CHAPTER 43
Abdominal Aortic Aneurysms
Peter G. Kalman
K. Wayne Johnston
INTRODUCTION
The first reported case of successful replacement of an
abdominal aortic aneurysm (AAA), performed by Charles
Dubost in 1951, ushered in the era of the current standard of
endoaneurysmorrhaphy and intraluminal graft insertion.[1]
The impetus for continuing to advance our knowledge
regarding the natural history of abdominal aortic aneurysms is
the serious risk of rupture. As recently reported in two
institutional studies, the overall 30-day mortality rate for
patients presenting to hospital with rupture was between 50
and 70%.[2,3] However, these studies derived their mortality
rates by including only those patients who arrived at the
emergency department after rupture in time for a diagnosis to
be made. Undoubtedly, the true mortality for all ruptured
aneurysms is higher, potentially reaching 90 –95%. The
prevalence of both small and large abdominal aneurysms
appears to be increasing, which may be the result of improved
imaging techniques and increased physician awareness,[4] but
a consensus has yet to be reached regarding the natural history
and indications for elective surgery.[5]
PATHOGENESIS, NATURAL HISTORY,
AND INDICATION FOR REPAIR
According to suggested standards, the definition of a true
arterial aneurysm is a permanent, localized (i.e., focal)
dilation of an artery with at least a 50% increase in diameter
compared with the normal. The most common site for a true
arterial aneurysm is the infrarenal abdominal aorta.
Arteriomegaly is a diffuse arterial enlargement (i.e., nonfocal)
with an increase in diameter of greater than 50% by
comparison with the normal diameter. Ectasia is characterized
by dilation less than 50% of the normal arterial diameter.[6]
Abdominal aneurysms are fusiform dilations that most
commonly begin distal to the renal arteries and are either
confined to the aorta or extend to involve the iliac arteries.
The average age at the time of surgical repair is 69–70 years,
with women accounting for 15 – 20% of all patients
undergoing both elective and emergency aneurysm repair as
Hobson/Wilson/Veith: Vascular Surgery: Principles and Practice, Third Edition, Revised and Expanded
DOI: 10.1081/0819-9-120024926
Copyright q 2004 by Marcel Dekker, Inc.
631
reported in the surgical literature.[7] As with cardiac disease, it
has been suggested that perhaps gender bias exists in patient
selection. However, the observed gender difference is not
significantly different when a family history for abdominal
aortic aneurysms is present.[8]
The landmark study in 1966 by Szilagyi et al. reported
observations in a large cohort of patients with asymptomatic
abdominal aneurysms and concluded that late survival as well
as the 5-year risk of rupture were related to aneurysm size.[9]
For aneurysms 6 cm or smaller in diameter, the 5-year
survival was 48% and risk of rupture was 20%, compared
with the 5-year survival of 6% and a rupture incidence of 43%
for aneurysms greater than 6 cm in diameter.[9] This report
had huge impact on decision making for several years and was
the basis for the 6 cm cut-off as the indication for elective
repair. This conclusion was made despite the extreme
variability by which aneurysms were measured in this study
(physical examination, plain x-ray at laparotomy, or autopsy).
The next report that affected surgical decision making was by
Darling et al. in 1977,[10] when 24,000 consecutive autopsies
at the Massachusetts General Hospital were reviewed over a
23-year period. This study supported the theory that aneurysm
rupture was related to size, but it was noteworthy that rupture
was also found in aneurysms less than 4 cm in diameter. On
the basis of these observations, the authors recommended that
even small aneurysms should be repaired because they are all
potentially lethal. The critical limitation of this and other
autopsy studies for the purpose of defining natural history is
the inaccuracy of size determination when the aneurysm is not
measured under conditions of physiologic blood pressure.
This would result in underestimating the actual size of the
aneurysm and therefore overestimating the risk at a given
size.
At present, there is general consensus among vascular
surgeons that the most significant predictor of rupture is size:
the 5-year risk for aneurysms between 5.5 and 5.9 cm is
approximately 20–25% (although this figure may be less), for
6 cm the risk is 35–40%, and for those greater than 7 cm the
rupture risk is greater than 75%. Most surgeons agree that
repair is indicated when, on balance, the risk of operation is
less than the risk of rupture for each size range. Although
many surgeons claim to have witnessed rupture of small
aneurysms, the risk of rupture is now generally considered to
www.dekker.com
632 Part Five. Aneurysms
be negligible and falls below the expected operative mortality
for elective repair.[11 – 16] Reports from population-based
studies support this view.[12,15] At the Mayo Clinic, Nevitt
et al. found that the risk of rupture for small aneurysms at
5 years was 0%.[12] Similar results were reported from a
population-based study from Sweden by Glimaker et al.[15]
Improved late survival has also been used as the
justification for early repair of small aneurysms, and it has
even been suggested to be a cost-effective procedure.[17]
Hallett et al. summarized a population-based cohort from the
Mayo Clinic and observed that the 5-year survival of patients
undergoing aneurysm repair was 62%, compared with the
expected survival of 83% for the general population.[16] The
decreased survival was primarily due to the prevalence of
coronary disease and questions the rationale for elective
surgery in this group, particularly in patients with small
aneurysms. Almost identical late survival (68% for 5 years)
was observed in the Canadian Aneurysm Registry.[18] Because
initial aneurysm size has been insufficient to reliably predict
risk, the next question to ask is “What is the growth rate for
small aneurysms, and is this important?” Bernstein and Chan
followed 99 patients who were at high general risk for surgery
for an average of 2.4 years (range 1 –9 years) with serial
ultrasonography at 3-month intervals.[19] For aneurysms
initially less than 6 cm, the mean expansion rate was
0.4 cm/year. The rupture risk for aneurysms less than 6 cm
in dimension was less than 5% during the follow-up period,
which supported the continuation of conservative therapy. The
protocol that was followed dictated that surgery was indicated
when the aneurysm reached 6 cm or expanded rapidly (greater
than 0.4 cm) at consecutive ultrasound follow-up. This study
had long-lasting influence with the conclusion that an
expansion rate of 0.5 cm between consecutive 6-month
follow-up sessions was a strong indication for elective
surgery. Later studies, however, failed to demonstrate the
relationship between expansion rate and risk of rupture.[12,20]
Whether or not aneurysm expansion is related to rupture risk,
there is significant variability observed in growth rate.[19,21,22]
In the Kingston aneurysm study, Brown et al. found that the
mean growth rate of aneurysms with an initial diameter range
of 4.5–4.9 cm was 0.7 cm/year and recommended that low-
risk patients should be considered for elective repair because
of the inevitable expansion of 5 cm.[14] Sterpetti et al. observed
a mean expansion of 0.48 cm/year, but the rate was found to be
extremely variable.[21] Using Cox regression, Cronenwett et al.
conducted a multivariate analysis of the variables predictive of
small aneurysm rupture[20] and found that the combination of
diastolic blood pressure, initial AP diameter, and degree of
chronic obstructive pulmonary disease were predictive of
aneurysm rupture at 5 years. The growth rate of small
aneurysms at The Toronto Hospital was determined from a
registry of 430 patients, 214 of whom had more than 3
evaluations at 6-month intervals.[23] Patients were followed on
average for 3.3 years, and the initial aneurysm size averaged
4 cm. During follow-up, 58.4% of patients had no change or a
decrease in aneurysm size, 25.3% had an expansion between
0.1 and 0.25 cm, 12.6% had an increase greater than 0.25 cm,
and only 3.7% enlarged greater than 0.5 cm.
There are pitfalls contained in the early studies of the
natural history of aneurysm expansion and rupture, not the
least of which is the source of the data, which originate from a
variety of designs (autopsy data and referral- and population-
based studies). New information from the large UK and
ADAM trials indicate that the rupture rate for aneurysms
between 4 and 5.5 cm is approximately 0.6–1% per year.
However, this must be monitored at 6-month intervals when
observation is selected for management.[24 – 26] The indication
for elective aneurysm repair in the elderly should generally
follow the same guidelines as repair in younger individuals. It
must be emphasized that patient selection is individualized,
and the final decision for management should be based on
physiologic rather than chronologic age. Numerous reports
have claimed that aneurysm repair can be conducted with an
acceptable operative mortality and morbidity in the
octogenarian, but it must be stressed that these cases are
usually highly selected.[27,28]
The clustering of abdominal aneurysms in families has been
cited in several studies and has raised the possibility that genetic
factors may be involved with both X chromosome–linked and
autosomal dominant patterns. Although no founder or common
link mutation has been identified,[29] this familial association
has been found to occur at an estimated incidence of
approximately 15–20%.[8,30 – 32] Powell et al. reported the
identification of an abnormality on the long arm of chromosome
16 and an association with familial aneurysms.[33] Additionally,
molecular defects of Type III procollagen have been identified
in Ehlers-Danlos syndrome (Type IV).[34] Type III procollagen
is a structural component of arterial walls, and it has been
postulated that the defect is related to aneurysm formation.
Recent advances in molecular biology have provided evidence
that altered gene expression may cause abnormalities in elastin
and collagen contents in aneurysms.[35] Because it is presently
difficult to determine the populations at risk for the development
of significant abdominal aneurysms, identification of familial or
genetic tendencies would be invaluable for initiating cost-
effective screening programs. Comprehensive genetic analysis
may serve a useful role in the future by identifying those
individuals who have a significant risk for aneurysm
development.
DIAGNOSIS
Seventy-five percent of abdominal aneurysms are asympto-
matic when first detected,[36] either on routine physical
examination or as an incidental finding on plain x-ray,
ultrasound, or computed tomographic (CT) scan. The
majority of those identified are small, usually measuring
less than 5 cm in dimension. An important feature to establish
when performing a physical examination on a patient with an
abdominal aneurysm is to try to determine the upper border of
the pulsation. If the palpating hand cannot get between the
upper border of the aneurysm and the costal margin, then
suprarenal extension should be suspected.
The most expeditious way to confirm the diagnosis of an
abdominal aneurysm and to accurately determine the size is to
obtain an ultrasonographic scan. Similarly, ultrasound is the
simplest method for serial follow-up of small aneurysms to
detect any change in size. Once it has been decided that
surgical intervention is indicated according to the sizing
obtained by ultrasound, CT scan provides valuable additional
 Chapter 43. Abdominal Aortic Aneurysms 633

Figure 43-1. (A) Spiral CT scan at the level of the renal arteries; left renal vein visualized crossing normal diameter aorta. (B) Three-
dimensional reconstruction of spiral CT (from A) demonstrating AAA and bilateral iliac aneurysms as well as visceral vessels.

information for operative planning. CT scan accurately length of neck, the location of the left renal vein, and the
delineates the anatomy of the aneurysm and in particular origins of major vessels. More recently, the spiral or helical
defines the proximal and distal extent of iliac involvement. CT complements and augments the anatomic information
Operative planning is enhanced by demonstration of the provided by conventional CT (Fig. 43-1). Moreover, the
634 Part Five. Aneurysms
resolution of spiral CT allows relatively accurate screening of
associated renal artery disease with a reported 92% sensitivity
and 83% specificity for a stenosis greater than 70%.[37]
Associated abnormalities can also be detected by CT scan
including venous abnormalities such as left-sided vena cava,
caval duplication, retroaortic renal vein or venous collar, as
well as nonvascular pathology such as various malignancies,
cholelithiasis, horseshoe kidney, and renal tumors and cysts.
Contrast aortography is playing a less significant role in
the routine preoperative treatment of the patient, although it
remains the standard for some vascular surgeons. The
majority obtain aortograms only in selected situations—for
example, when associated occlusive disease is suspected and
the aortogram would assist the surgeon in planning the
procedure or in the case of poor definition of the aortic neck as
a result of aortic lengthening and buckling. An arteriogram is
valuable in the case of internal iliac aneurysms for
determining pelvic blood flow because at least one internal
iliac artery should be maintained to avoid colon ischemia (and
vasculogenic impotence in men). When this is not possible,
reimplantation of a large patent inferior mesenteric artery can
be performed. Other indications for an arteriogram include
juxtarenal or suprarenal aneurysms that require detailed
anatomy of visceral arteries and, likewise, clinical suspicion
of visceral arterial occlusive disease (i.e., severe hypertension
or postprandial pain and weight loss). Less commonly, as with
cases of horseshoe and pelvic kidneys, an arteriogram is
useful for demonstration of the unpredictable arterial supply
or when an aberrant, low renal artery may have been
suggested on CT scan. Finally, potential candidates for
endovascular repair require detailed mapping of the aorta and
iliacs for sizing and positioning of the endoluminal prosthesis.
Magnetic resonance imaging has all the benefits of CT scan
and aortography combined, and the availability is increasing.
The main disadvantages at present include the cost and
contraindications in many patients because of metallic devices
such as monitoring lines, pacemakers, and surgical clips. A
major disadvantage is the slow acquisition time and the resulting
claustrophobic distress experienced by some patients.
MEDICAL RISK ASSESSMENT
Coronary artery disease (CAD) is the most common cause of
death after elective aneurysm repair, and considerable effort
is directed toward preoperative detection of cardiac dysfunc-
tion and CAD.[38 – 40] Noninvasive evaluations are the most
frequently used screening methods because features of the
medical history are unreliable for accurately predicting
cardiac risk,[41 – 43] and it has been estimated that silent
myocardial ischemia occurs in 2.5–10% of asymptomatic
patients with no previous documentation of CAD.[44]
Unfortunately, the false-positive rates for exercise tread-
mill testing have been reported to be as high as 40%,[45,46] and
echography, radionuclide ventriculography, and dipyrida-
mole-thallium scanning all have low positive predictive
value. It has been reported that the latter tests identify 30 –
50% of vascular surgery patients who are at increased risk for
a cardiac event, but less than 25% of those identified actually
experience adverse cardiac events postoperatively.[47,48]
Guidelines have been established recently for preoperative
screening for patients undergoing noncardiac surgical
procedures.[49] These guidelines stratify patients into risk
groups based on history and symptoms and are designed to
help identify patients who may benefit from coronary
revascularization before their elective procedure.
Cardiac intervention is rarely necessary to simply lower
the risk of surgery, and those patients who ultimately undergo
coronary revascularization would have done so solely on the
merits of their severe symptoms (unstable or severe angina,
symptomatic arrhythmias, severe valvular disease). There is
no strong evidence demonstrating that prophylactic coronary
revascularization improves perioperative mortality or long-
term survival rates.
OPERATIVE TECHNIQUES
The typical patient undergoing elective AAA repair is
monitored intraoperatively with an ECG monitor, radial
arterial line, urinary catheter, and selective use of pulmonary
artery catheters. A large-bore peripheral intravenous line and
a central venous line are available for rapid infusion if
required. It is becoming increasingly routine for surgeons to
use an autotransfusion device with increasing patient
awareness of the uncommon but potential transmission of
diseases with blood products.
For elective AAA repair, most surgeons favor the midline
transabdominal incision, although recently there has been
increasing interest in the retroperitoneal approach[50 – 53] (see
Chapter 84).
Supporters for the transabdominal approach cite surgeon
familiarity and the ability to inspect the viscera for potential
concomitant pathology. Proponents of the retroperitoneal
approach claim less intraoperative hypothermia, less third
space fluid loss, and fewer postoperative cases of respiratory
problems and ileus. Furthermore, the retroperitoneal approach
may be useful in patients who have had multiple abdominal
procedures, pararenal aneurysms or those with stomas.
Ultimately, the best approach is the one with which the
surgeon is most comfortable, although knowledge of both
procedures should be part of the surgeon’s armamentarium to
ensure that all situations and unusual aortic problems can be
managed most appropriately.
The feasibility of minimally invasive endoluminal AAA
repair has been demonstrated, but the long-term results are
unknown. May et al.[54] compared endoluminal versus open
repair and found that the endoluminal technique had the
disadvantage of a higher early failure rate but, when
successful, resulted in shorter hospital length of stay, shorter
ICU stay, and less blood loss than open repair. At this point it
is fair to say that this technology is still evolving but
promising and should still be considered experimental.
RESULTS OF OPEN REPAIR
Contemporary operative results are summarized in the
multicenter, prospective Canadian Aneurysm Study,[55,56]
 Chapter 43. Abdominal Aortic Aneurysms 635

which consisted of 680 consecutive patients who underwent successful outcome depends on accurate anatomic diagnosis
AAA repair performed by 72 participating members of the and choosing the optimal exposure and method for proximal
Canadian Society for Vascular Surgery between March 1 and aortic control.
December 1, 1986. The operative morbidity and mortality is
summarized in Table 43-1. Regular follow-up has been
maintained at 6- to 9-month intervals through contact with the
surgeon, family physician, or patient to update overall status,
JUXTARENAL ANEURYSM AND THE
morbidity, intercurrent illnesses, mortality, and cause of DIFFICULT PROXIMAL
death. This registry is a population-based study because the ANASTOMOSIS
patients represent a heterogeneous group free from referral
center bias; this classification is supported by the fact that the
overall operative mortality rate for patients in the study was When the proximal anastomosis is technically difficult because
4.7% ðn ¼ 32Þ and was unrelated to any surgeon character- it is close to the origin of the renal arteries, suprarenal cross-
istics (i.e., age, community vs. university practice type, city clamping or left renal vein ligation can be used to gain proximal
population, or hospital size). control and improve exposure. It is often safer and simpler to
obtain proximal control above the celiac rather than the
immediate suprarenal aorta because the risk of embolic debris to
the renal arteries is less significant. If a midline incision is used,
SITUATIONS ENCOUNTERED DURING the stomach is retracted inferiorly and the lesser sac is entered
through the gastrohepatic omentum. The right crus of the
AAA REPAIR AND THEIR SOLUTIONS diaphragm is carefully divided using cautery, and the
supraceliac aorta is exposed. With a left retroperitoneal
Certain situations that are encountered occasionally during approach, the upper viscera are rotated medially exposing the
AAA surgery make the procedure more difficult and add left crus of the diaphragm, which is then divided with cautery,
significant risk to the patient, thus encouraging preoperative thus exposing the aorta. In selected cases where a huge
recognition and demanding modification of the procedure. A juxtarenal aneurysm limits upper abdominal exposure, a low,
limited thoracoabdominal incision is helpful to obtain proximal
control of the thoracic aorta. Aortic control at each of these sites
Table 43-1. Operative Morbidity and is used only until the proximal anastomosis is completed, and
Mortality in 680 Nonruptured AAA then the clamp is moved distally to allow visceral perfusion
Repairs while the distal repair is performed. The proximal anastomosis
Postoperative bleeding of a juxtarenal repair often includes the lower margins of the
Transfusion 2.3% renal arteries, and one of the challenges is preservation of renal
Repeat operation 1.4% function. Patients with preexisting renal dysfunction are at even
Limb ischemia 3.5% greater risk.
Graft thrombosis 0.9% In the Canadian Aneurysm Study[55] a suprarenal clamp
Distal thromboembolism 3.3% was necessary in 6.8% of cases, and this group suffered a
Amputation 1.2% higher incidence of renal damage. The mortality rate and
Graft infection 1 case incidence of cardiac events was not increased, therefore
Cerebrovascular event 0.6% suprarenal clamping is an option when indicated. For
Paraplegia 1 case facilitation of the upper anastomosis, the left renal vein was
Cardiac event 15.1% ligated in 7.9% of cases, which resulted in an increased risk of
MI 5.2% renal damage (i.e., elevation of creatinine and increase in
CHF 8.9% renal failure requiring dialysis). Left renal vein ligation
Arrythmia 10.5% should rarely be performed and only in difficult cases where
New arrythmia 8.4% retraction of the vein gives inadequate exposure.
Respiratory failure 8.4%
Renal damage 5.4%
requiring dialysis 0.6% PLANNING THE DISTAL
Diarrhea
No ischemic colitis 7.1%
ANASTOMOSIS
With ischemic colitis 0.6%
Prolonged ileus 11% An aortic tube graft or bi-iliac graft is recommended unless
Wound infection significant iliofemoral occlusive or aneurysmal disease is
Superficial 1.5% present because patients rarely require subsequent reoperation
Deep 0.5% for occlusive or aneurysmal disease of the iliofemoral segment.
Coagulopathy 1.1% In the Canadian Aneurysm Study[55] the distal anastomosis was
Mortality (all causes) 4.7% performed as a tube graft in 38.5%, a bi-iliac graft in 30.7%, an
Cardiac 3.3% iliac/femoral graft in 6.5%, and a graft to both femoral arteries in
24.3%. In contrast to patients with a totally intra-abdominal
Source: Ref. 56. graft, those with a femoral anastomosis had an increased
636 Part Five. Aneurysms
incidence of wound infection (0.9% vs. 3.0%, respectively) and
graft thrombosis (0.2% vs. 2.5%, respectively). Other morbidity
and mortality rates were the same.
MAINTENANCE OF HINDGUT AND
PELVIC PERFUSION
There is an increased risk of distal colon ischemia when
pelvic blood flow is significantly reduced, and it is an
established surgical principle that internal iliac artery flow
should be maintained on at least one side, although recently
questioned by Mehta and Veith. The criteria for reimplanta-
tion of the inferior mesenteric artery is not clearly defined but
certainly should be considered in the case of an unusually
large inferior mesenteric artery or angiographic evidence of
superior mesenteric artery stenosis or if the collateral
circulation between the superior and inferior mesenterics is
poorly developed. Further considerations while in the
operating room include poor backflow from a patent inferior
mesenteric artery even after completion of the distal
anastomosis, concern that pelvic flow has been reduced by
the reconstructive procedure and concern about the
appearance of the colon. Methods such as inferior mesenteric
stump pressure measurement, intraoperative Doppler, photo-
plethysmography, or colon pH measurement provide
objective assessment, but there is no evidence that these are
superior to clinical assessment.
In the Canadian Aneurysm Study [55] the inferior
mesenteric artery was reimplanted in 4.8% of cases. When
internal iliac flow was maintained to one or both sides, the
incidence of colon ischemia was 0.3%, whereas, when it was
interrupted bilaterally, the incidence increased to 2.6%.
INFLAMMATORY ANEURYSMS
Inflammatory aneurysms occur in approximately 5–10% of
surgical cases and are therefore usually unexpected until the
time of elective repair unless a preoperative CT scan is routinely
performed. There are many proposed etiologies for inflamma-
tory aneurysms, but none has been unanimously embraced.[57]
They are important to recognize because the periaortic fibrotic
tissue can be densely adherent to the duodenum, sigmoid colon
and mesocolon, the ureters, vena cava and left renal vein, which
may complicate the operative repair. These aneurysms are
characterized histologically by extensive adventitial fibrosis and
mononuclear cell infiltration with lymphoid follicle formation.
The erythrocyte sedimentation rate is frequently elevated and
the test for C-reactive protein may be positive. CT typically
shows a 1-cm-thick, homogeneous wall with contrast enhance-
ment around the aneurysm, which may be visualized external to
the rim of wall calcification (Fig. 43-2).
The principles of operative management are now well
established: (1) no dissection of the adherent duodenum or
sigmoid mesocolon off the aneurysm, (2) perform proximal
cross-clamping of the aorta at the diaphragm if impossible
below the renal arteries, (3) perform balloon occlusion of the
iliac arteries as the inflammatory reaction usually makes iliac
dissection hazardous, and (4) perform the proximal
anastomosis by the inclusion method if requrired.
In the Canadian Aneurysm Study[48,49] inflammatory aortic
aneurysms were observed in 4.5% of cases, and there was no
difference in age, sex, or atherosclerotic risk factors. The
incidence of pain was not significantly higher in patients with
inflammatory aneurysms; unlike previously reported series,
however, there was no specific diagnostic feature that
distinguished an inflammatory aneurysm from a standard aortic
aneurysm. The surgery appeared more difficult as reflected by
the higher volume of blood transfused and more frequent use of a
cell saver, as well as the higher frequency of renal vein ligation,
although morbidity and mortality was not increased.
HORSESHOE KIDNEY
The horseshoe kidney is relatively uncommon, occurring with a
frequency of 0.25% in the general population. The majority are
fused at the lower poles with an isthmus, which may simply be a
fibrous band or renal tissue with a separate blood supply. The
surgical challenges are the presence of bulky isthmus,
anomalous ureters, and renal blood supply.[58] The ureters may
be multiple and cross in aberrant places anterior to the isthmus,
and preservation of the renal blood supply and collecting system
are the goals of reconstruction. Renal ischemia may result if a
bulky isthmus is divided, and urine leakage may occur, which
may be a serious problem because of the prevalence of coexisting
chronic urinary infections. A retroperitoneal approach is ideal
because the left kidney and isthmus can be elevated to expose the
aorta without division of the isthmus.
All patients with the diagnosis made preoperatively should
undergo arteriography to define the renal artery anatomy,
which can range from single renal arteries to multiple arteries
from the aorta, iliac, and visceral arteries. The surgical options
include bypass or reimplantation of an artery or cuff of aorta
into the graft depending on the individual circumstance.
CONCOMITANT INTRA-ABDOMINAL
PATHOLOGY
Concomitant intra-abdominal pathology frequently makes
surgical judgment more challenging. Important questions
arise with respect to priority and performance of a one- or
two-stage procedure. As a general rule, AAA repair should
not be combined with other procedures that may result in
bacterial contamination (e.g., gastrointestinal and genitour-
inary), and management is dependent on the type and clinical
activity of the associated condition, where the symptomatic
condition always takes priority.
COLORECTAL TUMORS
The priority decision with colorectal tumors depends on the
disease that requires intervention most urgently. If the tumor is
found incidentally during elective, asymptomatic AAA repair,

Figure 43-2. Spiral CT scan of inflammatory AAA. Note thick, homogeneous enhancing rind external to the rim of wall calcification.
most surgeons would repair the aneurysm first and recommend
colon resection after a 4- to 6-week delay. In the unusual
circumstance where the incidental tumor appears obstructive,
then colon resection would take priority. If the aneurysm and
colon tumor are both detected preoperatively, then the priority is
given to the most ominous lesion (e.g., a colon obstruction
would be relieved before an asymptomatic AAA, and, similarly,
a symptomatic AAA would be dealt with before a nonobstruct-
ing colon lesion). Combined procedures would only be
entertained on rare occasions when a symptomatic AAA is
encountered at the same time as an obstructive colon tumor. In
this last scenario, the aneurysm is repaired first followed by the
colon resection, after careful retroperitoneal closure.
RENAL TUMORS
Renal tumors are occasionally found at the same time as an
asymptomatic AAA. In general, there is no contraindication
for simultaneous repair unless obvious sepsis is evident from
an obstructive lesion.
GALLBLADDER DISEASE
Cholelithiasis is the most common abdominal pathology
found in the AAA patient, with estimates of prevalence that
range from 5 to 20%.[59] Gallstones are most commonly
asymptomatic and rarely cause acute symptoms after AAA
repair. Ouriel et al. found an incidence of cholecystitis in only
1.1% of 703 elective AAA repairs postoperatively, and the
Chapter 43. Abdominal Aortic Aneurysms 637
underlying cause was acalculous in 75%.[59] Asymptomatic
gallstones are generally left alone, whereas concomitant
cholecystectomy is occasionally considered when symptoms
from cholecystitis occurred relatively recently and the AAA
repair was entirely uneventful.
RUPTURED AAAS
The sudden onset of severe abdominal and/or back pain and
syncope should alert one to the presence of a ruptured AAA.
Important physical findings include hypotension (measured or
a history of syncope, perspiration), tachycardia, abdominal
pain, and a mass that may or may not be pulsatile. With
symptomatic but intact aneurysms, the severe back and
abdominal pain may be indistinguishable from that of a
rupture, but the important feature by history is the absence of
hypotension and confirmation of an intact aneurysm by CT
scan. Symptoms in the latter situation may be related to acute
expansion of the aneurysm wall, intramural hemorrhage, or
wall degeneration. Symptomatic, intact aneurysms should be
considered urgent, but not necessarily emergent because in
many cases they can be managed surgically in a more elective
manner.
With a suspected diagnosis of rupture, the patient is
immediately transferred to the operating room. In this setting,
insertion of large-bore intravenous access and resuscitation
with fluid and blood products can proceed while preparation
for operative intervention is begun. If the patient’s condition
is stable preparation can proceed in a controlled manner,
whereas if the patient suddenly decompensates the surgical
team is ready for immediate intervention. Arterial access is
638 Part Five. Aneurysms
established to allow accurate blood pressure measurements
and for sampling for hematocrit and blood gases. The patient
is prepped and draped awake followed by rapid induction and
intubation, which frequently causes hypotension when the
adaptive sympathetic drive is released.
The usual exposure is through a generous midline incision,
and rapid control of the aorta is achieved with digital
compression or compression with an aortic occluder (against
the vertebrae at the supraceliac level), an aortic cross-clamp
(infrarenal, suprarenal or supraceliac), and occasionally an
intra-aortic balloon. Distal control can usually be obtained by
clamping the common iliac arteries, but balloon occlusion
catheters are sometimes safer when visualization of the iliacs
is poor. Once proximal and distal control is securely achieved,
graft placement is performed as in the elective situation once
the decision regarding configuration is made (tube vs.
bifurcation graft).
The immediate and late survival rates after repair of a
ruptured AAA remain low in spite of improvements in
surgical care. In the Canadian Aneurysm Registry the in-
hospital survival rate for patients with a ruptured AAA was
50% and 49% at 1 month,[60] which is similar to the 53%
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Chapter 43. Abdominal Aortic Aneurysms 639
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640 Part Five. Aneurysms
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CHAPTER 44
Thoracoabdominal Aortic
Aneurysms
Larry H. Hollier
Marcus D’ayala
Alfio Carroccio
INTRODUCTION
Thoracoabdominal aortic (TAA) aneurysms can be defined as
aneurysms that involve the descending thoracic and
abdominal aorta. Although less common than abdominal
aortic aneurysms, TAA aneurysms appear to be associated
with a worse prognosis.[1,14] In these reports, the 2-year
survival rate of untreated patients with these extensive
aneurysms was less than 30%, with about half of all deaths
occurring as a result of aneurysm rupture.[2] The surgical
repair of these complex aneurysms can improve this poor
survival rate significantly.
As demonstrated by Crawford and colleagues, a 2-year
survival rate of about 70% can be expected following opera-
tive intervention.[3] However, this operative procedure
requires entering both the thoracic and abdominal cavities
and is associated with significant morbidity and mortality.
Such procedures can challenge even the most experienced
vascular surgeons. Although progress in the perioperative
care of patients with TAA aneurysms has led to a decrease in
the complication rate associated with this procedure, death,
paraplegia, and renal failure are still commonly seen. Most
authors now quote operative mortality rates of less than 10%,
with an overall rate of paraplegia of approximately 4 –20%,
depending upon the extent of the aneurysm, and a 5 –30%
incidence of renal failure.[4 – 9]
The recommendation to proceed with surgical repair must,
therefore, take into account this high complication rate, which
must be balanced against the risk of aneurysm rupture.
Careful preoperative assessment of coexistent comorbidities,
standardized surgical techniques, and specific guidelines for
postoperative management of these patients can have a
favorable impact on the morbidity and mortality associated
with this procedure, usually allowing for safe and effective
repair.
Hobson/Wilson/Veith: Vascular Surgery: Principles and Practice, Third Edition, Revised and Expanded
DOI: 10.1081/0819-9-120024927
Copyright q 2004 by Marcel Dekker, Inc.
641
ETIOLOGY AND CLASSIFICATION
Most TAA aneurysms are true aneurysms that involve all layers
of the aortic wall. They occur most commonly as a result of
degenerative disease associated with atherosclerosis but may
also be seen as a result of cystic medial necrosis, seen in
association with Marfan’s syndrome and other connective tissue
disorders such as Ehlers – Danlos syndrome.[10] Another
common cause of TAA aneurysms is chronic dissection.
Currently, degenerative aneurysms are considered to be
multifactorial in nature but are frequently referred to as
atherosclerotic. Elastin degradation and collagen failure are
believed to be the primary initiating events, and the importance
of genetic factors is well recognized.[11] Giant cell arteritis, such
as Takayasu’s arteritis, and other arteritides, trauma, and
bacterial or fungal infections are etiologies seen less
commonly.[10] Risk factors for patients with TAA aneurysms
are shown in Table 44-1. When compared to patients with
nondissecting aneurysms, patients with dissecting aneurysms
differ with respect to several important risk factors. This
difference has an effect on the operative mortality, incidence of
postoperative complications, and late survival following repair
(Tables 44-2 and 44-3).[12,13]
Whereas the incidence of hypertension is equally high in
both groups, preexisting coronary artery disease, chronic
obstructive pulmonary disease (COPD), chronic renal failure,
and cerebrovascular disease are more prevalent in patients with
nondissecting aneurysms. These patients have a higher
incidence of postoperative cardiac, pulmonary, and renal
complications, whereas neurologic deficits occur more common
in patients with dissecting aneurysms. Additionally, dissecting
aneurysms generally are associated with a worse prognosis, with
higher operative mortality and lower late survival rates.
Regardless of their etiology, TAA aneurysms can be
classified according to the extent of aneurysmal involvement
www.dekker.com
642 Part Five. Aneurysms

Table 44-1. Comorbid Conditions in Patients with TAA Aneurysms

Author/year COPD (%) CAD (%) CVD (%) Renal failure (%) Hypertension (%) DM (%) Smoking (%)

Hollier/1988 42 67 12 38 NA 6 90
Golden/1991 37 42 NA 16 71 NA 66
Cox/1992 41 63 15 16 77 8 84
Svensson/1993 40 31 15 13 73 5 NA
Schepens/1994 27 17 12 34 66 NA NA
Safi/1994 36 13 12 29 67 NA NA
Kashyap/1997 NA 67 NA 24 85 8 NA

TAA = Thoracoabdominal aortic.

COPD = Chronic obstructive pulmonary disease.
CAD = Coronary artery disease.
CVD = Collagen vascular disease.
DM = Diabetes mellitus.
NA = Not applicable.

affecting the descending thoracic and abdominal aorta. Type I
TAA aneurysms are those that arise just distal to left subclavian
artery and involve the entire thoracic aorta and upper abdominal
aorta proximal to the renal arteries. Type II TAA aneurysms
involve most of the descending thoracic aorta and the abdominal
aorta, from the left subclavian artery to the level of the iliac
bifurcation. Type III TAA aneurysms extend from the mid-
descending thoracic aorta and include the abdominal aorta with
involvement of the visceral segment. Type IV TAA aneurysms
are those that involve the abdominal aorta and extend above the
visceral vessels to the level of the diaphragm. This classification
system, proposed initially by Crawford and colleagues,[3] has
led to uniform reporting standards that allow for meaningful
comparisons between series. It is also of prognostic significance
because complication rates following surgical repair vary
according to the extent and type of aneurysm undergoing repair,
with the more extensive type I and II aneurysms carrying a
higher postoperative complication rate, particularly with respect
to spinal cord ischemia and renal failure.
NATURAL HISTORY
Few studies in the literature are available on the natural history
of TAA aneurysms. However, it appears that the natural history
of these aneurysms is similar to that of aneurysms elsewhere.
With time, most TAA aneurysms increase in size and rupture
rates, with larger aneurysms expanding at a faster rate and
rupturing more frequently. Although aneurysm rupture is seen
most commonly in patients with large aneurysms, some large
aneurysms can remain stable for years, making expansion rates
and rupture unpredictable in any individual patient.
TAA aneurysms seem to have a worse prognosis when
compared with abdominal aortic aneurysms. In a population-
based study, Bickerstaff and colleagues reported a 2-year
survival rate of 29% for untreated patients with large thoracic
and TAA aneurysms.[14] Aneurysm rupture occurred in 74% of
patients observed during this period, with an associated
mortality rate of 94%. Rupture and death were seen more
commonly in patients with dissecting aneurysms as opposed to
nondissecting aneurysms. The overall 5-year survival rate
following diagnosis was only 13%, which compared poorly with
the 75% survival rate for an age-matched population of patients
without aneurysms.
Other reports confirmed the poor results associated with
nonoperative management of TAA aneurysms. In a study by
Crawford and DeNalale, 76% of patients with TAA aneurysms
who remained untreated because of the small size of their
aneurysms, advanced age, or associated comorbidities died
within 2 years of diagnosis.[2] Fifty-two percent of these deaths
occurred as a result of aneurysm rupture.

Table 44-2. Incidence of Postoperative Complications

According to Etiology Table 44-3. Survival Rate Following TAA Aneurysmal
Repair
Complication Nondissecting (%) Dissecting (%)
Year Nondissecting (%) Dissecting (%)
Respiratory 32 12
Cardiac failure 11 7 1 80 74
Stroke 3 4 5 61 50
Paraplegia 13 25 10 33 –
Renal failure 21 18
TAA = Thoracoabdominal aortic.
Source: Modified with Permission from Panneton, J.M.; Hollier, L.H. Source: Modified with Permission from Panneton, J.M.; Hollier, L.H.
Nondissecting Thoracoabdominal Aortic Aneurysms: Part I. Ann. Vasc. Nondissecting Thoracoabdominal Aortic Aneurysms: Part I. Ann. Vasc.
Surg. 1995, 9, 503– 514 and Panneton, J.M.; Hollier, L.H. Dissecting Surg. 1995, 9, 503–514 and Panneton, J.M.; Hollier, L.H. Dissecting
Descending Thoracic and Thoracoabdominal Aortic Aneurysms: Part II. Descending Thoracic and Thoracoabdominal Aortic Aneurysms: Part II.
Ann. Vasc. Surg. 1995, 9, 596–605. Ann. Vasc. Surg. 1995, 9, 596–605.
 Chapter 44.
More recently, Cambria and colleagues evaluated 57 patients
with nondissecting TAA aneurysms who were initially managed
nonoperatively.[15] Thirty-four of these 57 patients or 60% died
during the follow-up period, which averaged 37 months. The
most common cause of death was cardiopulmonary disease,
accounting for 24% of all mortalities; followed by aneurysm
rupture, responsible for 19% of deaths. The 2- and 5-year
survival rates for those patients who remained untreated were
52% and 17%, respectively. While these results are more
favorable than those reported by other investigators, this study
excluded patients with dissecting TAA aneurysms, which are
known to have a worse prognosis. Currently, we recommend
elective aneurysm repair for those patients in whom the
maximum aortic diameter exceeds 6 cm in good risk patients or
greater than 7 cm in patients who represent a greater than
average risk of surgery.
DIAGNOSIS
TAA aneurysms usually cause no specific symptoms and are
diagnosed incidentally as a result of imaging studies
undertaken for other reasons; occasionally they may present
with a number of signs and symptoms depending upon their
extent and location. In a recent study of over 1500 patients
Figure 44-1. Chest x-ray showing widening of the mediastinal shadow by an aneurysm of the descending thoracic aorta.
Thoracoabdominal Aortic Aneurysms 643
who underwent TAA aneurysmal repair over a 30-year
period, only 38% were truly asymptomatic; but while most
patients described one or more symptoms, they were not
generally thought to be related to their aneurysm.[7] The
median age of patients with TAA was 66 years, with males
outnumbering females and accounting for 65% of the patients.
As TAA aneurysms enlarge, they can compress adjacent
structures, which may result in pain that can be referred to the
chest, back, flank, or abdomen. However, pain may also be
indicative of aneurysm rupture or dissection, which is associated
with a high morbidity and mortality. Therefore, the complaint of
pain in a patient with a known TAA aneurysm, irrespective of its
location, mandates rapid preoperative evaluation and expedi-
tious repair if rupture appears imminent.
Other signs and symptoms may include dyspnea, cough,
wheezing, or recurrent pulmonary infections, which occur as
a result of tracheobronchial obstruction from extrinsic
compression in the superior mediastinum. Dysphagia and
weight loss from esophageal obstruction have also been
reported, and erosion into the tracheobronchial tree or
esophagus may lead to hemoptysis or hematemesis. Erosion
can also occur into the vena cava, resulting as an aortocaval
fistula, presenting with lower-extremity edema and con-
gestive heart failure. A less common complaint is hoarseness,
which can occur from stretching of the left recurrent laryngeal
nerve by the enlarging aneurysm. Finally, embolization of
644 Part Five. Aneurysms
Figure 44-2. Operative photography of a thoracoabdominal aneurysm.
thrombotic or atheromatous debris may result in visceral or
lower extremity ischemia, or paraplegia may occur from
embolization or thrombosis of the spinal arteries.
In asymptomatic patients, the presence of a pulsatile
abdominal mass or suspicious chest x-ray (CXR) (Fig. 44-l)
may suggest the diagnosis of a TAA aneurysm (Fig. 44-2).
This diagnosis may be confirmed by computed tomography
(CT) scan with intravenous contrast (Fig. 44-3), magnetic
resonance imaging (MRI) (Fig. 44-4), transesophageal
echocardiography, or conventional angiography (Fig. 44-5).
It is our belief that the combination of CT scanning with IV
contrast and angiography provide the optimum anatomic
information necessary before surgical reconstruction. These
imaging studies accurately establish the proximal and distal
extent of the aneurysm, and ascertain the presence or absence
of dissection, rupture, or associated occlusive disease that
might involve the lower extremities, renal or visceral arteries.
PREOPERATIVE EVALUATION
Patients with TAA aneurysms frequently have comorbid
conditions, such as advanced age, pulmonary dysfunction,
cardiovascular disease, cerebrovascular disease, and renal
insufficiency (Table 44-1) which increase the morbidity and
mortality associated with aneurysm repair. A thorough
preoperative evaluation, therefore, is necessary to improve
the overall results associated with operative intervention.
A large percentage of patients undergoing TAA aneurysm
repair are heavy smokers and suffer from underlying COPD.
Respiratory complications have been the most common
complications seen in the postoperative period and have been
a major cause of morbidity and mortality. Their presence
decreased the 30-day survival rate from 98% to 80%. In a
study by Svensson and colleagues, only 19% of patients with
TAA aneurysms had never smoked. COPD was present in
56% of the patients, and 58% of these developed respiratory
failure following surgical repair.[16] Overall, 43% of patients
required ventilatory support for more than 2 days after
operative intervention and 15% required a tracheostomy.
Other studies have also established respiratory failure as
the most common complication following TAA aneurysm
repair.[17] However, certain measures, such as cessation of
smoking for at least one week before surgical repair, the use
of bronchodilators, corticosteroids, and antibiotics for
treatment of bronchitis, as well as good pulmonary toilet in
the postoperative period, can substantially decrease the high
incidence of respiratory complications.
A history of heavy smoking, productive cough, dyspnea on
exertion, or the diagnosis of COPD are generally considered
indications for preoperative pulmonary function tests and
arterial blood gas analysis. The finding of a significant
decrease in forced vital capacity (FVC) or forced expiratory
volume over one second (FEV1) is associated with an increase
 Chapter 44.
Figure 44-3. Computed tomographic scan demonstrating an inflammatory thoracoabdominal aneurysm. Note the contrast-enhancing
inflammatory wall of the aneurysm (arrow).
in postoperative pulmonary complications. Preoperative
optimization of respiratory function in these difficult patients
is of utmost importance and appears to modify the
postoperative pulmonary complications.
Cardiovascular and cerebrovascular disease are also
common comorbid conditions found in patients with TAA
aneurysms. As demonstrated by Svensson and colleagues,
over 30% of patients with TAA aneurysms will have
associated significant cardiac disease, with an additional 15%
having cerebrovascular disease defined by the presence of a
previous transient ischemic attack, stroke, or carotid
endarterectomy.[7] Echocardiography and a dipyridamole
thallium scan are obtained routinely in asymptomatic and in
sedentary, minimally symptomatic patients, because of the
high incidence of underlying silent cardiovascular disease.
These studies attempt to assess cardiac risk by evaluating
ventricular function, excluding valvular insufficiency, and
determining whether a significant segment of myocardium is
at risk for ischemia. Patients with more severe cardiac
symptoms or those with poor ventricular function or evidence
of significant thallium redistribution should undergo coronary
angiography.[18] Cardiac revascularization before aneurysm
repair is recommended in the presence of severe reconstruc-
tible coronary artery disease.
Carotid artery duplex studies are also performed routinely
as part of the preoperative assessment of patients with TAA
Thoracoabdominal Aortic Aneurysms 645
aneurysms, regardless of whether symptoms of cerebrovas-
cular insufficiency are present. Carotid endarterectomy is
recommended before aneurysm repair in the presence of a
high-grade stenosis. This approach, which is usually well
tolerated, will not significantly delay aneurysm repair yet
decreases the incidence of postoperative stroke.
OPERATIVE TREATMENT
Successful repair of TAA aneurysms requires close
cooperation between the anesthesiologist and surgeon. Before
induction of general endotracheal anesthesia, a pulmonary
artery catheter and right radial arterial catheter are placed to
monitor the patient’s hemodynamics and optimize cardiac
function. Intraoperative transesophageal echocardiography is
also used throughout the procedure to follow the patient’s
volume status and detect wall-motion abnormalities sugges-
tive of myocardial ischemia. At least two large-bore IV
catheters are inserted, with one connected to a rapid infusion
device (RIS, Haemonetics). Additionally, an autotransfusion
device (Cell Saver, Braintree, MA) is used to minimize the
need for banked blood. An indwelling urinary catheter is
placed, and a dose of IV antibiotics is administered before
646 Part Five. Aneurysms

Figure 44-4. (A) Magnetic resonance imaging demonstrating an intercostal artery arising from a thoracoabdominal aortic aneurysm.
(B) High-resolution magnetic resonance imaging showing the anterior spinal artery originating from the artery of Adamkiewicz.
 Chapter 44.
Figure 44-5. Aortogram of a patient with a thoracoabdominal
aortic aneurysm.
incision. The patient is then intubated with a dual lumen
endotracheal tube, which allows for selective deflation of the
left lung, a maneuver that facilitates exposure of the thoracic
aorta to the level of the left subclavian artery. Proximal
exposure to this level is often necessary, particularly for
patients with type I and II TAA aneurysms. For cerebrospinal
fluid (CSF) drainage, we also insert a spinal catheter into the
4th lumbar interspace, draining fluid as needed to maintain
CSF pressure below 10 mmHg. In both experimental and
clinical studies this technique has been shown to decrease the
incidence of postoperative paraplegia from spinal cord
ischemia.[9,22,23] An epidural catheter is placed above the
spinal catheter for postoperative pain control.
A decision is then made regarding the need for distal aortic
perfusion, which can be achieved through one of several
techniques and allows for retrograde perfusion of the
intercostal, lumbar, renal, celiac, superior mesenteric, and
iliac arteries. This technique reduces the extent and severity
of ischemia distal to the aortic cross-clamp while the proximal
anastomosis is constructed and critical intercostals are
reimplanted. Whereas several authors have reported a
decrease in the incidence of postoperative complications
(e.g., paraplegia and renal failure) by using distal aortic
perfusion to reduce ischemia time to the spinal cord and
Thoracoabdominal Aortic Aneurysms 647
abdominal viscera, others have noted equally good results by
using a simple clamp-and-sew technique.[8,9,19,20]
We favor distal aortic perfusion for most patients with type
I and II aneurysms, reserving a clamp-and-sew technique for
those patients with type III and IV aneurysms in whom
reconstruction can usually be achieved in under 30 minutes.
Distal aortic perfusion has an additional advantage in that it
also minimizes the increase in afterload associated with
placement of a proximal aortic cross-clamp, decreasing the
need for pharmacologic control of proximal hypertension and,
therefore, the incidence of cardiac complications.
Different options are available for distal perfusion,
including femorofemoral bypass, atriofemoral bypass, an
external heparin-bonded shunt from the ascending aorta to the
descending or abdominal aorta, and axillofemoral bypass.
Each has certain advantages and disadvantages.
Femorofemoral bypass involves placing a venous cannula
through the femoral vein into the right atrium, with an arterial
cannula placed into the distal aorta or proximal iliac artery by
way of the femoral artery. This approach requires the use of
pump perfusion along with a membrane oxygenator and heat
exchanger, with full systemic heparinization. Exposure of the
femoral vessels through a separate incision is also required. In
general, flow rates of about 2–3 L per minute are sufficient to
maintain a distal perfusion pressure above 60 mmHg.
Atriofemoral bypass may be more beneficial since it does
not require full heparinization. Placement of a cannula
directly into the left atrium eliminates the need for a
membrane oxygenator and heat exchanger, which itself
reduces the requirement for full anticoagulation. A separate
incision to expose the femoral artery and allow for placement
of an arterial cannula is also required with this approach.
Both of the techniques mentioned previously involve the
use of pump perfusion, which can possibly activate clotting
factors and induce a fibrinolytic state. Passively shunting
blood from the ascending to descending thoracic or
abdominal aorta by means of an external, heparin-bonded
shunt is another option available for distal perfusion.
However, this technique requires more extensive exposure
and is rarely used by us. In some instances, however, we do
use a temporary right axillary-to-right femoral artery bypass
using 10 mm externally supported polytetrafluorethylene
(PTFE) graft, as reported by Comerota and White.[21] This
procedure is done with the patient in a supine position just
before starting the TAA aneurysmal repair. The graft itself is
not tunneled in the subcutaneous tissue and is removed after
completing the procedure. This approach avoids the need for
heparinization, but has the disadvantage of lengthening the
procedure and adding two additional wounds, with the
potential for complications. It also requires repositioning the
patient before proceeding with aneurysm repair.
After completing the above preparatory steps, the patient is
positioned on the operating room table right side down. The
table is slightly flexed in the lumbar region and the shoulders
are placed at a 90 degree angle to the table with the hips at a
30 degree angle. This position is maintained by use of an
deflatable beanbag. The left arm is elevated and moved to the
right and secured on an overhead arm board. After the patient
has been prepped and draped, a left posterolateral
thoracotomy incision is performed and carried onto the
abdominal wall, curving downwards along the midline or
648 Part Five. Aneurysms
extending obliquely across the abdomen. The precise location
of this incision depends on the type of aneurysm undergoing
repair. For patients with type I and II TAA aneurysms, the
thoracotomy incision is centered over the 4th, 5th, or 6th
intercostal space, with additional exposure gained by
resecting one of these ribs, if necessary. In patients with
less extensive disease undergoing repair of type III or IV TAA
aneurysms, the thoracotomy incision is made over the 7th,
8th, or 9th interspace.
Following entry into the chest, the left lung is deflated and
the inferior pulmonary ligament is divided. This procedure
permits mobilization of the left lung, which is retracted
superiorly and medially. The mediastinal pleura is then
incised to expose the underlying descending thoracic aorta. If
necessary, this dissection is extended proximally to the level
of the left subclavian artery. The left vagus and recurrent
laryngeal nerves are identified and preserved. Occasionally,
aneurysmal dilatation of the descending thoracic aorta
involves the origin of the left subclavian artery, requiring
separate control of this vessel and more proximal control of
the aortic arch.
After completing this proximal dissection, the diaphragm
is divided in a circumferential fashion, with marking sutures
placed along the edges of the divided diaphragm to facilitate
later reapproximation. The crus of the diaphragm is also
divided, exposing the underlying aorta. The abdominal
dissection is then performed through either a transperitoneal
or retroperitoneal route. Dissection proceeds along the left
paracolic gutter, elevating the abdominal viscera and rotating
these structures medially. Care is taken to avoid splenic injury
while dividing the splenophrenic ligament. The left kidney is
elevated along with the abdominal viscera, exposing the left
renal artery—usually easily identified. The left renal vein is
located just below the left renal artery. A lumbar branch
originating from the inferior, posterior aspect of the left renal
vein must be identified and divided to fully rotate the left
kidney medially. The right renal artery is not visualized in this
approach, though the celiac and superior mesenteric vessels
are usually readily visible. This dissection is carried distally in
a plane posterior to the inferior mesenteric artery, exposing
the abdominal aorta down to the bifurcation. However,
exposure of the distal right common iliac artery is somewhat
limited.
After proximal and distal control have been obtained, the
patient is systemically heparinized, with the extent of
anticoagulation determined by the method chosen for distal
aortic perfusion. Mannitol and furosemide are administered
to induce a brisk diuresis, and mild hypothermia along with
a dose of corticosteroids are used as additional means of
spinal cord protection. The proximal cross-clamp is then
placed, usually distal to the left subclavian artery, with a
distal cross-clamp placed a short distance away. This
sequential cross-clamping technique permits retrograde
distal perfusion. The aneurysmal aorta is opened lon-
gitudinally and the proximal descending aorta completely
divided to avoid incorporating the esophagus into the
anastomosis. A properly sized, collagen-impregnated
Dacronw graft is then sewn to the descending aorta with
a running stitch of 3-0 prolene suture material. In the
presence of a friable aortic wall, this proximal anastomosis
is reinforced with a Teflonw felt strip.
After completing this anastomosis, the cross-clamps are
moved distally and the suture line is tested for hemostasis.
Next, the distal aortic clamp is moved lower on the aorta
and the aneurysm is opened more extensively to expose the
origins of the distal intercostal arteries and the visceral
vessels. Endarterectomy of the origin of the visceral vessels
occasionally may be necessary in the presence of
associated visceral occlusive disease, but we try never to
endarterectomize the intercostal artery orifices because of
the high risk of dissection of these vessels. Critical
intercostal arteries are then reimplanted using a patch-
inclusion technique, done by creating a defect in the
posterior aspect of the graft and incorporating the segment
of aortic wall containing the critical intercostal arteries
with a running suture of 3-0 prolene. A similar patch
inclusion technique is used to incorporate the celiac,
superior mesenteric, and right renal arteries. Usually, the
origin of the left renal artery is located too far away from
the other visceral vessels to allow for incorporation into
this patch, necessitating separate anastomosis of the left
renal artery to the graft. However, in some patients a
separate graft to the left renal artery may be needed. If the
origins of the visceral vessels are widely spaced, or in the
presence of dissection, separate grafts to each of the
visceral vessels may be necessary.
Backbleeding lumbar arteries are oversewn and a decision
is made regarding the need to reimplant the inferior
mesenteric artery. Finally, the distal anastomosis is completed
by suturing the distal end of the graft to the aortic bifurcation.
When aneurysmal dilatation extends into the iliac arteries, a
bifurcation graft may be needed to accomplish distal
perfusion to the lower extremities. Care should be taken to
insure that one maintains flow through at least one
hypogastric artery to minimize the added risk of colon or
cauda equina ischemia.
After completing the reconstruction, the aneurysm sac is
closed over the graft to prevent contact between the graft and
the abdominal viscera. Additionally, closing the sac of the
aneurysm over the graft minimizes bleeding from the edges of
the aneurysm and aids with hemostasis. If the aneurysm sac
cannot be reapproximated over the graft, a PTFE membrane is
used for coverage. Platelets, fresh frozen plasma (FFP), and
cryoprecipitate are administered while the aneurysm sac is
being closed to help ensure adequate hemostasis. Protamine
may also be needed, depending upon the amount of heparin
administered. The diaphragm is then closed using the marking
sutures placed previously as a guide. The chest is closed in
multiple layers, leaving two 32 Fr thoracostomy tubes
inserted through separate stab wound incisions in the thoracic
cavity.
Next, the abdominal viscera are inspected, proper
positioning of a nasogastric tube is verified, and the
abdomen is closed in standard fashion. A closed-suction
drain is rarely placed in the retroperitoneum before closure.
If distal aortic perfusion was used, all cannula are removed
and the femoral vessels repaired. The groin wound is then
closed in layers, with the skin closed using a running
subcuticular stitch to avoid potential wound complications.
Likewise, if a temporary axillofemoral bypass was used,
the graft is removed and the axillary and femoral vessels
repaired.

POSTOPERATIVE CARE
Following TAA aneurysmal repair, the patient is transferred
to the surgical intensive care unit (SICU). Particularly close
attention is given to the patient’s blood pressure, heart rate,
respiratory rate, and urine output. The CSF drainage is
continued for an additional 2 –3 days to minimize delayed-
onset paraplegia that may result from progressive spinal cord
edema. Central venous pressure, pulmonary capillary wedge
pressure, cardiac output, and peripheral vascular resistance
are monitored frequently, and laboratory indicators such as a
complete blood cell (CBC) count, coagulation studies, serum
electrolytes, serum creatinine, and arterial blood gases are
checked regularly. Blood products are often necessary in the
postoperative period to optimize the patient’s hemodynamics
and correct any residual coagulopathy. Electrolyte disturb-
ances, particularly hypokalemia and hypoxemia, are avoided
because they may rapidly precipitate a lethal cardiac
arrhythmia.
No attempts at extubation are made during the first
postoperative day; rather, the patient is maintained intubated
and sedated. In the presence of significant facial edema, the
dual lumen endotracheal tube is not exchanged until the
following day for fear of losing control of the airway. A chest
x-ray and an electrocardiogram are obtained immediately
postoperatively and on a daily basis until the patient is
sufficiently stable to leave the SICU.
The patient’s sedatives are discontinued on the second
postoperative day, when weaning from the ventilator is
initiated. At this time it is usually possible to more adequately
assess the patient’s neurologic function, which is followed
closely.
The spinal catheter is discontinued on the third post-
operative day. If a delayed neurologic deficit occurs,
reinsertion of the spinal catheter is performed rapidly,
draining fluid to maintain a CSF pressure of less than
10 mmHg while the patient’s hemodynamics are optimized.
In a recent report by Safi and colleagues, this approach
resulted in significant improvements in neurologic function in
all those patients who developed a delayed deficit.[22]
Maintenance fluids initially are given at the rate of
125 mL per hour and additional IV fluids are given to
match the urine output on a cc/cc basis. This is necessary
Table 44-4. Postoperative Complications Following TAA Aneurysmal Repair
Author/year 30-day mortality (%) Paraplegia (%)
Hollier/1988 15 5 4
Golden/1991 5 16
Cox/1992 35 21
Svensson/1993 8 16
Schepens/1994 6 14
Safi/1994 4 9
Acher/1998 10 8 NA
TAA = Thoracoabdominal aortic.
MI = Myocardial infarction.
NA = Not applicable.
Chapter 44. Thoracoabdominal Aortic Aneurysms 649
since after the period of intraoperative renal ischemia, there
is an obligatory high output loss of fluids while the renal
tubules are temporarily dysfunctional. The fluid replace-
ment for urine losses can usually be discontinued the day
after surgery and the maintenance IV fluids are usually
decreased from 125 mL per hour on the first postoperative
day to 100 mL per hour on the second postoperative day
and 60 mL per hour on the third day, in anticipation of
third-space fluid mobilization. Diuretics are frequently
administered on the third postoperative day, when chest
tubes, nasogastric tubes, and closed-suction drains can
usually be removed. An oral diet is resumed after bowel
function has returned. Ambulation is encouraged after the
patient has been extubated and the epidural catheter is
removed.
RESULTS
The morbidity and mortality associated with TAA aneurysm
repair has decreased significantly since the procedure was first
performed over 40 years ago. Careful preoperative evaluation
and advancements in perioperative care and surgical
technique, the introduction of the graft inclusion technique,
and the use of CSF drainage largely have been responsible for
these improved results. Hollier, Safi, Acher, and Brewster
now report operative mortality rates of less than 10% and
paraplegia rates of less than 10%. Nontheless, despite this
progress, mortality, neurologic injury, and renal dysfunction
rates are still greater than desirable. The incidence of these
devastating complications are still noted to vary according to
extent of the aneurysm undergoing repair, cross-clamp times,
age of the patient, and presence of comorbid conditions. As
seen in Table 44-4, the incidence of paraplegia reported in the
literature varies from 5% to 20%, with renal failure rates of
5% to 30%.
As described previously, several methods have been used
successfully to decrease the incidence of these devastating
complications. Spinal cord protection can be improved by
CSF drainage, distal aortic perfusion, reimplantation of
critical intercostals, mild hypothermia, and IV corticoster-
oids.[9,19,20,23] Distal aortic perfusion and/or selective visceral
artery perfusion can also help decrease renal failure rates and
Renal failure (%) Respiratory failure (%) MI/cardiac failure (%)
33 9
29 26 5
29 36 10
18 33 12
14 26 23
7 47 9
NA NA
650 Part Five. Aneurysms
minimize hemorrhagic complications. Renal dysfunction can
be minimized by adequate preoperative hydration, admini-
stration of mannitol and furosemide prior to cross-clamping,
and endarterectomy or renal bypass in the presence of
associated renal artery occlusive disease. Cold perfusion of
the kidneys may also useful, and some authors have reported
improved results using this technique.[24,25]
CONCLUSION
The surgical treatment of TAA aneurysms has improved
significantly in recent years. Whereas the operative mortality
associated with elective repair has been reduced to under
10%, the morbidity of this procedure still remains high due to
the high incidence of postoperative complications.
Equally good results have not been attained for patients
undergoing repair of ruptured TAA aneurysms. In one recent
report, Acher and colleagues documented an operative
mortality rate of 1.6% for patients undergoing elective repair,
but a 21% mortality rate for a similar group of patients who
presented with acute symptoms.[26] Crawford et al. reported
operative mortality of about 25% for patients with ruptured
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Aneurysms: Observations Regarding the Natural Course of
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3. Crawford, E.S.; Crawfors, J.L.; Safi, H.J.; et al.
Thoracoabdominal Aortic Aneurysms: Preoperative and
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357– 370.
8. Schepens, M.A.; Defauw, J.J.; Hamerlijnck, R.P.; et al.
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TAA aneurysms,[27] but others report much higher mortality.
A review by Johansson and colleagues noted an operative
mortality rate of 97 –100% for patients with ruptured TAA
aneurysms.[28] This high mortality rate associated with
rupture mandates an aggressive approach in the management
of these difficult patients. Therefore, for thoracoabdominal
aneurysms of significant size, we favor operative intervention
for most asymptomatic patients and virtually all symptomatic
patients, particularly if they present with rupture.
In general, the risks associated with aneurysmal rupture
exceed the risk of surgical treatment when aneurysm size
exceeds 6 – 7 cm, although the presence of significant
comorbid conditions may require deferring surgical recon-
struction in extremely high-risk patients. Further experience
with endovascular techniques may, in the future, offer the
patient additional options for repair of these difficult
aneurysms. Until then, however, careful preoperative
assessment, optimization of the patient’s overall condition,
good surgical technique, and specific guidelines for post-
operative care of these patients remains the best approach to
achieve successful repair of these complicated aneurysms. It
is our hope that future advances in this field may help further
decrease the morbidity and mortality associated with this
procedure.
9. Safi, H.J.; Bartoli, S.; Hess, K.R.; et al. Neurological Deficit
in Patients at High Risk with Thoracoabdominal Aortic
Aneurysms: The Role of Cerebral Spinal Fluid Drainage
and Distal Aortic Perfusion. J. Vasc. Surg. 1994, 20 (3),
434– 443.
10. Pitt, M.P.; Bonser, R.S. The Natural History of Thoracic
Aortic Aneurysm Disease: An Overview. J. Cardiovasc.
Surg. 1997, 12 (Suppl.), 270 – 278.
11. Patel, M.I.; Hardman, D.T.; Fisher, C.M.; et al. Current
Views on the Pathogenesis of Abdominal Aortic Aneur-
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12. Panneton, J.M.; Hollier, L.H. Nondissecting Thoraco-
abdominal Aortic Aneurysms: Part 1. Ann. Vasc. Surg.
1995, 9, 503–514.
13. Panneton, J.M.; Hollier, L.H. Dissecting Descending
Thoracic and Thoracoabdominal Aortic Aneurysms: Part
II. Ann. Vasc. Surg. 1995, 9, 596– 605.
14. Bickerstaff, L.K.; Pairolero, P.C.; Hollier, L.H.; et al.
Thoracic Aortic Aneurysms: A Population Based Study.
Surgery 1982, 92, 1103– 1108.
15. Cambria, R.A.; Gloviczki, P.; Stanson, A.W.; et al.
Outcome and Expansion Rate of 57 Thoracoabdominal
Aortic Aneurysms Managed Nonoperatively. Am. J. Surg.
1995, 170, 213– 217.
16. Svensson, L.G.; Hess, K.R.; Coselli, J.S.; et al. A
Prospective Study of Respiratory Failure After High Risk
Surgery on the Thoracoabdominal Aorta. J. Vasc. Surg.
1991, 14 (3), 271 – 282.
17. Money, S.R.; Rice, K.; Crockett, D.; et al. Risk of
Respiratory Failure After Repair of Thoracoabdominal
Aortic Aneurysms. Am. J. Surg. 1994, 168, 152– 155.
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18. Hollier, L.H. Cardiac Evaluation in Patients with Vascular
Disease—Overview: A Practical Approach. J. Vasc. Surg.
1992, 15, 726– 728.
19. Kouchoukos, N.T.; Wareing, T.H.; Izumoto, K.; et al.
Elective Hypothermic Cardiopulmonary Bypass and
Circulatory Arrest for Spinal Cord Protection During
Operations on the Thoracoabdominal Aorta. J. Thorac.
Cardiovasc. Surg. 1990, 99, 659– 664.
20. Frank, S.M.; Parker, S.D.; Rock, P.; et al. Moderate
Hypothermia, with Partial Bypass and Sequential Repair
for Thoracoabdominal Aortic Aneurysm. J. Vasc. Surg.
1994, 19, 687– 697.
21. Comerota, A.J.; White, J.V. Reducing the Morbidity of
Thoracoabdominal Aneurysm Repair by Preliminary
Axillofemoral Bypass. Am. J. Surg. 1995, 170, 218– 222.
22. Safi, H.J.; Miller, C.C.; Azizzadeh, A.; et al. Observations
on Delayed Neurological Deficit After Thoracoabdominal
Aortic Aneurysm Repair. J. Vasc. Surg. 1997, 26, 616– 622.
23. McCullough, J.L.; Hollier, L.H.; Nugent, M. Paraplegia
After Thoracic Aortic Occlusion: Influence of Cerebro-
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spinal Fluid Drainage. Experimental and Early Clinical
Results. J. Vasc. Surg. 1988, 7, 153– 160.
24. Svensson, L.G.; Crawford, E.S.; Hess, K.R.; et al.
Thoracoabdominal Aortic Aneurysms Associated with
Celiac, Superior Mesenteric, and Renal Artery Occlusive
Disease: Methods and Analysis of Results in 271 Patients.
J. Vasc. Surg. 1992, 16, 378– 390.
25. Kashyap, V.S.; Cambria, R.P.; Davison, J.K.; et al. Renal
Failure After Thoracoabdominal Aortic Surgery. J. Vasc.
Surg. 1997, 26, 949– 957.
26. Acher, C.W.; Wynn, M.M.; Hoch, J.R.; et al. Cardiac
Function Is a Risk Factor for Paralysis in Thoracoabdom-
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27. Crawford, E.S.; Hess, K.R.; Cohen, E.S.; et al. Ruptured
Aneurysm of the Descending Thoracic and Thoraco-
abdominal Aorta. Analysis According to Size and
Treatment. Ann. Surg. 1991, 213, 417– 426.
28. Johansson, G.; Markstrom, U.; Swedenborg, J. Ruptured
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CHAPTER 45
Popliteal Artery Aneurysm
Timothy P. Connall
Samuel E. Wilson
Popliteal artery aneurysms are the most common peripheral
artery aneurysms, comprising 70% of these lesions. Surgical
treatment of these aneurysms dates to Antyllus, a third-
century Greek physician who ligated both poles of the
aneurysm and incised and packed the aneurysm sac. In 1785
John Hunter treated a coachman with a popliteal aneurysm by
simply ligating the superficial femoral artery above the
aneurysm (in what today is called Hunter’s canal ).[1] Matas
performed endoaneurysmorrhaphy by ligating all branch
vessels from within the aneurysm and suturing the walls of the
aneurysm together; he performed this surgery on 154
popliteal aneurysms from 1888 to 1920. In the 1950s,
aneurysm excision with vein interposition and aneurysm
exclusion with venous bypass became the primary methods of
treatment.
EPIDEMIOLOGY
Though popliteal aneurysm (Fig. 45-1) is the most common
peripheral artery aneurysm, its prevalence in the general
population is low. In a series from the Henry Ford Hospital,
popliteal aneurysm accounted for 1 in 5000 hospital
admissions; there was 1 popliteal aneurysm per 15 abdominal
aortic aneurysms. Popliteal aneurysm is a disease found
almost exclusively in men, most often in the sixth decade of
life (Table 45-1). Most popliteal aneurysms are fusiform and
associated with atherosclerosis as their presumed primary
etiology. Less common etiologies include trauma such as
after knee dislocation, knee replacement, or knee arthro-
scopy,[2] inflammatory arteritides such as Behçet’s or
Kawasaki disease,[3] infected emboli, and bacteremia such
as with Staphylococcus and Salmonella.[4]
Nearly all popliteal aneurysms are atherosclerotic. Other
etiologies include popliteal artery entrapment syndrome,
trauma, and infection, but these causes are uncommon,
occurring in less than 10% of cases.[5 – 9] Diseases frequently
associated with atherosclerosis are found in patients with
popliteal aneurysm. Coronary artery disease and cerebral
vascular disease occur, respectively, in 35 and 10% of
patients; hypertension is present in 45%; and diabetes mellitus
in 13%.[3,7 – 13]
Hobson/Wilson/Veith: Vascular Surgery: Principles and Practice, Third Edition, Revised and Expanded
DOI: 10.1081/0819-9-120024928
Copyright q 2004 by Marcel Dekker, Inc.
653
There is an astonishingly high rate of additional aneurysms
in patients with popliteal aneurysm (Table 45-1). Bilateral
popliteal aneurysms are found in about 50% of cases. Extra-
popliteal aneurysms are found in 40– 75% of patients with a
single popliteal aneurysm; if bilateral popliteal aneurysms are
present, there is a 68–87% incidence of extrapopliteal
aneurysm disease.[5,6,14,17] The abdominal aorta is most often
affected, followed by the femoral and iliac arteries. These
high rates of associated aneurysms suggest that popliteal
aneurysm represents a more aggressive form of “aneurysm
disease” than that seen in standard infrarenal aortic
aneurysms. The specific genetic defects that lead to end
arterial damage are yet to be fully elucidated.[18,19] In the
patient with a popliteal aneurysm, a thorough search must be
made for additional aneurysms, particularly of the abdominal
aorta and contralateral popliteal artery.
CLINICAL FEATURES
Approximately 70% of patients with popliteal aneurysms will
be symptomatic at initial presentation. Popliteal aneurysms
present the vast majority of the time with complications of
thromboembolic disease ranging from claudication to rest
pain and ischemic gangrene. Popliteal aneurysms, in contrast
to aortic aneurysms, present with rupture less than 5% of the
time.[13,15,17,20] Popliteal aneurysms present with symptoms
of compression of neighboring structures such as the sciatic
nerve and popliteal vein 10% of the time.[13,15,17,20]
Compression may lead to radiculopathy, venous thrombosis,
and even arteriovenous fistula.[21]
DIAGNOSIS
Physical exam by a person familiar with a normal popliteal
pulse is usually an accurate and adequate screening test for
low-risk patients. Occasionally a nonvascular mass such as a
Baker’s cyst may be mistaken on exam for an aneurysm.
When a definitive diagnosis is important, duplex ultrasound is
the procedure of choice. A popliteal artery greater than 2 cm
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654 Part Five. Aneurysms

Prior to elective operative intervention it is prudent to

screen for other aneurysms because of their relatively high
coincidence. Depending on the findings of these screening
tests, the order of treatment may need to be altered.
Ultrasound provides adequate sensitivity and specificity
for most clinical situations. Computed tomography (CT) and
magnetic resonance imaging (MRI) provide equal and, in
some cases, superior images. The CT scan with recent
advances to allow three-dimensional reconstruction and
luminal “angiographic” reconstruction can provide angio-
graphic quality pictures to the level of the popliteal artery.
The tibial vessels are too small to be meaningfuly visualized
with current CT technology. The MRI/MRA has higher
resolution of small vessels and can often provide enough
information regarding popliteal and tibial runoff to obviate
the need for arterial angiography, especially when angio-
graphic morbidity is high as with renal insufficiency.

MANAGEMENT

Symptomatic Aneurysms
Thromboembolic disease from the popliteal arterial aneurysm
typically has a progressive natural history. Given the
relatively low rates of limb salvage once extensive
embolization has occurred, any embolization should be
considered a strong indication for surgery. Complete
aneurysm and artery thrombosis without embolization may
also occur. The natural history of this condition is presumed
by some to be more benign and similar to simple
atherosclerotic occlusion. Despite surgical intervention, 16 –
50% of extremities that present with acute thrombosis or
thromboembolism go on to major amputation as either a
primary or secondary procedure.[5,12 – 14,16]
Figure 45-1. A typical angiogram of a popliteal aneurysm.

[14]
in diameter is usually considered aneurysmal. To avoid
misinterpretation of a slight dilatation as an aneurysm in
patients with arteriomegaly, it is appropriate to compare the
diameter of the dilated vessel to the diameter of the distal
superficial femoral artery. In such instances a vessel with a
diameter 1.5–2.0 times the diameter of the proximal vessel is
considered aneurysmal.[12,14]
Asymptomatic Aneurysms
The management of asymptomatic popliteal aneurysms is a
subject of some controversy. Accumulation of prospective
natural history data on asymptomatic popliteal aneurysms is
difficult as even large centers usually see fewer than 10 of
these lesions per year. The retrospective data available
suggest that anywhere from 29 to 59% of popliteal aneurysms
will become symptomatic.[6,22 – 24] The variables that will

Table 45-1. Epidemiology and Percentage of Additional Aneurysms in Patients with Popliteal Aneurysm

Percentage of other aneurysms

Series Number of patients Mean age Male: female AAAa Iliac Femoral Bilateral popliteal

Reilly et al.[11] (1983) 70 70 15:1 32 8 15 53

Whitehouse et al.[12] (1983) 61 67 30:1 62 36 38 44
Vermilion et al.[13] (1981) 87 60 28:1 40 25 34 68
Shortell et al.[16] (1991) 39 63 39:0 39 18 14 24
Halliday et al.[5] (1991) 40 64 19:1 30 5 22 50
a
Abdominal aortic aneurysm.

predispose to thromboemmbolism likely include size and
intraluminal thrombus, but this is not well defined. Dawson
et al.[24] retrospectively followed 42 patients for an average of
6.2 years with asymptomatic popliteal aneurysms with an
average aneurysm size of 3.1 cm. At 18 months 59%
developed symptoms, culminating in three leg amputations,
one peroneal nerve palsy, and eight limbs with claudication.
Delaying therapy until the onset of symptoms may avoid
operation in high-risk individuals, but it will also adversely
effect surgical outcome because of the loss of outflow. Varga
et al.[25] followed 137 patients newly diagnosed with popliteal
aneurysms to look at variables affecting outcome. Grafts
placed emergently had a 10% early bypass failure rate as
opposed to 1.2% of those placed electively. Regarding safety
and efficacy, in four series reporting operation on patients
with asymptomatic aneurysms there were no operative deaths,
long-term limb loss was 0 –3%, and 89 –97% of patients
remained symptom-free.[5,11,13,14]
In summary, the indications for repair of popliteal
aneurysms requires some surgical judgment. In contrast
with aortic aneurysms, the complications of popliteal
aneurysms are never life-threatening, and in the high-risk
patient a case can always be made for nonoperative
management. For most patients elective repair of a popliteal
aneurysm (femoral-popliteal bypass with autologous vein) is
a definitive, safe operation that has clinical results that rival or
exceed similar operations done for occlusive disease.[26] We
recommend that an isolated asymptomatic popliteal aneurysm
large enough to cause arterial turbulence or thrombus
formation be considered for operative repair. These criteria
would typically include aneurysms greater than 2.5 cm. In the
future, should less morbid methods of treatment be proven,
such as endovascular therapy, the indications for repair could
be further liberalized. As mentioned above, the presence of
thromboembolism defined either clinically or radiologically
should be considered a strong indication for surgery to avoid
limb loss.
Thrombolytic Therapy
Thrombolytics such as urokinase, streptokinase, and t-PA are
medications that catalyze endogonous fibrinolytic pathways.
They have been shown effective at lysis of thrombus both
acute and chronic, venous and arterial, and in situ or embolic.
Whether vascular patency will be preserved after thombolytic
recanalization depends on the nature of the primary lesion.
The use of thrombolytics in the treatment of popliteal
aneurysms has strong theoretical appeal where the most
frequent cause of graft failure is thomboembolic occlusion of
outflow vessels.
The use of surgical thrombectomy is not necessarily easier
because of frequent concomitant athero-occlusive disease and
the difficulty in surgically managing inframalleolar throm-
boembolism. As was shown in the Topas trial, the use of
initial thrombolytics for acute ischemia may be associated
with similar limb salvage and lower mortality when compared
to initial surgery.
Thrombolytics may stimulate additional embolism from
the aneurysm sac. Catheter-based infusion directly into the
distal embolus may help prevent additional embolization
Chapter 45. Popliteal Artery Aneurysm 655
from the aneurysm sac. Preoperative thrombolytic use on a
known thrombosed popliteal aneurysm without emboliza-
tion is unnecessary and unwise. The diagnosis of popliteal
aneurysm is occasionally made incidentally after thera-
peutic thrombolysis for presumed atherosclerotic occlusion.
The overall effect of thrombolyics in a patient with
thromboembolic outflow compromise appears to be
beneficial.
Hoelting et al.[27] retrospectively compared 11 patients
who received primary bypass surgery for acute popliteal
aneurysm –related ischemia to 9 similar patients who received
thrombolytics prior to bypass surgery. There were 5
“occlusive complications” and one secondary amputation in
the primary bypass group as opposed to none in the
thrombolytic group. In a similar retrospective review
Carpenter et al.[26] compared 38 patients who received
primary bypass surgery for acute popliteal aneurysm –related
ischemia to 7 similar patients who received thrombolytics
prior to bypass surgery. These 7 patients are described as
having thrombosis of all three of their run-off vessels. The
patients with preoperative thrombolytics had better graft
patency ð p , 0:005Þ and limb salvage ð p , 0:01Þ than the
patients that underwent emergency primary operation.
Varga et al. prospectively compared 23 patients who
received thrombolytics to 56 patients who had primary bypass
surgery and concluded that “intraarterial thrombolysis is of
value in restoring the distal run-off before bypass in popliteal
aneurysms presenting with acute limb-threatening ische-
mia.”[25]
Surgery
The procedure of choice for popliteal aneurysm is construc-
tion of a reversed saphenous vein arterial bypass and
exclusion of the aneurysm. (As a second choice, polytetra-
fluoroethylene, or PTFE, is used as the arterial conduit.) A
medial approach to the popliteal artery is taken, as described
by Szilagyi et al.[17] Definitive treatment of popliteal
aneurysms consists of aneurysm ligation and bypass. The
typical bypass usually consists of an above-knee popliteal to
below-knee popliteal bypass, although this can vary
considerably in either direction, depending on the extent of
aneurysmal disease. The best conduit for bypass is autologous
vein.
The popliteal aneurysm can be exposed, ligated, and
bypassed by either the medial or posterior approach. The
medial approach allows exposure of the greater saphenous
vein, the above- and below-knee popliteal artery, and the
tibial vessels for selective tibial thrombectomy or more distal
bypass. Without division of the hamstring tendons, the medial
approach does not permit surgery directly on the aneurysm
sac. When direct sac exposure is required, as in a patient with
compressive symptoms requiring sac debridement, the
posterior approach is best. The posterior approach allows a
bloodless and superficial dissection of the entire popliteal
artery. This exposure readily allows dissection and debride-
ment of the aneurysm off neighboring structures. For
aneurysms limited to the popliteal fossa, the posterior
approach may also permit a shorter bypass because of better
exposure. When necessary an additional 4 –5 cm of superficial
656 Part Five. Aneurysms
femoral artery can be exposed posteriorly by division of
overlying adductor muscle fibers. Distal tibial exposure
through the posterior approach, while possible, is more
difficult than from a medial approach. With the posterior
approach, unless the lesser saphenous vein is of sufficient
size, an additional incision will be required for harvesting of
the greater saphenous vein.
Results
Patients with asymptomatic aneurysms have higher long-term
graft patency rates than do patents with symptomatic
aneurysms that have undergone repair.[15,16]
Endovascular treatment of aneurysms is currently being
aggressively pursued in the treatment of infrarenal aortic
aneurysms. Its theoretical advantages include lower surgical
morbidity. Such an advantage is especially important in
popliteal aneurysm, where many of the lesions are
asymptomatic and none are life-threatening. There are
currently only case reports describing the endovascular
treatment of popliteal aneurysms.
Puech-Leaao et al., through a posterior popliteal artery
exposure, passed a Palmaz stent sewn to a saphenous vein
graft up the superficial femoral artery to perform a proximal
anastomosis (stent expansion) beyond the limits of surgical
exposure.[28] May et al. reported one case of successful
deployment of an endovascular graft to exclude a popliteal
pseudoaneurysm caused by knee replacement surgery.[29]
Krajcer and Diethrich reported one case of successful
REFERENCES
1. Schechter, D.C.; Bergan, J.J. Popliteal Aneurysm: A
Celebration of the Bicentennial of John Hunter’s Operation.
Ann. Vasc. Surg. 1986, 1, 118.
2. Potter, D.; Morris-Jones, W. Popliteal Artery Injury
Complicating Arthroscopic Meniscectomy. Arthroscopy.
1995, 11 (6), 723.
3. Bradway, M.W.; Drezner, A.D. Popliteal Aneurysm
Presenting as Acute Thrombosis and Ischemia in a
Middle-Aged Man with a History of Kawasaki Disease.
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4. Wilson, P.; Fulford, P.; Abraham, J.; Smyth, J.V.; Dodd,
P.D.; Walker, M.G. Ruptured Infected Popliteal Artery
Aneurysm. Ann. Vasc. Surg. 1995, 9 (5), 497.
5. Halliday, A.W.; Taylor, P.R.; Wolfe, J.H.; Mansfield, A.O.
The Management of Popliteal Aneurysm: The Importance
of Early Surgical Repair. Ann. R. Coll. Surg. Engl. 1991,
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6. Farina, C.; Cavallaro, A.; Schultz, R.D.; et al. Popliteal
Aneurysms. Surg. Gynecol. Obstet. 1989, 169, 7.
7. Jimenez, F.; Utrilla, A.; Cuesta, C.; et al. Popliteal Artery
and Venous Aneurysm as a Complication of Arthroscopic
Meniscectomy. J. Trauma. 1988, 28, 1404.
8. Gillespie, D.L.; Cantelmo, N.L. Traumatic Popliteal Artery
Pseudo-Aneurysms: Case Report and Review of the
Literature. J. Trauma. 1991, 31, 412.
treatment at 8 months of an atherosclerotic popliteal
aneurysm treated percutaneously with a Wallstent and
PTFE graft.[30] Mercadae reported 6 patients with popliteal
aneurysms that were percutaneously treated with an
endoluminal graft.[31] In this series with follow-up less than
1 year, there was one case of thrombosis and one case of
incomplete exclusion with recurrence. Mercadae concludes
that “stent-grafting of popliteal aneurysms seems still to be
reserved for elderly and poor condition patients.”
CONCLUSIONS
Popliteal aneurysms are relatively rare lesions. Their
natural history typically consists of thromboembolic
occlusion of the infrapopliteal vessels. It would appear
that roughly one third of patients with these lesions will
become symptomatic within 3 years. If treatment is
delayed until the onset of limb-threatening ischemia, the
rate of limb loss is approximately 10 times that when
treated electively. The treatments of popliteal aneurysms
are ligation and bypass. When outflow vessels are
compromised, consideration should be given for preopera-
tive thrombolytic therapy. Popliteal aneurysms can be
surgically reached by both the medial and posterior
approaches. Endovascular exclusion and bypass is a
promising new technology but is yet without significant
experience.
9. Rosenbloom, M.S.; Fellows, B.A. Chronic Pseudoaneur-
ysm of the Popliteal Artery After Blunt Trauma. J. Vasc.
Surg. 1989, 10, 187.
10. Cole, C.W.; Thijssen, A.M.; Barber, G.G.; et al. Popliteal
Aneurysms: An Index of Generalized Vascular Disease.
Can. J. Surg. 1989, 32, 65.
11. Reilly, M.K.; Abbott, W.M.; Darling, R.C. Aggressive
Surgical Management of Popliteal Artery Aneurysms. Am.
J. Surg. 1983, 145, 498.
12. Whitehouse, W.M.; Wakefield, T.W.; Graham, L.M.; et al.
Limb-Threatening Potential of Arteriosclerotic Popliteal
Artery Aneurysms. Surgery. 1983, 93, 694.
13. Vermilion, B.D.; Kimmins, S.A.; Pace, W.G.; Evans, E. A
Review of One Hundred Forty-Seven Popliteal Aneurysms
with Long-Term Follow-Up. Surgery. 1981, 90, 1009.
14. Dawson, I.; Van, B.J.; Brand, R.; Terpstra, J.L. Popliteal
Artery Aneurysms. Long-Term Follow-up of Aneurysmal
Disease and Results of Surgical Treatment. J. Vasc. Surg.
1991, 13, 398.
15. Schellack, J.; Smith, R.B.; Perdne, G.D. Nonoperative
Management of Selected Popliteal Aneurysms. Arch. Surg.
1987, 122, 372.
16. Shortell, C.K.; DeWeese, J.A.; Ouriel, K.; Green, R.M.
Popliteal Artery Aneurysms: A 25-Year Surgical Experi-
ence. J. Vasc. Surg. 1991, 14, 771.

17. Szilagyi, D.E.; Schwartz, R.L.; Reddy, D.J. Popliteal
Arterial Aneurysms. Arch. Surg. 1981, 116, 724.
18. Kontusaari, S.; Tromp, G.; Kuivaniemi, H.; et al. A
Mutation in the Gene for Type III Procollagen (COL 3AI)
in a Family with Abdominal Aneurysms. J. Clin. Invest.
1990, 86, 1465.
19. Kuivaniemi, H.; Tromp, G.; Prockop, D.J. Genetic
Causes of Aortic Aneurysms: Unlearning at Least Part
of What the Textbooks Say. J. Clin. Invest. 1991, 88,
1441.
20. Hands, L.J.; Collin, J. Infra-Inguinal Aneurysms: Outcome
for Patient and Limb. Br. J. Surg. 1991, 78, 996.
21. Reed, M.K.; Smith, B.M. Popliteal Aneurysm with
Spontaneous Arteriovenous Fistula. J Cardiovasc Surg
(Torino) 1991, 32, 482.
22. Gifford, R.W.; Hines, E.A.; Janes, J.M. An Analysis and
Follow-Up of One Hundred Popliteal Aneurysms. Surgery.
1953, 33, 284.
23. Wychulis, A.R.; Spittel, J.A.; Wallace, R.B. Popliteal
Aneurysms. Surgery. 1970, 68, 942.
24. Dawson, I.; Sie, R.; van Baalen, J.M.; van Bockel, J.H.
Asymptomatic Popliteal Aneurysm: Elective Operation
Versus Conservative Follow-Up. Br. J. Surg. 1994, 81 (10),
1504.
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25. Varga, Z.A.; Locke-Edmunds, J.C.; Baird, R.N. A Multi-
center Study of Popliteal Aneurysms. Joint Vascular
Research Group. J. Vasc. Surg. 1994, 20 (2), 171.
26. Carpenter, J.P.; Barker, C.F.; Roberts, B.; Berkowitz, H.D.;
Lusk, E.J.; Perloff, L.J. Popliteal Artery Aneurysms: Current
Management Outcomes. J. Vasc. Surg. 1994, 19 (1), 65.
27. Hoelting, T.; Paetz, B.; Richter, G.M.; Allenberg, J.R. The
Value of Preoperative Lytic Therapy in Limb-Threatening
Acute Ischemia from Popliteal Artery Aneurysm. Am.
J. Surg. 1994, 168 (3), 227.
28. Puech-Leaao, P.; Kauffman, P.; Wolosker, N.; Anacleto,
A.M. Endovascular Grafting of a Popliteal Aneurysm Using
the Saphenous Vein. J. Endovasc. Surg. 1998, 5 (1), 64.
29. May, J.; White, G.H.; Yu, W.; Waugh, R.; Stephen, M.S.;
Harris, J.P. Endoluminal Repair: a Better Option for the
Treatment of Complex False Aneurysms. Aust. NZ. J. Surg.
1998, 68 (1), 29.
30. Krajcer, Z.; Diethrich, E.B. Successful Endovascular
Repair of Arterial Aneurysms by Wallstent Prosthesis and
PTFE Graft: Preliminary Results with a New Technique.
J. Endovasc. Surg. 1997, 4 (1), 80.
31. Mercadae, J.P. Stent Graft for Popliteal Aneurysms. Six
Cases with Cragg Endo-pro System I Mintec. J. Cardiovasc.
Surg. 1996, 37 (Suppl. 1), 41.
CHAPTER 46
Splanchnic Artery Aneurysms
Russell A. Williams
Samuel E. Wilson
Splanchnic artery aneurysms involve the celiac, superior
mesenteric, and inferior mesenteric arteries and their
branches. They occur relatively infrequently when compared
to aneurysms of the aorta and iliac vessels, partly because
there is a lower overall incidence of atherosclerosis in the
splanchnic circulation. Atherosclerosis, responsible for the
great majority of aortic and iliac aneurysms, is thought to be
responsible for less than half of splanchnic artery aneurysms.
While atherosclerosis can be found in the majority of
splanchnic artery aneurysms, it is thought to be a secondary
process.[1] Splanchnic artery aneurysms have a diverse
etiology and a correspondingly diverse natural history.
Inflammation is an important primary cause of splanchnic
artery aneurysms. It may occur from a primary vasculitis such
as polyarteritis nodosum, a metastatic infection such as
emboli from endocarditis, or an extravascular process such as
pancreatitis or a penetrating peptic ulcer. Peripancreatic
pseudoaneurysms are estimated to occur in 10% of patients
with chronic pancreatitis.[2] Polyarteritis nodosa is an
autoimmune vasculitis which causes multiple aneurysms,
typically less than 1 cm in diameter, of the small and medium-
sized muscular arteries of the abdominal viscera and kidneys.
Due to their small size, intraparenchymal location, and natural
history, these aneurysms rupture only occasionally and do not
often require surgery. In contrast, embolomycotic aneurysms
have a very unpredictable natural history, which often ends in
fatal rupture and, unless completely resolved on follow-up
angiography, are best treated with surgery. Other important
causes of splanchnic artery aneurysms include hemodynamic
and connective tissue alterations as well as trauma.
Splanchnic artery aneurysms may be single or multiple
depending on etiology, and the wall may contain the three
layers of the normal arterial wall or they may be false
aneurysms. Sixty percent of splanchnic artery aneurysms
occur in the splenic artery, 20% in the hepatic artery, 8% in
the superior mesenteric artery, 4% in the celiac artery, 4%
in the gastric and gastroepiploic arteries, and 4% in the
remaining splanchnic branches.[3] Splenic artery aneurysms,
the most common splanchnic artery aneurysms, have
been variously estimated to occur in 0.8 –4% of patients
undergoing angiography,[4] 10% of elderly patients
at autopsy; and 0.05% of autopsies of the general
population.[5,6]
Hobson/Wilson/Veith: Vascular Surgery: Principles and Practice, Third Edition, Revised and Expanded
DOI: 10.1081/0819-9-120024929
Copyright q 2004 by Marcel Dekker, Inc.
659
In general, a majority of splanchnic artery aneurysms are
asymptomatic prior to rupture.[7] When pain is present, it
often signifies acute aneurysmal growth. Rupture rates and
subsequent mortality rates are reported to be 2 –90% and
25–75%, respectively, depending on location and etiology.[4]
Rupture may occur into the peritoneal cavity, causing
hemorrhagic shock, or, as is common with inflammatory
aneurysms, into adjacent structures such as the pancreas or GI
tract, causing related symptoms.
Angiography provides the anatomical detail necessary for
the diagnosis and the planning of treatment of splanchnic
artery aneurysms mainly because these aneurysms are often
small, multiple, and surrounded by or in direct connection
with neighboring vasculature or viscera. Other less invasive
modalities, such as x-ray, ultrasound, computed tomography
(CT), and magnetic resonance imaging (MRI), are often
diagnostic and useful in following aneurysmal growth over
time. CT angiography can provide excellent images without
arterial injection.
Surgical therapy, consisting of ligation or resection of an
aneurysm with or without reconstruction, is the most
conservative method of treatment and is effective in many
instances. Percutaneous embolization is often a less invasive
alternative and is considered by some to be the procedure of
choice for visceral aneurysms where the risk of end-organ
ischemia from embolization is low or where the associated
surgical morbidity is substantial, as with peripancreatic
pseudoaneurysms.[8,9] In a limited number of situations, as
with small atherosclerotic splenic artery aneurysms, these
lesions may be safely observed.
SPLENIC ARTERY ANEURYSMS
Splenic artery aneurysms (SAA) have been recognized with
certainty since 1770, when Beaussier[10] described one in a
woman aged 60, at autopsy. Over 50 years ago, the first SAA
was successfully treated by operation.
A majority of patients with SAA are 50 –70 years of age,
but 20% are 20 –50 years of age, and among these younger
patients the female-to-male ratio is 20:1.[7] Overall, 87% of
patients with SAA are females, and 80% are multiparous
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660 Part Five. Aneurysms
females. Ninety-five percent of patients who experience
SAA rupture are pregnant.[4] Such epidemiology has led to
the common speculation that changes in arterial connective
tissue as well as increases in blood volume, portal
congestion, and splenic arteriovenous shunting related to
pregnancy all contribute to splenic artery medial degener-
ation and aneurysm formation. One-eighth of women with
SAA will also have fibromuscular dysplasia, an arteriopathy
which predisposes to aneurysm formation.[1,11]
Nonpregnant patients with splenic artery hyperdynamic
flow from causes such as cirrhosis, portal-systemic shunts, or
liver transplantation are also at increased risk for developing
SAA. Splenic artery flow in cirrhotics has been found, on
average, to be a least twice that in noncirrhotics. Seven
percent of patients with portal hypertension undergoing
angiography will have incidental SAA, and additional
patients will have generalized splenic artery dilatation.
Patients may also develop SAA from trauma, infected
emboli, and extravascular inflammatory processes, most
notably pancreatic (historical note, President James A. Garfield
died secondary to rupture of a traumatic SAA produced by
a bullet wound during his attempted assassination).
Clinical Presentation
Approximately 80% of patients with SAA are asymptomatic.
In these patients the diagnosis is evident from the appearance
of typical aneurysmal calcifications seen on a plain
radiograph, incidental findings on angiography, or symptoms
of spontaneous aneurysmal rupture (Fig. 46-1). Characteristic
curvilinear aneurysmal calcifications can be found in 70% of
patients with SAA. These findings, while easily identifiable,
are not associated with lower incidence of rupture.
Spontaneous aneurysmal rupture may cause bleeding into
the peritoneal cavity or, as happens with inflammatory
aneurysms, into adjoining structures such as the pancreas, GI
tract, or (rarely) the splenic vein. Some 25% of the time
intraperitoneal rupture is transiently contained within the
lesser sac, after which massive uncontained bleeding occurs
through the foramen of Winslow or a rupture of the lesser
omentum. This clinical phenomenon of “double rupture”
provides a window of opportunity for diagnosis and surgical
intervention before the onset of hemorrhagic shock. The
symptoms of aneurysmal rupture during pregnancy or after
delivery may be mistaken for other common obstetric
emergencies such as uterine rupture, abruptio placentae, or
amniotic fluid embolism especially since SAA rupture may
occur during labor. Inflammatory aneurysms rupturing into
pancreatic pseudocysts may create symptoms of abdominal
pain and hypotension, as these cysts, when large, may
sequester a large amount of blood. When such cysts
communicate with the pancreatic duct patients may develop
acute or chronic GI bleeding. The syndrome, described as
hemosuccus pancreatitis, usually requires angiography for a
definitive diagnosis.[12]
Patients with noninflammatory SAA have a 2 –10%
incidence of aneurysm rupture. The mortality of rupture may
be as high as 70% in pregnancy and up to 25% in those who
are not pregnant. The fetal mortality under these circum-
stances is high. Since the risk of mortality from prophylactic
surgical treatment of noninflammatory SAA is low, patients
should undergo surgery if they are or may become pregnant, if
the aneurysm is greater than 1.5 –2.5 cm, or if they have
referable abdominal symptoms.
Operation for SAA due to pancreatitis has an associated
mortality of 30% because of the persistent intra-abdominal
sepsis presence of extensive inflammatory adhesions,
pancreatic pseudocysts, multiple feeding vessels, and enteric
erosions as well as the possible need for splenectomy and
partial pancreatectomy. Once rupture has ensued, the
mortality increases to 50%.
Exposure for the surgical treatment of SAA provided by
an upper midline incision or, alternatively, a left subcostal
incision, which can be extended in a chevron fashion by
adding a right subcostal incision, is also useful, especially
in the obese or pregnant patient. The latter incision is more
time-consuming to perform and inadvisable in an
emergency, even if the diagnosis is known. The aneurysm
itself is exposed by dividing the gastrocolic ligament to
enter the lesser sac. Splenic preservation should be
attempted, but this may not be possible if the aneurysm
extends into the hilum of the spleen or if emergency
surgery is being done for rupture.
Splenic artery aneurysms secondary to pancreatitis may
be densely adherent to the pancreas or may have ruptured
into a pseudocyst or the pancreatic duct. They pose a more
difficult technical problem because the dense inflammatory
adhesions usually make operation difficult. Double ligation
may even be very difficult; percutaneous arterial embolism
and thrombosis of the aneurysm is often preferable and
safer. Management of the patient who has rupture of a
SAA into a very large pseudocyst that extends high under
the left diaphragm and liver and which may be adherent to
portal vein or even the inferior vena cava can be
technically different and hazardous. Opening the pseudo-
cyst to control the bleeding point usually leaves the
surgeon with an obscured field that wells full of blood, at
times making hemostasis impossible. In this situation
the authors have introduced a balloon catheter into the
abdominal aorta via the femoral artery to occlude the
origins of mesenteric vessels. The gross size and situation
of the cyst may preclude the use of a cross clamp of the
aorta at the diaphragmatic hiatus. Once control of bleeding
within the pseudocyst is achieved, a drain is placed, as
many of these cysts communicate with the pancreatic duct
and a pancreatic fistula or even pancreatic ascites is likely
to ensue. Patients at high operative risk—such as cirrhotics,
the elderly, or those with extensive fibrosis from
pancreatitis—may benefit from nonoperative percutaneous
catheter embolization of the splenic artery and aneurysm.
An increasing number of reports of success using this
technique are emerging. With the patient under local
anesthesia, the catheter is selectively placed within the
lumen of the aneurysm.[13] The more commonly used small
embolic particles of Teflon, Ivalon, or Silastic are not used
to cause thrombosis, as they are not retained in the
aneurysm but embolize distally to the spleen. Instead a
Gianturco steel coil, which has woolly thrombogenic
strands attached, is introduced. This expands after
extrusion from the catheter, wedging itself within the
lumen and making embolization unlikely. Once in place,

Figure 46-1. Calcified splenic artery aneurysm in a 60-year-old woman.
the coil acts as a baffle and the other thrombogenic
materials can be injected.
HEPATIC ARTERY ANEURYSM
Hepatic artery aneurysms (HAA) are one-third as common as
SAA and affect males two to three times as often as females,
which is a reversal of the sex ratio found in SAA. The reversal
in gender occurrence may be because medial degeneration,
responsible for most SAA, accounts for only 25% of HAP.
Other important causes of HAA are trauma, atherosclerosis,
and inflammation. Trauma, which may be environmental or
iatrogenic, accounts for 22% of HAP. Both blunt and
penetrating trauma causes HAA, which may be true or false
and intrahepatic or extrahepatic. Twenty percent of all HAA
are intrahepatic, and a majority of these are caused by
environmental trauma.[14] Iatrogenic trauma typically occurs
from biliary surgery such as cholecystectomy, causing
extrahepatic aneurysms of the right or common hepatic
arteries. Percutaneous transhepatic procedures also can lead
to HAA, usually of the intrahepatic type.
Inflammation, which accounts for 28% of HAA, occurs
most frequently from embolism in a patient with infective
endocarditis. Other, less common causes of inflammation
Chapter 46. Splanchnic Artery Aneurysms 661
causing HAA include pariarteritis nodosa, cholecystitis, and
pancreatitis.
Clinical Presentation
Most patients with HAA are asymptomatic prior to
rupture.[15] In these patients the diagnosis is based on
vascular calcifications or detection of spontaneous aneur-
ysmal rupture. In patients who have large aneurysms,
displacement of neighboring structures such as the biliary
and GI tracts provides a diagnostic clue. Pain, when it does
occur, is often associated with aneurysmal growth. Spon-
taneous HAA rupture occurs into the biliary tract as
frequently as into the peritoneal cavity. One-third of patients
with hemobilia will have the classic triad of hemobilia, pain,
and jaundice.[16] Rarely, these aneurysms will rupture into the
portal vein, creating acute portal hypertension and bleeding
varices. Rupture rates and subsequent mortality rates for HAA
are 20– 44% and 35% respectively.[14,17]
Investigations
On plain x-rays, atherosclerotic aneurysms will often appear
as a rim of eggshell-like calcification; ultrasonography and
computed tomography (CT) delineate the aneurysm, showing
its relation to the bile ducts or portal vein.
662 Part Five. Aneurysms
The definitive study for planning treatment is selective
celiac or hepatic artery angiography. Angiography delineates
the site and extent of the aneurysm, shows an arteriovenous
fistula, and demonstrates any arterial collaterals that have
formed or enlarged portal venous collaterals if portal
hypertension is present. It also outlines the anatomy of the
liver’s blood supply, which is via aberrant vessels in up to
40% of people. This is important information, as the arterial
blood supply to the liver should be maintained following
treatment, either through collaterals, normal aberrant arteries,
or a prosthetic or autologous vein graft to replace the excised,
diseased segment of artery.
Operations
Aneurysms located on the main hepatic artery proximal to the
origin of the gastroduodenal artery may be excised or ligated,
the blood supply to the liver being maintained through
collaterals from the superior mesenteric artery entering the
gastroduodenal branch of the common hepatic artery.
Excision, rather than double ligation, is desirable if the
aneurysm is infected, large enough to produce obstructive
symptoms of the biliary or intestinal system or if it
communicates with part of the GI tract. In some cases it is
safer to remove the aneurysm only partially, reducing its size
by “debridement” and leaving the sac, which may be adherent
to the adjacent vital tissues. Occasionally patients may have
had the gastroduodenal artery divided at a previous operation
on the biliary system or the duodenum. In these patients, if
collaterals are poorly developed, a saphenous vein graft can
be used to restore arterial continuity after aneurysmal
resection.
The 40% of patients who are found on arteriogram to have
alternative origins of the hepatic arteries will have the origin
of the anomalous artery from the left gastric or superior
mesenteric artery. Identification of such vessels on pre-
operative angiography usually precludes the need to restore
hepatic artery continuity. At operation, adequacy of arterial
collateral blood flow to the liver is demonstrated if there is
profuse backbleeding from the distal, divided end of the
hepatic artery. Liver blood flow may also be restored by
anastomosing the distal divided stump of the hepatic artery to
an artery other than the celiac, such as the splenic, utilizing a
segment of prosthetic material or a venous autograft.
Invasive angiography has been used to thrombose hepatic
artery aneurysms and is the preferred method for treatment of
intrahepatic aneurysms that otherwise would be treated by
ligation of the right or left hepatic artery or even by hepatic
lobectomy. Percutaneous embolization and thrombosis is
generally not recommended for the treatment of an
extrahepatic aneurysm because of the importance of
maintaining the arterial blood supply to the liver. However,
there are reports of extrahepatic aneurysms being successfully
treated by arteriographic embolization in patients with
additional illnesses, such as staphylococcal endocarditis,
involving several heart valves where multiple mycotic
aneurysms had developed, liver malignancy,[11] or previous
surgery at which the diagnosis of leaking hepatic artery
aneurysm was missed but subsequently found on an
angiogram. There is one cautionary report of percutaneous
hepatic aneurysm embolization proving fatal in a 73-year-old
man with malignant obstruction of the bile duct who was
treated by introducing an endoprosthesis for biliary drainage.
A hepatic artery aneurysm complicated the initial procedure
and was embolized, resulting in extensive hepatic necrosis.[18]
Postoperatively, hepatic viability may be aided by inspired
oxygen, bowel rest, and hypertonic dextrose until liver
function tests return to normal.
SUPERIOR MESENTERIC ARTERY
ANEURYSMS
Unlike SAA and HAA, superior mesenteric artery
aneurysms (SMAA) are rarely caused by trauma or medial
degeneration, thus their overall incidence is proportionately
lower. Most patients have subacute bacterial endocarditis
or are intravenous drug addicts. Streptococcus species are
commonly grown from the aneurysm, although in drug
addicts Staphylococcus is also likely. Approximately 60%
of SMAA are caused by embolism from infective
endocarditis. Medial degeneration, when present, causes
not only SMAA but also dissections. Embolomycotic
aneurysms and dissections happen more often in the SMA
than in the other splanchnic vessels. In the minority of
patients, SMAA are atherosclerotic in origin, and plain
radiograph may show ring-like calcification in the upper
abdomen near the midline.
Clinical Presentation
Superior mesenteric artery aneurysms are also unique in that
the majority of these patients will manifest symptoms, usually
of intestinal ischemia, prior to rupture.
In patients who have had bacterial endocarditis, the
development of a SMAA should be considered, especially if
there are complaints of abdominal symptoms, such as
epigastric pain unrelated to meals. In some patients,
especially those who are thin, a palpable, tender mass
which is mobile from side to side may be felt. At times, a
pulsation can be appreciated and the patient may have
positive blood cultures.
Those patients who have a SMAA from another cause can
present with similar pain but no antecedent history. The
aneurysm will then be discovered during investigation (see
Fig. 46-2). With an atherosclerotic aneurysm, a plain
radiograph of the abdomen often shows signet-ring – like
calcification to the side of the midline with a posterior defect
in the circumference, representing the origin of the superior
mesenteric artery from the aorta. Otherwise, the aneurysm
may be identified only at laparotomy.
The natural history of mycotic aneurysms with persistence
of infection in the arterial wall is of unrelenting enlargement
and ultimately rupture. The history of atherosclerotic or other
types of aneurysms is uncertain, though one could expect
progressive enlargement and ultimate rupture. Abdominal
apoplexy due to rupture into the peritoneal cavity and rupture
of a traumatic superior mesenteric artery false aneurysm into

Figure 46-2. Mycotic superior mesenteric artery aneurysm in an intravenous drug abuser. (Dr. A. Yellin’s case.)
the duodenum some years after an initial penetrating bullet
injury to that area has been described.
Operations
The first SMAA to be treated successfully was a mycotic
aneurysm operated upon by DeBakey and Cooley in 1949 by
resection without restoring continuity of the SMAA.[19]
Following aneurysmectomy, the viability of the small
bowel surprisingly may not be threatened, obviating the need
for any additional procedure to restore arterial continuity.
Progressive constriction of the aneurysmal lumen of the SMA
and other splanchnic arteries is believed to stimulate
hypertrophy of arterial collaterals. However, should aneur-
ysmectomy result in an inadequate blood supply, the jejunal
continuation of the artery may be anastomosed to the
remaining SMA directly or by interposing a saphenous vein
graft.
Following resection of a mycotic aneurysm, the use of a
prosthetic graft or even a venous homograft, especially if it
courses through the aneurysm bed, is best avoided. If flow is
to be restored, an “extraanatomic” route from adjacent vessel
such as the aorta to the jejunal or ileal segment of the superior
mesenteric artery is chosen.
Other techniques for the treatment of saccular aneurysms
include endoaneurysmorrhaphy. After inflow and outflow
Chapter 46. Splanchnic Artery Aneurysms 663
control, the aneurysm is opened and its orifice with the main
artery, which may be only an ovoid slit several centimeters long,
is oversewn from within the aneurysm, maintaining patency of
the native vessel. This technique is particularly recommended
for mycotic and traumatic false aneurysms, of which both
originate from a limited area of weakness in the arterial wall.[20]
As part of the management of mycotic aneurysms, the infected
aneurysmal sac and contents are excised or debrided without
necessarily excising the native vessel. A prolonged course of the
appropriate antimicrobial agent is given, starting before
operation and continuing for 6 weeks or more after operation.
If this is discontinued too early, residual arterial infection may
lead to reformation of an aneurysm.
A variant of aneurysmorrhaphy may be helpful to treat
large saccular or fusiform aneurysms: the sac is opened after
control of its inflow and outflow, and the orifices of native
artery attached to the aneurysmal segment are oversewn from
inside the sac. This, in fact, obliterates the involved segment
of the artery, so it should be ascertained that no distal
ischemia results.
Excision of many of these SMAAs may be difficult, as they
can be adherent to important adjacent structures, including the
superior mesenteric vein. An injury or deliberate surgical
procedure that occludes the superior mesenteric vein is poorly
tolerated and may produce ischemia of the small bowel along
with ascites. With such an aneurysm, the sac may be excised,
leaving the section of its wall adherent to the vein.
664 Part Five. Aneurysms

Figure 46-3. (A ) CT scan with enhancement of celiac artery aneurysm (A) compressing the extrahepatic bile ducts (B) producing biliary
obstruction. (B ) Angiogram of the same celiac artery aneurysm.
 Chapter 46. Splanchnic Artery Aneurysms 665

Operations of the main trunk of the SMA are usually done

through a vertical abdominal incision. To expose the artery and
its origin more proximally, the duodenojejunal flexure is
mobilized, reflected medially, and the pancreas elevated. The
patient with a ruptured, freely bleeding SMAA often requires
clamp control of the aorta at the diaphragmatic hiatus to stop
bleeding and so permit operation on the aneurysm itself. Some
very proximally situated aneurysms of the SMA may be
operated on by exposing the origin of the artery extra-
peritoneally, reflecting the left colon and duodenum to the right.
In some cases a thoracoabdominal incision facilitates this
maneuver.

OTHER SPLANCHNIC ARTERY

ANEURYSMS

These are very uncommon and include aneurysms of the

celiac, gastric, gastroduodenal, and pancreaticoduodenal
arteries, the ileal and jejunal branches of the superior
mesenteric trunk, and—most rarely of all—the inferior
mesenteric artery. The majority are atherosclerotic degen-
erative aneurysms, but some arise following trauma to the
arterial wall or from local inflammation, particularly in the
case of the pancreaticoduodenal and gastroduodenal arteries
in patients with pancreatitis. Figure 46-4. Pancreaticoduodenal artery aneurysm.
The rarity of these aneurysms makes them reportable and
has led to many sporadic case reports from which
recommendations have been extrapolated. It is thought that Often only the hepatic artery will require revascularization. In
they, like aneurysms elsewhere, will all enlarge and, other instances complete revascularization, either from celiac
depending on their site, will obstruct adjacent organs, artery reapproximation or placement of an interposition graft,
particularly the biliary system, and will ultimately thrombose is required.
or rupture (Fig. 46-3A and B).
Pancreaticoduodenal and gastroduodenal artery aneurysms
caused by pancreatitis usually present as bleeding following Gastroduodenal and Pancreaticoduodenal
rupture into the pancreatic duct, the biliary system, or Aneurysms
adjacent bowel. These aneurysms should always be
considered as possible points of origin of intestinal bleeding The close anatomic relationship of the gastroduodenal and
in patients with pancreatitis. pancreaticoduodenal arteries to the pancreas puts these arteries,
like the splenic artery, at risk for development of inflammatory
aneurysms (Fig. 46-4). Sixty percent of gastroduodenal and
Celiac Artery Aneurysms 30% of pancreaticoduodenal aneurysms are caused by
pancreatitis.[22] Patients with pancreatitis-related aneurysms
The celiac artery does not appear to be predisposed to a
may have symptoms prior to rupture, but these may be
particular type of aneurysm, although it has been reported that
difficulty to differentiate from symptoms of pancreatitis. When
38% of patients with celiac artery aneurysms (CAA) have
these aneurysms rupture, over half will do so into adjacent
other splanchnic artery aneurysms and 18% have abdominal
structures, including the GI tract, pancreas, and (rarely) the
aortic aneurysms.[21] Atherosclerosis is associated with 27%
biliary tract, creating symptoms of acute or chronic GI
of CAA.[21] Trauma and embolism are unusual causes of
bleeding.[23] Other aneurysms will rupture directly into the
CAA.
peritoneal cavity. Surgical intervention may be complicated
As in the case of SMA, 60% of patients with CAA have
and has an associated mortality of up to 30%.[24]
abdominal discomfort prior to rupture and 30% have a
pulsatile mass.[21] Rupture rates and subsequent mortality
rates are 13% and 40% respectively. Operation is successful Gastric and Gastroepiploic Aneurysms
in about 90% of cases. Surgical exposure, unless the
aneurysm is small, will require a thoracoabdominal incision. Aneurysms of the gastric and gastroepiploic arteries occur
Also as in the case of SMAA, approximately one-third of through various mechanisms, the most common of which are
patients with CAA will tolerate celiac ligation without atherosclerosis and medial degeneration. Gastric artery
reconstruction. Whether ligation is feasible should be dissection also occurs, with a total of 50 cases reported to
determined from temporary intraoperative celiac artery date.[22] An unusual cause of gastric artery aneurysms is the
occlusion. In 50% of cases, revascularization is performed. so-called caliber-persistent artery of the stomach, also called
666 Part Five. Aneurysms
cirsoid aneurysm, miliary aneurysm of the stomach, or
Dieulafoy’s vascular malformation. These lesions are
probably congenital anatomic variants in which gastric
vessels penetrate the submucosa without decreasing in size or
joining in the normal submucosal anastomotic plexus of
vessels. In the presence of a caliber-persistent artery of the
stomach, even the smallest of mucosal disruptions may lead to
massive and usually lethal gastric bleeding.[25,26]
Gastric artery aneurysms most commonly develop in the
gastric and not the gastroepiploic vessels. Unlike other
splanchnic aneurysms, the majority of gastric artery
aneurysms (70%) will rupture into the GI tract and not the
peritoneal cavity.[27] Ninety percent of patients with these
lesions present with aneurysm rupture as their initial
symptom. The mortality rate for patients after rupture is
70%.[14] Because of the high rate of rupture, emergency
surgery is the most common form of treatment. Ligation of
the affected gastric vessel will not cause gastric ischemia.
Arterial pathology may extend into the gastric wall, in which
case local gastric resection should be performed.
REFERENCES
1. Stanley, J.C.; Fry, W.J. Pathogenesis and Clinical
Significance of Splenic Artery Aneurysms. Surgery 1974,
76, 898.
2. Hofer, B.O.; Ryan, J., Jr.; Freeny, P.C. Surgical
Significance of Vascular Changes in Chronic Pancreatitis.
Surg. Gynecol. Obstet. 1987, 164, 499.
3. Deterling, R.A. Aneurysms of the Visceral Arteries.
J. Cardiovasc. Surg. 1971, 12, 309.
4. Stanley, J.C.; Fry, W.J. Pathogenesis and Clinical
Significance of Splenic Artery Aneurysms. Surgery 1974,
76, 898.
5. Owens, J.C.; Coffey, R.J. Aneurysms of the Splenic Artery,
Including a Report of Six Additional Cases. Int. Abstr.
Surg. 1953, 97, 313.
6. Foremore, S.W.; Guida, P.M.; Schmacher, H.W. Splenic
Artery Aneurysm. Bull. Soc. Int. Chir. 1970, 29, 210.
7. Trastek, V.F.; Bairolero, P.C.; Joyce, J.W.; et al. Splenic
Artery Aneurysms. Surgery 1982, 91, 694.
8. Ku, A.; Kadir, S. Embolization of a Mesenteric Artery
Aneurysm: Case Report. Cardiovasc. Interv. Radiol. 1990,
13, 91.
9. Mandel, S.R.; Jaques, P.F.; Sanofsky, S.; Mauro, M.A.
Nonoperative Management of Peripancreatic Arterial
Aneurysms. A 10-Year Experience. Ann. Surg. 1987, 2, 126.
10. Beaussier, M. Sur un Aneurisme de I’artere Splenique
Dont les Parios se Sont Ossifees. J. Med. Toulouse 1770,
31, 157.
11. Bedford, P.D.; Lodge, B. Aneurysm of the Splenic Artery.
Gut 1960, 1, 312.
12. Lambert, C.J., Jr.; Williamson, J.W. Splenic Artery
Aneurysm: A Rare Cause of Upper Gastrointestinal
Bleeding. Am. Surg. 1990, 56, 543.
13. Probst, P.; Castaneda-Zuniga, W.R.; Gomes, A.S.; et al.
Nonsurgical Treatment of Splenic Artery Aneurysms.
Diagn. Radiol. 1978, 128, 619.
INTESTINAL BRANCH ARTERY
ANEURYSMS
Aneurysms of the jejunal, heart and colic arteries are rare. A
total of 6 jejunal arterial branch artery aneurysms and 13
inferior mesenteric artery aneurysms have been reported to
date. The etiology of solitary intestinal branch aneurysms is
often difficult to ascertain; they may therefore be called
“congenital.” Multiple intestinal branch aneurysms are
usually associated with a vasculitis, either autoimmune or
embolomycotic. Symptoms of these lesions may include a
palpable mesenteric mass or symptoms referable to
intraluminal or intraperitoneal aneurysm rupture. These
aneurysms tend to be small; preoperative angiography, if
the patient’s condition permits, is often very helpful in
operative localization and in ruling out the possibility of
multiple lesions. Surgical treatment can include arterial
ligation, aneurysm resection, and, if necessary, resection of
involved bowel.
14. Stanley, J.C.; Thompson, N.W.; Fry, W.J. Splanchnic
Artery Aneurysms. Arch. Surg. 1971, 101, 689.
15. Salo, J.A.; Aarnio, P.T.; Jarvinen, A.A.; Kivilaakso, E.O.
Aneurysms of the Hepatic Arteries. Am. Surg. 1989, 5,
705.
16. Contryman, D.; Norwood, S.; Register, D.; et al. Hepatic
Artery Aneurysm: Report of an Unusual Case and Review
of the Literature. Am. Surg. 1983, 49, 51.
17. Busuttil, R.W.; Brin, B.J. The Diagnosis and Management
of Visceral Artery Aneurysms. Surgery 1980, 88, 619.
18. Sjovall, S.; Hoevels, J.; Sundqvist, K. Fatal Outcome from
Emergency Embolization of an Intrahepatic Aneurysm.
Surgery 1980, 87, 347.
19. Boijsen, E.; Efsing, H.O. Aneurysm of the Splenic Artery.
Acta Radiol. Scand. 1969, 8, 29.
20. Olcott, C.; Ehrenfeld, W.K. Endoaneurysmorrhaphy for
Visceral Artery Aneurysms. Am. J. Surg. 1977, 133,
636.
21. Graham, L.M.; Stanley, J.C.; Whitehouse, W., Jr.; et al.
Celiac Artery Aneurysms: Historic (1745 – 1949)
Versus Contemporary (1950 – 1984) Differences in
Etiology and Clinical Importance. J. Vasc. Surg. 1985,
5, 757.
22. Eckhauser, F.E.; Stanley, J.C.; Zelenock, G.B.; et al.
Gastroduodenal and Pancreaticoduodenal Artery Aneur-
ysms: A Complication of Pancreatitis Causing Spon-
taneous Gastrointestinal Hemorrhage. Surgery 1980, 88,
335.
23. Gangahar, D.M.; Carveth, S.W.; Reese, H.E.; et al. True
Aneurysm of the Pancreaticoduodenal Artery: A Case
Report and Review of the Literature. J. Vasc. Surg. 1985, 2,
741.
24. Stabile, B.E.; Wilson, S.E.; Debas, H.T. Reduced Mortality
from Bleeding Pseudocysts and Pseudoaneurysms Caused
by Pancreatitis. Arch. Surg. 1983, 18, 45.

25. Eidus, L.B.; Rasuli, P.; Manion, D.; Heringer, R. Caliber-
Persistent Artery of the Stomach (Diculafoy’s Vascular
Malformation). Gastroenterology 1990, 99, 1507.
26. Miko, T.L.; Thomazy, V.A. The Caliber Persistent Artery
of the Stomach: A Unifying Approach to Gastric
Chapter 46. Splanchnic Artery Aneurysms 667
Aneurysm, Diculafoy’s Lesion, and Submucosal Arterial
Malformation. Hum. Pathol. 1988, 19, 914.
27. Thomford, N.R.; Yurko, J.E.; Smith, E.J. Aneurysm of
Gastric Arteries as a Cause of Intraperitoneal Hemorrhage:
Review of Literature. Ann. Surg. 1968, 168, 294.
CHAPTER 47
Infected Aneurysms
Bruce A. Perler
Calvin B. Ernst
Arterial infection is one of the most demanding problems
encountered by the vascular surgeon. Although improvements
in surgical technique and better antimicrobial prophylaxis
have reduced septic complications of vascular reconstruction,
the infected aneurysm continues to pose a threat to life and
limb. Even in an era of rapidly expanding diagnostic and
therapeutic technology, diagnosis remains difficult and is
often delayed, treatment is demanding, and the results, while
improving, are far from satisfactory. It is the purpose of this
chapter to offer a pragmatic definition of infected aneurysms,
to highlight the appropriate diagnostic approach, to provide
an overview of the microbiology and anatomic distribution of
these lesions, and to outline therapeutic options.
HISTORY AND EVOLUTION OF
TERMINOLOGY
Infected aneurysms are among the oldest arterial lesions
described in the western literature. As early as the sixteenth
century, Ambrose Paré recognized that aneurysms could
develop secondary to microbial infection, specifically
syphilis. In 1844 Rokitansky[1] described abscesses in the
walls of arteries and proposed that they resulted from the
lodgement of infected emboli. Koch,[2] in 1851, described a
22-year-old man who died suddenly from a ruptured
aneurysm of the superior mesenteric artery while being
treated for endocarditis. In 1853 Tufnell[3] reported a 25-year-
old man with endocarditis and a popliteal aneurysm.
It was against this background that Sir William Osler,[4] in
the first of his Gulstonian Lectures to the Royal College of
Physicians in London in March 1885, coined the term mycotic
aneurysm. Osler described several cases in which he believed
valvular vegetations characteristic of endocarditis spread
directly to the aortic wall and led to aneurysmal degeneration.
Osler’s work firmly established mycotic aneurysms as a
clinical entity and stimulated other workers to make further
observations. By 1923, Stengel and Wolferth[5] had identified
217 cases of mycotic aneurysm from a review of the world
literature.
Hobson/Wilson/Veith: Vascular Surgery: Principles and Practice, Third Edition, Revised and Expanded
DOI: 10.1081/0819-9-120024930
Copyright q 2004 by Marcel Dekker, Inc.
669
Terminology
Confusion exists concerning the classification and nomencla-
ture of infected aneurysms (Table 47-1). Presumably, Osler[4]
called these lesions “mycotic” because of the “fresh fungus
vegetations” in the mulitple beadlike aneurysms he described.
Although mycotic is synonymous with fungal, the term mycotic
aneurysm has been used inappropriately to describe any
arterial aneurysm caused by microorganisms, fungal or
bacterial. To be accurate and minimize confusion, a mycotic
aneurysm should be considered a lesion that develops as a
complication of bacterial endocarditis, as Osler described.
Eppinger[6] introduced the term embolomycotic to describe
these aneurysms. Although others postulated that emboliza-
tion of endocardial vegetations led to aneurysm formation
through purely traumatic effects, Eppinger identified the same
bacterial strains at the site of emboli as found in endocardial
vegetations. He postulated that lodgement of bacteria-laden
emboli in the arterial wall initiated the development of an
exudative periarteritis with subsequent destruction of the
elastic and muscular elements of the wall, with eventual
aneurysm formation. The term embolomycotic recognizes
both the traumatic and infectious elements in development of
these aneurysms.[7]
Although over 90% of the mycotic aneurysms reported in
the early literature were associated with endocarditis, there
were sporadic reports describing patients with infected
aneurysms but without endocardial disease.[8] In 1937
Crane[9] described a patient with a multilocular aortic
aneurysm who had no evidence of endocardial infection. He
coined the term primary mycotic aneurysm to describe this
entity. Revell,[10] in a 1943 review of the literature, found only
23 cases of primary mycotic aneurysms and added one of his
own. He emphasized that a mycotic aneurysm should be
classified as primary if it results from a bacteremia from an
obscure focus, reiterating Crane’s definition.[9,10] According to
these criteria, Osler’s mycotic aneurysms would be classified
as secondary mycotic aneurysms, since they developed as a
result of the emobilization of infected vegetations or from the
direct spread of aortic valve vegetations to the sinus of
Valsalva or the aortic wall. Likewise, direct spread of sepsis
from an infected lymph node or osteomyelitis to an adjacent
artery would lead to secondary mycotic aneurysm formation.[8]
www.dekker.com
670 Part Five. Aneurysms

Table 47-1. Historical Nomenclature for Arterial Infection
Mycotic aneurysm
Primary mycotic aneurysm
Secondary mycotic aneurysm
Cryptogenic mycotic aneurysm
Embolomycotic aneurysm
Bacterial aortitis
Nonaneurysmal suppurative aortitis
Microbial arteritis
Compounding the confusion as to nomenclature was the
introduction of the term cryptogenic mycotic aneurysms by
Blum and Keefer[11] in 1962. They noted that infected
aneurysms resulted from the deposition of organisms upon a
diseased intimal surface. In cryptogenic mycotic aneurysms,
the source of the bacteremia was unknown, as opposed to a
known albeit extravascular or noncontiguous source in the
primary mycotic aneurysm.[12] Since pathophysiology, bac-
teriology, clinical presentation, and proper therapy of these
lesions are similar to those of the primary mycotic aneurysms
described in most series (see below), this additional
terminology seems superfluous.
Rokitansky’s observation of abscess formation within the
arterial wall remained unnoticed for many years.[7] Even-
tually, however, cases of arterial sepsis without aneurysm
formation were reported. Parkhurst and Decker[12] described
12 patients with bacterial infection of the aortic wall but with
aneurysm formation in only 9. In the 3 patients without
aneurysms, the disease entity was termed bacterial aortitis.
Bardin et al.[13] note that arterial infection without aneurysm
formation represents a midpoint on the continuum from
asymptomatic bacterial colonization to invasive infection
with aneurysm formation; they therefore coin the term non-
aneurysmal suppurative aortitis. Microbial arteritis has
recently been proposed to describe arterial infection without
aneurysm development.[14]
CONTEMPORARY CLASSIFICATION
Although most of the nomenclature has been well defined by
the respective proponents, the multiplicity of terms has led to
confusion regarding the appropriate classification of spon-
taneous arterial infection (Table 47-1). Patel and Johnston[15]
proposed a comprehensive classification in which an infected
aneurysm is categorized according to the preexisting arterial
condition (normal, arteriosclerotic, aneurysmal, or arterial
prosthesis) and the source of infection (intravascular or
extravascular). Intravascular sources of infection included
septic embolism, septicemia, or extension of adjacent
endocardial infection. Extravascular sources included spread
from adjacent foci or iatrogenic infection. Wilson and his
colleagues[16] classified all forms of spontaneous arterial
infection into seven categories (Table 47-2).
Review and study of the pathophysiology, bacteriology,
and epidemiology of these lesions supports a natural
distinction between mycotic aneurysms associated with
infective endocarditis as defined by Osler and those arterial
infections not associated with infective endocarditis. There-
fore, for the purposes of this chapter, these lesions are
classified as follows:
Mycotic aneurysms
Infected aneurysms (nonendocarditis)
Microbial arteritis with aneurysm formation
Secondarily infected aneurysm
Microbial arteritis without aneurysm formation
Infected anastomotic aneurysms
Colonized aneurysms
MYCOTIC ANEURYSMS
Incidence
Mycotic aneurysms may occur in a normal or arteriosclerotic
artery secondary to embolization or direct extension of septic
valvular vegetations in a patient with infective endocardi-
tis.[4,16] Prior to the introduction of antimicrobial drugs, this
type represented the most common form of arterial
infection.[5,7] In a 1923 review, Stengel and Wolferth[5]
identified 217 patients, in 186 (87%) of whom the aneurysms
developed secondary to endocardial infection. Pulmonary
infection and osteomyelitis were much less frequent causes. It
is difficult to ascertain how frequently mycotic aneurysms
develop in patients with infective endocarditis. In one report,

Table 47-2. Classification of Spontaneous Arterial Infection

I. Mycotic aneurysm Aneurysm occurring in a normal or atherosclerotic artery resulting from emboli or
endocardial origin.
II. Infected aneurysm Established aneurysm infected by bacteremia.
III. Microbial arteritis Infection of normal or atherosclerotic vessel by a bacteremia, often resulting in rupture
of the artery and pseudoaneurysm formation.
IV. Traumatic infected pseudoaneurysm Aneurysm due to trauma (penetrating or blunt); Inatrogenic injury; injection sites in
narcotic addicts.
V. Contiguous arterial infection Arterial invasion from an adjacent septic focus.
VI. Septic arterial emboli Infection seeded from other primary site.
VII. Spontaneous aortoenteric fistula Primary erosion.

Source: After Wilson et al.[16]


13% of patients with endocarditis died of mycotic aneurysm
rupture.[16]
The introduction of antimicrobial drugs has reduced the
mortality and morbidity of bacterial endocarditis, with a
consequent reduction in the incidence of mycotic aneurysms.
In 20,201 autopsies performed at the Mayo Clinic through
1954, a total of 178 abdominal aortic aneurysms were
identified and only 6 (3%) were infected.[17] None were
associated with endocarditis. On the other hand, in a 1967
report Perdue and Smith noted that 10 of 16 infected
aneurysms were secondary to endocarditis.[18]
Furthermore, while mycotic aneurysms secondary to
endocarditis compromise a much smaller component of
arterial infection than they did in the early part of this century,
it must be emphasized that endocarditis has not been
eradicated; its potential for septic arterial complications
remains an ongoing clinical concern. In a 1986 study, for
example, Dean et al. reported 9 patients with bacterial
endocarditis and 25 mycotic aneurysms/emboli at Vanderbilt
University. Multiple vessels were involved in 7 (78%) of
these patients.[19] This experience underscores the necessity
for comprehensive cerebral, visceral, and peripheral angio-
graphic examination of the patient who presents with a
mycotic aneurysm, since multiple vessel involvement is
common and, not infrequently, some lesions are clinically
silent. The use of contaminated needles by intravenous drug
abusers and the spread of acquired immunodeficiency
syndrome (AIDS) in this society may unfortunately contribute
to an increase in the prevalence of mycotic aneurysms in the
future.[20]
Pathogenesis
Mycotic aneurysms develop from infected heart valves either
by direct extension or by embolization. Eppinger[6] was the
first investigator to isolate identical bacterial strains from
mycotic aneurysms and endocardial vegetations in patients
with endocarditis, providing circumstantial evidence in
support of the embolic mechanism. Direct spread of infection
from the aortic valve to the ascending aorta occurs in a
substantial number of cases.[21,22] Embolization of infected
debris also occurs to the vasa vasorum or to small arterial
branches of the main vessel. Finding intact intima in the aorta
at sites of the mycotic aneurysm development suggests that
these intramural abscesses were seeded from the vasa
vasorum.[23 – 25] Infected emboli may cause thrombosis of
the vasa vasorum and resulting vessel wall ischemia;
compounded by the local sepsis, degeneration of elastic and
muscular elements may ensue, resulting in aneurysm
development.[26] This is probably the mechanism responsible
for aneurysm formation in large vessels such as the thoracic
aorta. Lodgement of septic emboli in small peripheral arterial
branches and the subsequent destructive infectious process
results in infected aneurysms of peripheral vessels.
In some patients, histologic examination of mycotic
aneurysms has documented intramural abscesses in the intima
and inner portions of the media, areas supplied not by the vasa
vasorum but by the intraluminal circulating blood.[27] Such
transmural inoculation leads to intimal and medial damage,
resulting in aneurysmal dilatation. This mechanism is
Chapter 47. Infected Aneurysms 671
probably operative in the smaller, more peripheral arteries.
The final common pathway is destruction of the arterial wall,
with progressive aneurysmal dilatation and eventual rupture.
Histology
The grossly normal vessel adjacent to the aneurysm may
harbor microscopic signs of inflammation. Although histo-
logic findings may be quite variable, the inflammatory reaction
is less acute in mycotic than in infected aneurysms. The most
characteristic findings in mycotic aneurysm are damage and
loss of intima, destruction of elastic lamellae—especially the
internal elastic lamina—periarteritis, or mesoarteritis. When
the inflammatory reaction is less acute, plasma cells and
lymphocytes may predominate. Usually, the inflammatory
reaction is most prominent around the vasa vasorum, which
may be thickened or obliterated in areas of the greatest
inflammation. In chronic aneurysms, an infiltration of
fibroblasts may be identified as well as calcification.[8,17]
INFECTED ANEURYSMS: MICROBIAL
ARTERITIS WITH ANEURYSM;
INFECTED ANEURYSM
Incidence
As our population ages and the incidence of aneurysmal
disease increases, more patients are being identified with
secondary infection of preexisting arterial aneurysms,
usually of the abdominal aorta.[28,29] In addition, microbial
inoculation of a diseased but nonaneurysmal arterial wall may
result in infection, mural weakening, and aneurysm
formation. Such lesions are classified as microbial arteritis
with aneurysm. Since pathogenesis and bacteriology of both
infected aneurysms and microbial arteritis with aneurysm are
similar, histologic differentiation is often impossible, and
treatment is the same, these lesions should be considered a
variant of the same disease process: infected aneurysms. As
with mycotic aneurysms, it is difficult to determine the
incidence of infected aneurysms. Most studies have evaluated
aortic aneurysms. In an autopsy series from Boston City
Hospital covering the years 1902 –1951, a total of 338 aortic
aneurysms were noted, and yet only 12 aortic infections
(3.5%) were recognized. Of these, 7 were associated with
bacterial endocarditis; thus, the incidence of nonendocarditis
infected aneurysms was 1.5%.[12] Some have estimated the
incidence of infected abdominal aortic aneurysms to be as
high as 3–5%.[30] In a recent study, Klontz identified 23
patients with infected aneurysms discharged from all
Veterans Administration hospitals from 1986 to 1990.[31]
However, in another review of 2585 aneurysm cases, the
incidence of infection was only 0.9%.[32] Reddy et al.
reported an overall incidence of infected aortic aneurysms
of 0.65% at Henry Ford Hospital during the last
30 years, although the incidence had increased from
0.13% in the 1960s to 0.54% in the 1970s and 1.61% in the
1980s.[33]
672 Part Five. Aneurysms

Pathogenesis In addition to these anatomic factors, depressed host

Available data suggest that inoculation of an intimal lesion
during transient bacteremia is the mechanism by which both
microbial arteritis and infection of a preexisting arterial
aneurysm are initiated. Since intact intima is known to be
highly resistant to bacterial infection, a defect in the intimal
surface appears necessary for microbial arteritis to
develop.[34,35] Arteriosclerosis significantly diminishes resist-
ance of the arterial wall to bacterial infection and is the
underlying abnormality in the majority of patients with
infected aneurysms.[36] Thrombus within arterial aneurysms
and the large area of intimal disruption makes these lesions
particularly suspectible to infection. Whether the infection
develops in a nonaneurysmal atherosclerotic plaque or within
an aneurysm, results are similar. Localized sepsis results in a
disintegration of mural elastic and muscular elements, with
resultant progressive dilatation of the vessel. Once a nidus of
infection is established within a plaque or aneurysm
thrombus, it becomes difficult or impossible for systemic
antimicrobial agents to eradicate the infection.
Although atherosclerosis is the most common lesion
predisposing to the development of infected aneurysms, any
condition that causes irregularity of the luminal surface,
such as coarctation, may predispose to secondary bacterial
infection.[37] It has been suggested that the thickened intima
characteristically located just distal to the coarctation is
particularly suspectible to bacterial invasion.[38] Infected
aneurysms may also develop secondary to chronic arteriove-
nous fistulas.[39] Progressive dilatation of the proximal artery
and associated degenerative changes of the arterial wall
appear to increase susceptibility to bacterial infection.[40] An
infected aneurysm may develop at the reentry site of a chronic
aortic dissection.[41] Spontaneous arterial infections have also
developed in segments of cystic medionecrosis and areas of
syphilitic aortitis.[16,42]
Some infected aneurysms have been identified with
apparently intact intimal surfaces. Under these circumstances
it is presumed that hematogenous infection seeded the arterial
wall via the vasa vasorum.[25] An association has been
demonstrated between infected aortic aneurysms and both
lumbar osteomyelitis and infected paraaortic lymph nodes. In
one study,[43] 18% of the patients with infected aneurysms of
the abdominal aorta also had apparent involvement of adjacent
lumbar vertebrae. It is possible that infection within the
vertebrae or lymph nodes reaches the aorta via the lymphatic
channels or the vasa vasorum, although evidence in support of
this mechanism is speculative.[25]
immunity has been implicated in the genesis of infected
aneurysms in at least 25% of cases reviewed.[44] Solid or
hematopoietic malignancy, lymphoproliferative disorders,
chronic alcoholism, the use of corticosteroids or chemother-
apeutic agents, chronic renal insufficiency, autoimmune
diseases, and diabetes mellitus have been noted in some
patients developing infected aneurysms.[44]
Histology
Infected aneurysms can usually be distinguished from the
classic mycotic aneurysms histologically. In an infected
aneurysm, the inflammatory reaction is very localized, in
contrast to the diffuse inflammatory involvement in mycotic
aneurysms; it is so localized that the diagnosis may be missed
unless multiple microscopic sections are examined. Whereas
the intima may be absent in mycotic aneurysms, identifiable
fragments of all layers of the arterial wall are usually found in
the infected aneurysms. Inflammatory reaction is consistently
acute in infected aneurysms, whereas subacute or even more
chronic changes may be noted in mycotic aneurysm.[28]
ANATOMIC DISTRIBUTION
Mycotic and infected aneurysms have involved almost every
artery (Table 47-3).[45 – 48] Excluding intracranial vessels, the
most common sites are the aorta, visceral arteries, and upper
and lower extremity vessels.
Aorta
All segments of the aorta (Fig. 47-1) have been affected, from
the ascending thoracic aorta to the bifurcation. When bacterial
endocarditis was prevelant, mycotic aneurysms frequently
developed in the ascending aorta and arch. As infected
arteriosclerotic aneurysms have become more prevalent than
true mycotic aneurysms, the infrarenal abdominal aorta, due
to its predilection for arteriosclerotic degeneration, has been
more commonly involved.[34] To date at least 39 infected
aneurysms of the suprarenal abdominal and/or descending
thoracic aorta have been reported,[32] and the incidence
appears to be increasing.[49 – 53] For example, in a 1998 report
of 17 infected aortic aneurysms from Oregon Health Sciences
University, 7 (41%) were suprarenal.[53]

Table 47-3. Anatomic Distribution of Mycotic and Infected Aneurysms

Strengel[5] Lewis[7] Revell[10] Mundth[34] Anderson[47] Brown[48] Total

Aorta 66 (25%) 12 (11%) 21 (75%) 13 (76%) 2 (12%) 3 (30%) 117 (27%)

Visceral 69 (26%) 31 (29%) 4 (14%) 1 (6%) 0 0 105 (24%)
Arm 23 (9%) 13 (12%) 2 (7%) 0 3 (19%) 1 (10%) 42 (10%)
Leg 31 (12%) 11 (10%) 1 (4%) 2 (12%) 7 (44%) 2 (20%) 54 (12%)
Iliac 10 (4%) 3 (3%) 0 1 (6%) 4 (25%) 1 (10%) 19 (4%)
Other 65 (34%) 37 (35%) 0 0 0 3 (30%) 105 (24%)
Total 264 107 28 17 16 10 442
 Chapter 47. Infected Aneurysms 673

Figure 47-1. Lateral (left) and AP (right) aortograms showing typical saccular appearance of a mycotic aortic aneurysm.

Carotid Artery other penetrating trauma.[60 – 63] Nevertheless, bacterial endo-

Fortunately, since they represent special problems in manage-
ment (see below), infected aneurysms involving the extracranial
carotid artery are uncommon. In one institution, over an 11-year
period during which 23,000 arterial aneurysms were treated,
only 11 infected carotid aneurysms were seen.[54] In a
review of the literature, Jebara et al. identified 26 cases of
infected carotid artery aneurysms.[55] Prior to availability of
antimicrobial drugs, many infected carotid aneurysms resulted
from pharyngeal or cervical streptococcal infections.[56]
Spontaneous carotid artery infections have been reported
following dental extractions and carotid angiography, as well as
with septic arthritis.[57 – 59] Most recently, infected carotid
aneurysms have been associated with intravenous drug use and
carditis continues to be a cause of mycotic carotid aneurysm.[64]
All age groups have been affected; one report described a
pediatric patient who developed an infected carotid artery
aneurysm secondary to a chronic immunosuppressive state.[65]
Visceral Arteries
Infection remains one of the most common causes of visceral
artery aneurysms (Fig. 47-2).[66] In the preantibiotic era, it was
estimated that 20% of splenic artery aneurysms were mycotic.
Presumably, such aneurysms resulted from emboli from
infected cardiac vegetations.[67] In a 1969 review[68] of 350
splenic artery aneurysms, 38 mycotic or infected lesions were

Figure 47-2. Selective celiac arteriogram of mycotic common hepatic (large arrow) and proper hepatic (small arrow) arterial
aneurysms.
674 Part Five. Aneurysms

identified. It is not known how often arteriosclerotic aneurysms Table 47-4. Microbiology of Infected Aneurysms
of the splenic artery become infected. Although superior (Excluding Colonized Aneurysms)
mesenteric artery (SMA) aneurysms are not common, infection
has been responsible for about 60% of these lesions.[65,69,70] No. positive cultures
Parenteral drug abuse has contributed to the development of
infected SMA aneurysms,[71] which may involve the main trunk Organisms Pre-1984 1984 –1990 1991– 1998
or branch arteries.[72 – 75]
Staphylococcus 23 22 13
The hepatic artery is rarely aneurysmal (Fig. 47-2). As
Salmonella 17 18 20
with the SMA, however, infection is the most common
E. coli 10 5 3
etiology.[76] The majority of hepatic arterial lesions reported
Streptococcus 7 7 19
have resulted from septic emboli from endocarditis. Since
Pseudomonas 7 – 1
1960, however, only 16% of hepatic artery aneurysms have
Enterobacter 5 3 –
been infected.[76] Most recently, infected hepatic artery
Klebsiella 4 2 2
aneurysms have been seen as a complication of orthotopic
Proteus 4 – 1
liver transplantation. The incidence has been estimated to be
Pneumococcus 2 – 1
1 – 3%, and previously most cases were identified at
Mycobacterium 2 1 1
autopsy.[70 – 79] Aneurysms have involved the main hepatic
Yersinia 1 – –
as well as the donor gastroduodenal artery.[80] Recently,
Arizona hinshawii 1 – –
Fichelle et al. reported successful repair of an infected hepatic
Enterococcus 1 1 –
artery pseudoaneurysm in a 35-year-old liver transplant
Campylobacter fetus 1 4 3
patient using a saphenous vein renal-hepatic artery bypass.[81]
Citrobacter – 2 1
Deitch et al. recently reported the first case of an infected
Haemophilus 1 3 –
renal artery pseudoaneurysm secondary to renal artery
Edwardsiella – 1 –
percutaneous transluminal angioplasty (PTA) and stent
Brucella – – 2
placement, with a successful surgical repair.[82] It was
Anaerobes 7 9 9
postulated that the deposition of platelets and thrombus at the
Fungal 5 1 2
angioplasty site may stimulate a localized arteritis, thus
97 79 78
predisposing to bacterial seeding. As is customary in most
endovascular procedures, prophylactic antibiotics had not Source: Refs. 13,14,29,32–35,39,41,43,47,51,57,60,63,67,71,77,84,88,
been administered. In view of the increasing performance of 89,96–107,111,113,128,135,143,147,150,163,166,200,226,242.
percutaneous endovascular procedures in the non –operating
room setting, one may see further cases of arterial infection
related to this etiology. Although experience to date is
anecdotal, prophylactic antibiotic administration may be depends upon the etiology of the aneurysm. When bacterial
appropriate peri-procedurally in this scenario. endocarditits was common, nonhemolytic streptococci,
pneumococci, and staphylococci were frequently identified.[5]
In a 1943 study[10] of 24 aneurysms, pneumococci (33%),
Extremities streptococci (33%), gonococci (22%), and staphylococci
(11%) were identified. In a review of cases recorded prior to
Mycotic and infected aneurysms involve arm and leg arteries 1960, streptococci and staphylococci were found to be the
in about 20% of cases (Table 47-3). Brachial and radial artery most common offenders (80%), followed by pneumococci
infection has resulted from arteriographic catheterization and enterococci.[16]
procedures and indwelling arterial cannulas for hemodynamic As endocarditis has become less prevelant, bacteriologic
monitoring.[83 – 85] Parenteral drug abuse appears to be patterns have likewise shifted. The incidence of staphylo-
superceding arterial cannulation procedures as the major coccal infection appears to be increasing (Table 47-4).
cause of femoral artery infection.[48,86,87] Due to the Salmonella species have also emerged as frequent pathogens
widespread nature of the drug problem, some centers now of infected aneurysms, particularly in the aorta. In three large
report that infected femoral artery aneurysms are more reviews[90 – 95] of arotic infection, Staphylococcus (25%) and
common than infected aortic aneurysms.[48] There has also Salmonella (31%) species predominate. Other reports[34]
been a recent increase in the incidence of infected iliac artery document isolation of Salmonella from 23 –66% of infected
aneurysm as a complication of kidney and pancreas aneurysms. In addition to the emergence of Salmonella and
transplantation.[88,89] Finally, sporadic cases of infected iliac the continued prevelance of staphylococcal species as
artery aneurysms, secondary to PTA and stent placement, are responsible pathogens, other gram-negative organisms and
being reported.[90 – 92] anaerobic bacteria are being identified with increasing
frequency.[47,96 – 106]
Aneurysm cultures are not always revealing. In one study,[28]
only 53% of aneurysm tissue sampled yielded growth of
BACTERIOLOGY organisms. In another,[34] 71% of aneurysm cultures were
positive. Universal failure to grow organisms from obviously
Numerous organisms have been isolated from mycotic and infected aneurysms relates to culture techniques, fagility of the
infected aneurysms (Table 47-4). The organism isolated organism, and intercurrent antibiotic therapy.

In addition to failure to culture organisms consistently, the
source of infection has been determined in only 54–71% of
cases.[28,34] Osteomyelitis was formally a common contribut-
ing etiology. Bacteremia secondary to gastroenteritis and
endocarditis was also frequently noted. Less commonly
encountered were urinary tract sepsis, esophageal fistula,
diverticulitis, otitis media, pulmonary infection, and cellulitis.
Recently, an infected abdominal aortic aneurysm was
reported secondary to an appendiceal abscess.[107] Clearly,
transient bacteremias from unknown foci are an important
factor in the pathogenesis of infected aneurysms.
In addition to identifying appropriate antibiotic therapy,
culture data may have some prognostic significance. Gram-
negative infections of abdominal aortic aneurysms appear
more ominous than gram-positive infections. In Jarrett’s
review,[43] the mortality rate was 84% among patients with
gram-negative infections, contrasted to only 50% when the
aneurysm contained gram-positive organsims. Rupture of the
aneurysm occurred in 5 of 6 patients with gram-negative
infections, compared to 1 of 10 with gram-positive organisms.
The greater tendency for rupture with gram-negative infection
and, hence, the increased mortality rate may reflect increased
organism virulence.
Salmonella Infection
One of the more fascinating yet incompletely understood
aspects of infected aneurysms, which deserves special
comment, is the tendency for Salmonella species to cause
arterial infection. Three types of vascular lesions may result
from Salmonella infection. First, a diffuse suppurative
arteritis may cause arterial rupture, resulting in a saccular or
false aneurysm. Second, Salmonella may initiate a focal
arteritis that leads to weakening of the arterial wall and
formation of a true infected aneurysm. Third, Salmonella
species may infect a preexisting aneurysm. Salmonella
arterial infections have been reported in the thoracic and
abdominal aorta as well as the iliac, femoral, popliteal, and
coronary arteries, although 75% affect the aorta and 50%
involve the abdominal aorta.[16,107 – 115] Recent studies
continue to demonstrate that Salmonella is a frequent source
of arterial infection.[116 – 123] Infection by Salmonella may be
faciliated by immunosuppressive diseases such as diabetes,
malignancy, human immunodeficiency virus, hemolytic
diseases such as sickle cell anemia and malaria, as well as
raw gastric acidity and alterations in the intestinal
flora.[44,115,124,125] Inoculation of the organisms on a diseased
intimal surface appears to be the initiating event in most
cases,[126] although invasion of previously healthy intima can
occur.[108]
Salmonella organisms are gram-negative flagellated
bacteria of the family Enterobacteriaceae, with over 2200
serotypes.[115] The most common isolates from infected
aortic aneurysms are S. choleraesuis (32%), S. typhimurium
(27%), and S. enteritides (9%).[127,128] Organism serotype
determines the specific clinical syndrome.[115] The high
incidence of Salmonella arteritis due to S. choleraesuis is
probably related to its propensity to cause a severe
bacteremia.[129 – 131] Fifty percent of all Salmonella bacter-
emias are due to S. choleraesuis, with localized suppurative
Chapter 47. Infected Aneurysms 675
infection occurring in 10%. In addition to arteritis, meningitis,
pleuropulmonary disease, endocarditis, and osteomyelitis,
there have been reports of splenic, hepatic, and soft tissue
abscesses.[114]
The recent increase in Salmonella arterial infection has led
to a rethinking of previous dogma concerning antibiotic
therapy for Salmonella gastroenteritis. Since antibiotics
prolong the fecal excretion of Salmonella and increase the
frequency of resistant stool isolates, most investigators
recommend no treatment for this otherwise self-limited
gastrointestinal ailment.[132] However, in an extensive
review[133] of state laboratory records of Salmonella
bacteremia in Massachusetts, it is noted that 10 of 105
patients with bacteremia developed endothelial foci of
infection. Of these 10 patients, 4 had preexisting untreated
gastroenteritis. Furthermore, all 10 were over 50 years of age.
Since only 40 patients older than 50 were noted to have
Salmonella bacteremia during the study period, the incidence
of endothelial infection in this group was 25%. Others have
corroborated a predilection of Salmonella arteritis for older
individuals.[134] Therefore, it has been suggested that
antibiotic treatment of patients over age 50 with Salmonella
gastroenteritis might reduce the incidence of endothelial
infection.[133]
Unusual Bacteria
Several unusual organisms have been increasingly isolated
from infected aneurysms in recent years. Plotkin and
O’Rourke[135] describe a 53-year-old man with an infected
aneurysm of the internal carotid artery due to Yersinia
enterocolitica, an aerobic and faculatively anaerobic nonen-
capsulated rod-shaped gram-negative organism. It was
presumed that a transient bacteremia in this patient resulted
in secondary infection of an arteriosclerotic carotid plaque
with eventual aneurysm formation. Arizona hinshawii and
Campylobacter fetus have also been isolated from infected
aneurysms.[136,137] Bacteremia of the genus Arizona are
among the Enterobacteriaceae that have been noted to cause a
variety of diseases in humans, including gastroenteritis,
urinary tract infection, cholecystitis, septic arthritis, osteo-
myelitis, and septicemia. Although taxonomically distinct
from other Enterobacteriaceae, these organisms were at one
time considered to belong to the genus Salmonella, since there
are a number of biochemical and serologic similarities
between these two groups of organisms.[138] Campylobacter,
like Salmonella, lacks the enterotoxin production, cytotox-
icity, and invasive properties exhibited by other enteric
organisms. Thus, although precise mechanisms of arterial
infection are not known, Campylobacter and Arizona
infections may share similar characteristics with Salmonella.
Clostridium septicum is a relatively uncommon anaero-
bic pathogen responsible for approximately 1% of all
clostridial infections, and often is identified in patients with
underlying malignant disease.[139] Over the past two
decades 10 patients, ranging in age from 68 to 85, have
been reported with infected aneurysms due to Clostridium
septicum. At least six of these patients had documented
malignancies.[105]
676 Part Five. Aneurysms
Fungal Infection
Despite the widespread use of the word mycotic (arising from
the Oslerian term fungus vegetations ) to describe infected
aneurysms, such aneurysms only rarely result from fungal
infection. The thoracic and abdominal aorta as well as the
major peripheral and intracranial arteries may be affected,
however. Histoplasma capsulatum, Aspergillus fumigatus,
Candida albicans, Actinomyces, and Penicillium species are
the only reported causative agents.[140 – 145]
Like systemic fungal infections, these arterial infections
tend to be associated with chronic immunosuppressive states,
diabetes mellitus, and the use of contaminated nee-
dles.[140,145,146] The precise mechanism of arterial infection
varies but is similar to that for bacterial involvement.
Inoculation of arteriosclerotic plaques by blood-borne
organisms has been documented only for Histoplasma.[140]
Embolization of infected valvular vegetations and contiguous
spread from adjacent foci of infection may also be responsible
for some cases.[140,146] Arterial infection via the vasa
vasorum, well established for bacterial organisms, has not
been conclusively documented for fungi.[140]
Fungal infection of arterial aneurysms may occur long
after recognition of the original fungal infection. Such
aneurysms are usually saccular; when they involve the
abdominal aorta, vertebral body erosion is frequently noted.
The risk of rupture of these lesions is significant. In a
review[140] of aortic aneurysms infected with Histoplasma
capsulatum, survival was only 33%. When fungal infection of
an aneurysm is suspected at operation, frozen section
specimens should be examined for confirmation. Principles
of surgical treatment are similar to those for aneurysm
infection with bacteria (see below).
INFECTED ANASTOMOTIC
ANEURYSMS
Infected anastomotic aneurysms bridge the gap between pure
arterial infection and prosthetic graft infection. Anastomotic
aneurysms occur following 2 –5% of bypass grafts, and a
majority involve the femoral anastomosis.[147] Traditionally,
the development of anastomotic aneurysms has been
attributed to a variety of factors such as structural weakness
of the artery (often after endarterectomy), suture fracture,
graft deterioration, and mechanical stress from patient activity
or hypertension. Infection has been considered an infrequent
cause. Only 12% of these lesions reported between 1972 and
1982 were infected.[148] However, a recent report suggests
that a occult infection may play an etiologic role in many of
these aneurysms. In a series of 45 anastomotic aneurysms,
Seabrook et al.[149] identified 32 bacterial isolates from 27
(60%) of these lesions. Coagulase-negative staphylococci
accounted for 24 (88%) of the isolates. These findings
suggested that bacterial contamination and colonization may
occur at implantation, resulting in a chronic, low-virulence
infectious process at the arterial suture line, with late
pseudoaneurysm formation. Furthermore, as the quality of
graft and suture materials improves, the incidence of
overtly infected anastomotic pseudoaneurysms is increasing,
having been noted in 28% of the cases in another recent
report.[150]
ENDOVASCULAR INFECTION
Arterial infection secondary to endovascular stent place-
ment also bridges the gap between pure arterial infection
and prosthetic graft sepsis. The true incidence of arterial
infection secondary to intravascular stent placement is not
known, is probably quite low, but, as noted above, is now
being increasingly seen in a variety of anatomic
locations.[82,90 – 92,151 – 154] Treatment of this complication
should follow the principles of native arterial infection
management, as described below.
COLONIZED ANEURYSMS
The isolation of positive bacterial cultures from the contents of
clinically noninfected arteriosclerotic abdominal aortic aneur-
ysms was first reported by Ernst et al.[155] Several subsequent
studies have demonstrated an incidence ranging from 7 to
20%.[156 – 161] Staphylococcal species have predominated.
Previous experience has failed to conclusively demonstrate an
increased risk of subsequent graft infection and positive
aneurysm cultures in the elective setting. Conversely, the
incidence of positive cultures is highest in symptomatic aortic
aneurysms. This subtle relationship between aneurysm
colonization and rupture may be more than coincidental,
although the mechanism remains unexplained.
NATURAL HISTORY
Complications of infected aneurysms include progressive
enlargement and rupture, thrombosis, and embolization. The
incidence of rupture is high, averaging 54%, compared to
20% for noninfected aneurysms.[162] In fact, without surgical
intervention infected aortic aneurysms were almost always
fatal. In one recent review, the mortality among patients
with Salmonella aortic aneurysms was 95% when treated
medically.[117] Furthermore, ruptured infected aneurysms are
usually smaller than ruptured noninfected aneurysms, and
progression to rupture occurs rapidly. Less commonly, a slow,
insidious course precedes rupture of an infected aueurysm. A
febrile illness lasting weeks and even months in some cases has
been described prior to eventual rupture.[28]
Outcome once an infected aneurysm has ruptured depends
upon the vessel involved. Infected aortic aneurysms represent
the greatest risk to life. Earlier studies of patients with ruptured
infected aortic aneurysms documented a mortality rate
approaching 95%.[162] More recent studies have reported a
much more favorable outcome, however. Aortocaval and
aortoenteric fistulas have also been reported secondary to
mycotic and infected aneurysms.[136,162] Limited perforation,
particularly of a peripheral vessel, results in pseudoaneurysm
formation with persistent sepsis.
Prior to rupture, both aortic and peripheral aneurysms may
shed emboli, causing septic arthritis and purpura.[163]
 Chapter 47. Infected Aneurysms 677

Although less common than rupture, thrombosis of myocotic Table 47-5. Clinical Characteristics of Infected Aneurysms
and infected aneurysms has been noted both in the aorta and
Epidemiology Males . females (4 to 1)
peripheral vessels. It has been suggested that thrombosis of
All age groups
these lesions may result in cure, but evidence in support of
Bacterial endocarditis
this contention is limited.[8]
Atherosclerosis; illicit drug use
History Intermittent febrile episodes
Malaise
DIAGNOSIS Weight loss
Pain
Exam Fever with chill (70 – 94%)
Clinical Presentation Pain (2 100%)
Rapidly expanding mass (50– 90%)
The clinical presentation (Table 47-5) of patients with
Laboratory Leukocytosis (65– 83%)
mycotic and infected aneurysms depends upon the pathogen-
Positive blood cultures (50%)
esis, underlying etiology, and vessel involved. Septic arterial
X-ray Noncalcified aneurysm
lesions have been noted in all age groups, from neonates to the
Lumbar osteomyelitis (AAA)
elderly.[5,22] Earlier reports documented these lesions most
Lobulated, saccular arteriographic
commonly in the second, third, and fourth decades, reflecting
appearance
the association with bacterial endocarditis.[5] More recently,
Operative findings Thin-walled aneurysm
however, there has been a shift in incidence to the elderly. In a
Surrounding inflammatory reaction
1967 study,[28] only 9% of infected aortic aneurysms occured
Succulent lymph nodes
in patients younger than age 40, whereas nearly three-fourths
Positive Gram stain
occurred in those over age 60. In a 1996 report of patients
with infected thoracic and abdominal aortic aneurysms,
patients ranged from 57 to 83 (mean, 70) years of age.[164]
The increasing age of patients affected with aortic infection or epigastric pain suggestive of cholecystitis or pancreatitis.
emphasizes the importance of diseased arterial intima, usually Likewise, SMA lesions may be confused with inflammatory
by arteriosclerosis, in the pathogenesis of microbial arteritis, diseases of the small or large bowel. Malabsorption has been
as well as the rising incidence of infected arteriosclerotic reported in association with an infected SMA aneurysm.[168]
aneurysms. Conversely, the prevelance of drug abuse and the Infected aneurysms of the peripheral vessels may be
use of contaminated needles—as well as AIDS—may lead to confused with localized soft tissue abscesses, cellulitis, or
an increased incidence of infectious arterial problems in lymphadenitis. A thrombosed, infected femoral artery
younger patients in the future.[19,165] aneurysm may mimic an incarcerated or strangulated groin
Most mycotic and infected aneurysms have been reported hernia. Failure to maintain a high index of suspicion can result
in males. Stengel and Wolferth[5] note that approximately in surgical disaster if one approaches these lesions without
two-thirds occurred in men; other studies[10,12,28] document a proper exposure and control.[14]
male predominance ranging from 82 to 91%. In contrast,
Jarrett and his colleagues[43] reported infected aortic
aneurysms in 7 women and 10 men.
Fever or history of a recent febrile illness are the most Laboratory Data
common complaints in patients with infected arterial lesions; Leukocytosis is the most consistently abnormal laboratory
these symptoms have been noted in 70–94% of patients with finding in patients with mycotic or infected aneurysms. A
proven mycotic or infected aneurysms.[34,43,47] The fever may leukocytosis above 10,000/mm3 has been noted in 65–83% of
be steady or intermittent and is usually associated with chills patients with proven infected aneurysms.[28,34,43] Antibiotic
and sweats.[14] Frequently, a long history of malaise, weight tibiotic therapy, however, may blunt this elevation.
loss, and increasing weakness is present. Pain is an almost Furthermore, leukocytosis may be noted following leakage
universal complaint. In patients with infected aortic from a noninfected aneurysm. Elevation of the erythrocyte
aneurysms, the discomfort may be localized to the abdomen sedimentation rate is a frequent but nonspecific finding. With
or back. In those with peripheral aneurysms, it is usually infected hepatic arterial aneurysms, liver function tests are
localized to the site of the lesion, where there may be usually unremarkable.[169]
overlying erythema, induration, and tenderness. Nearly 90%
of infected peripheral aneurysms are palpable, but only 50 –
65% of abdominal aortic aneurysms are.[34] Fever, along with Bacteriologic Studies
a tender abdominal aortic aneurysm, is presumptive evidence
of infection, since temperature elevation is rarely caused by Positive preoperative blood cultures provide strong con-
simple expansion or rupture.[43] When pain and tenderness of firmatory evidence for the presence of an infected aneurysm,
an infected aortic aneurysm are localized to the flank, although negative cultures do not rule out the diagnosis. In
differentiation from a perinephric abscess may be impos- one report,[47] only 50% of the patients had positive blood
sible.[166] Mistaken diagnosis of inflammatory intraabdominal cultures. In another,[34] positive blood cultures were found in
conditions may lead to confusion and catastrophy.[167] 53% of all patients and in only 46% of those with infected
Hepatic artery involvement may cause right-upper-quadrant aortic aneurysms. In contrast, Jarrett and his colleagues[43]
678 Part Five. Aneurysms
report that 70% of patients with infected aortic aneurysms had
positive blood cultures, and in each patient the organism
cultured from the blood was the same as that isolated from the
aneurysm. In a recent report from Henry Ford Hospital,
positive blood cultures were obtained from 69% of patients
with infected aortic aneurysms, and positive cultures were
noted more often in patients with ruptured in contrast to intact
aneurysms.[33] As many patients with infected aneurysms
may be receiving antibiotics at the time blood samples are
drawn, multiple samples may be required before bacteremia is
confirmed. Furthermore, the sampling of blood from an
arterial site downstream from the presumed focus of infection
may improve the yield of positive cultures.[170,171]
As with preoperative blood cultures, antibiotics may mask
bacterial growth from samples obtained at operation. It is
critically important, therefore, to perform a Gram-stain
examination in addition to bacterial cultures on material
obtained during operation. Positive operative cultures may be
obtained in 53 –94% of patients.[28,47] In most patients with
negative cultures, however, organisms will be identified on
histologic examination of tissue sections.[28] Mundth and his
colleagues[34] note that the responsible organism was isolated
in 71% of the aneurysm cultures. In the remaining 29%,
organisms were identified on Gram-stain examination of
the aneurysm wall or its contents. Reddy et al.[33] reported
positive intraoperative Gram stains in 50% of patients with
rupture but in only 1 of 8 patients with intact infected aortic
aneurysms. Operative cultures were positive in all patients
with ruptured and 89% of those with intact infected aortic
aneurysms.
RADIOLOGIC STUDIES
Plain Films
Frontal and lateral abdominal x-rays may provide useful
information in the patient with a suspected infected aortic
aneurysm. An association between osteomyelitis of the lumbar
vertebrae and infected aortic aneurysms has been documen-
ted.[29,43] Since vertebral body erosion is rarely noted within an
arteriosclerotic aortic aneurysm, such findings should raise
suspicion of aneurysmal infection. In addition, arteriosclerotic
abdominal aortic aneurysms are calcified in about 70% of cases,
and this calcification may be noted on standard lumbosacral
spine or frontal and lateral abdominal films.[172] Infected aortic
aneurysms, however, are less often calcified.[43] Therefore, a
noncalcified aneurysm in a patient with fever and leukocytosis is
strongly suggestive of an infected aneurysm.
Ultrasound
Abdominal ultrasound can confirm the presence of an aortic
aneurysm and provide a fairly accurate assessment of its size,
even in the absence of calcification.[172,173] Ultrasonography
is also helpful in documenting intraperitoneal abscesses, a
distended gallbladder suggestive of cholecystitis, pancreatic
masses, and other intraabdominal inflammatory conditions
that must be excluded in evaluating a patient for a possible
infected aortic aneurysm. To this end, ultrasonography is a
helpful screening procedure. No criteria have been described
which confirm aneurysm infection, however. Recently, Harris
and colleagues identified aortic wall thickening and false
aneurysm formation using transesophageal echocardiography
to evaluate two patients with aortic infection.[174]
Computed Tomography
The contrast-enhanced computed tomography (CT) scan is
extremely helpful in evaluating patients with suspected
infected aortic aneurysms. Several findings are highly
suggestive of the diagnosis, although none are patho-
gnomonic (Table 47-6).[175 – 181] An irregular, saccular
aneurysm noted in a febrile patient is highly suggestive,
particularly if there is disruption or absence of intimal
calcification. Gas within the aortic wall has been identified by
CT in patients with infected aneurysms.[175] More often, air or
fluid is identified adjacent to the aortic wall. An encasing or
adjacent mass—reflecting either hematoma, abscess, or
inflammatory nodal tissue—has also been seen with infected
aortic aneurysms. Finally, vertebral osteomyelitis adjacent to
an aortic aneurysm should raise the question of aneurysmal
infection. Clearly, CT examination may provide strong
circumstantial evidence of aortic infection prior to arterio-
graphically detected abnormalities.[181]
Radioisotope Examinations
Two new methods are currently available for the evaluation
of septic processes, particularly within the abdomen. Labeling
of human leukocytes with Indium-111, a gamma-emitting
agent, is now possible.[182] Indium-111 leukocyte scanning is
based upon external gamma camera detection of labeled
leukocytes that have accumulated at sites of infection or
inflammation. This technique has been utilized predominantly
to detect intraabdominal abscesses and has identified
prosthetic graft infection in a limited a number of
cases.[144,183] Bell et al.[184] reported the first case of an
infected aortic aneurysm detected by Indium-111 leukocyte
scanning. Leukocyte scintigraphy may complement CT
evaluation of patients with suspected arterial infection. Ben-
Haim and colleagues reported that four patients with infected
aneurysms were correctly identified by leukocyte scintingra-
phy, and the study was negative in 2 of 3 patients with
noninfected aneurysms.[185]
Table 47-6. CT Findings of Infected
Aneurysms
Saccular aneurysm
Irregular aneurysm lumen
Absence of calcification
Gas within aortic wall
Peri-aneurysmal gas
Peri-aneurysmal fluid
Encasing or contiguous mass
Associated para-aortic or psoas abscess
Vertebral osteomyelitis

Gallium-67 isotopic scans have been used to localize
intraabdominal abscessess. Radioactive Gallium-67 collects
in areas of inflammation and may be detected by external
scanning cameras. Successful use of Gallium-67 scanning in
the diagnosis of a Dacron aortic graft infection and
aortoenteric fistula has been reported.[186,187] The inflamma-
tory reaction inherent in a mycotic or infected aneurysm
should allow these arterial infections to be detected by
gallium scanning, although reports to confirm this suspicion
are not available.
Arteriography
An arteriogram is an essential part of the evaluation of any
patient with a presumably infected arterial aneurysm. In
addition to providing information for planning reconstruction,
arteriography may help confirm the diagnosis of infected
aneurysm. An excessively lobulated, saccular aneurysm
arising from an otherwise normal-appearing vessel that lacks
features of arteriosclerosis is highly suggestive of an
infectious etiology (Fig. 47-l).[188] The appearance of
localized smooth-walled aneurysmal changes, explained by
the rapidly progressive transmural inflammatory destructive
process, has been emphasized by others.[29] A particularly
eccentric aneurysm with a relatively small mouth in
comparison to its widest diameter also suggests infection.[189]
Despite these characteristic findings in some cases, the
angiographic appearance of many infected aneurysms may be
indistinguishable from that of typical arteriosclerotic,
traumatic, or congenital aneurysms.[190] Furthermore, angio-
graphic findings characteristic of infection typically occur late
in the course of the septic process.[181]
OPERATIVE FINDINGS
Certain findings at operation suggest infection within the
aneurysm, although such features may be quite subtle. Infected
aneurysms tend to be saccular, lobulated, and eccentric.[189]
The wall of the aneurysm is typically quite thin and friable.[28]
A moderate degree of surrounding inflammation may be noted,
and large, succulent lymph nodes adjacent to the aorta or in
proximity to a peripheral aneurysm may be encountered. The
typical inflammatory aneurysm of the abdominal aorta may
also be surrounded by large lymph nodes and be engulfed in an
inflammatory reaction. However, the wall of an inflammatory
aneurysm is usually thick and pearly white in contrast to the
thin-walled, red, mulberrylike infected aortic aneurysm. The
operating surgeon must maintain a high index of suspicion
when encountering unusual-appearing aneurysms in order to
make the diagnosis of infection.
TREATMENT
Successful management of the patient with arterial infection
remains one of the most difficult challanges encountered by
the vascular surgeon. The aim of therapy is to eradicate all
infection while maintaining adequate circulation. Principles
Chapter 47. Infected Aneurysms 679
of successful management are independent of the specific
lesion (mycotic aneurysm, microbial arteritis with or without
aneurysms, and secondarily infected aneurysm), mechanism
of infection (transmural bacteremic endothelial inoculation,
via vasa vasorum, or direct spread from contiguous sepsis), or
organism responsible.
Preoperative Management
Establishing the correct diagnosis preoperatively is the first
step in treatment. Multiple blood cultures should be obtained,
including several samples from a source downstream of the
presumed site of the aneurysm. Other potential sources of
infection such as urine, sputum, and open wounds should be
thoroughly cultured. High-dose intravenous organism-
specific antibiotic treatment must be started to prevent
continued hemotogenous spread of infection. The goal of
sterilization of the patient’s blood is important to prevent
possible contamination of a vascular prosthesis that might be
required for arterial reconstruction, although one should not
inordinately delay operative intervention for this purpose.
When attempts at identifying the offending organism(s) prove
futile, any combination of broad-spectrum bactericidal
antibiotics for both gram-positive and gram-negative organ-
isms (specifically Salmonella ) are appropriate. Although
sporadic cases of sterilization and spontaneous healing of
these lesions with antibiotics alone have been reported,[34,191]
this is the exception, if it occurs at all. Sudden rupture of
infected aneurysms has been observed while patients were
undergoing intensive antibiotic treatment.[17,28,188,192] Even
aneurysmal sterilization does not preclude progressive
enlargement and eventual rupture.[188,193,194]
Operative Management
Appropriate intravenous lines should be inserted. If
necessary, a Swan-Ganz catheter may be placed to monitor
pulmonary artery wedge pressure. The insertion of a radial
artery cannula in the nondominant wrist or the side opposite
anticipated axillofemoral reconstruction provides ready
access for blood sampling as well as systemic blood pressure
measurements.
Once the aneurysm has been exposed, infection must be
confirmed. When gross perivascular purulence is encoun-
tered, the diagnosis is obvious. In the absence of obvious
signs of sepsis, Gram stains should be obtained and frozen
sections of the aneurysm wall examined for bacteria or fungi.
Identification of microorganisms within the aneurysmal wall
or contents in the patient with fever, leukocytosis, positive
blood cultures, a particularly friable-appearing aneurysm or
an aneurysm surrounded by large lymph nodes is diagnostic
of aneurysm infection. Aerobic, anaerobic, and fungal
cultures must be obtained and plated immediately in
appropriate culture media.
Principles for managing infected aneurysms are generally
similar to those for dealing with an infected arterial
prosthesis. Wide debridement and copious irrigation with
antibiotic solution of all involved tissue is required. This
includes complete resection of the aneurysm if technically
possible. If rupture has occurred, a wider area will be involved
680 Part Five. Aneurysms
in the septic process and more aggressive debridement may be
required. Ligation of arteries should be performed in clean,
healthy-appearing tissue with synthetic monofilament or wire
sutures. Preoperative vascular laboratory data combined
with arteriography help document adequacy of collateral
circulation around the infected lesion. If, at the initial
operation, collateral circulation is adequate to support the
distal bed without arterial reconstruction, arterial ligation only
should be performed. If revascularization is necessary, the
method of reconstruction will depend upon the location and
extent of arterial involvement and the magnitude of the septic
process.[47,195]
Abdominal Aorta
Extraanatomic Reconstruction
The conventional management of the infected abdominal
aortic aneurysm is similar to the treatment of a secondary
aortoenteric fistula or an infected aortic prosthesis, namely,
excision of all septic tissue and extraanatomic arterial
reconstruction. Whether one is dealing with a ruptured or intact
abdominal aortic aneurysm, secure closure of the proximal
aortic stump distal to the renal arteries is mandatory for a
successful result and constitutes one of the more difficult aspects
of repair. Postoperative aortic stump dehiscence has been
documented in up to 33% of patients.[196] Healthy tissue that will
hold sutures may not be readily available. Under these
circumstances, temporary suprarenal aortic occlusion, at the
diaphragm through the lesser sac, permits complete mobili-
zation of the infrarenal aorta, unencumbered by an infrarenal
aortic clamp. A two-layer aortic closure with monofilament
suture has been recommended, and prevertebral fascia may be
used to strengthen the closure.[14,188,197] Although a pedicle of
omentum, transposed through the transverse mesocolon,
probably provides no strength, such coverage may facilitate
the resolution of periaortic infection (Fig. 47-3). Copious
irrigation of the retroperitoneum is performed and irrigating-
drainage catheters may be placed in the aortic bed for drainage
Figure 47-3. Methods of closing infrarenal aorta following aneurysm excision. A proximal row of continuous horizontal mattress
sutures is followed by a distal row of continuous over-and-over sutures (left). Prevertebral fascial flap buttress sutured over aortic stump
(center). Omental graft passed through transverse mesocolon provides additional protection (right). (From Ernst CB.[198] Reproduced by
permission.)
and postoperative through-and-through irrigation with anti-
biotic or povidone-iodine solutions during the early post-
operative period (Fig. 47-4).[115,198]
Although antecdotal reports[149,199,200] have described
successful management of infected aortic aneurysms by
resection without restoring arterial continuity, in the majority
of patients arterial reconstruction will be required to prevent
distal ischemia. The conventional approach dictates extra-
anatomic bypass through clean tissue planes. Axillofemoral
grafting as a means of extraanatomic bypass has gained
popularity since it was first introduced in the United States by
Blaisdell and Hall[201] in 1963, although long-term patency is
inferior to aortoiliac or aortofemoral reconstruction (Fig. 47-
4). When the infected aneurysm is small and limited to the
aorta and when, following excision and distal closure of the
aortic bifurcation, there is no significant iliac occlusive
disease, unilateral axillofemoral reconstruction is appropriate.
Under these circumstances, the contralateral leg will be
perfused retrograde around the bifurcation. If the bifurcation
must be excised and the common iliac vessels are free of
significant disease, they may be mobilized and anastomosed
end-to-end to form a neobifurcation, again allowing use of
unilateral axillofemoral reconstruction (Fig. 47-5).[29,195]
If recurrent occlusion of the axillofemoral graft becomes
a late problem, anatomic aortic reconstruction may be
performed provided the retroperitoneal infection has
completely resolved.[188] At least 6 – 12 months should
elapse from the original procedure before this option is
considered.
In the unstable patient with a suspected leaking or ruptured
infected aortic aneurysm, or in the patient in whom infection
has not been confirmed preoperatively, the abdomen must be
explored as the first step and the extraanatomic bypass
carried out with clean instruments after closure of the
abdomen. However, in view of the technical difficulty often
associated with the abdominal portion of the operation and
the time required, which may result in a protracted period of
limb ischemia, in the stable patient it appears that overall
results have improved most recently by performing the
extraanatomic bypass as the initial step.[36,188]

Figure 47-4. Infected aneurysm has been excised. The axillo-
bifemoral bypass maintains pelvic and leg circulation. Irrigation
drainage catheters are placed in retroperitoneal space (optional).
(From Ernst CB.[198] Reproduced by permission.)
In performing preliminary axillobifemoral reconstruction,
Cooke and Ehrenfeld[188] have advocated occluding the
common femoral artery proximal to the femoral anastomosis
to prevent acute graft thrombosis secondary to competitive
flow. However, based upon observations by Blaisdell and his
colleagues[202] as well as Ernst [203] it appears that
axillofemoral bypass grafts may remain patent for up to 4
months with competitive aortoiliac flow. Therefore, it does
not appear necessary to occlude host vessels proximal to groin
anastomoses for fear of failure of extraanatomic reconstruc-
tion due to competitive parallel blood flow. Bacteremic
contamination of the newly placed extraanatomic graft has
not been a problem.
In Situ Reconstruction
Over the last decade, in view of the continued significant
mortality and morbidity associated with the conventional
management of aortic infection, increasing numbers of
patients have undergone in situ revascularization following
resection and debridement of the infected tissues. This
strategy has elvolved from the management of patients with
suprarenal and thoracoabdominal aortic infection in whom
extraanatomic bypass is not an option. There are a number of
potential conduits which have been utilized.
Several workers have reported in situ reconstruction using
prosthetic conduits.[32,49,81,94,204 – 209] In the largest series
reported to date, Fichelle and colleagues replaced infected
infrarenal abdominal aortic aneurysms in 21 patients with
either Dacron[21] or polytetrafluoroethylene (PTFE)[2] grafts.
There were three (14%) deaths and no cases of recurrent
infection with a mean follow-up of 53 months[81] (see below).
In contrast, Pasic et al. reported an operative mortality of 33%
among 6 patients undergoing in situ prosthetic repair of
infected aortic aneurysms, and one survivor presented with a
late aortoenteric fistula.[204] Most recently, Gupta and
Chapter 47. Infected Aneurysms 681
Figure 47-5. After resection of infected aortic aneurysm and
ligation of infrarenal aortic stump, common iliac arteries have
been anastomosed and unilateral axillo-femoral bypass has been
performed. (From Scher LA, et al. [29] Reproduced by
permission.)
colleagues reported 2 patients who underwent in situ
replacement of infected aortic aneurysms with rifampin-
bonded Dacron grafts.[210] This preliminary clinical experi-
ence was based on prior studies demonstrating anti-
staphylococcal bactericidal activity on graft surfaces for at
least 2 days after aortic replacement as well as the lack of
thrombogenicity associated with rafampin bonding and the
absence of evidence suggesting the emergence of rifampin-
resistant organisms.[211 – 213] Another novel approach recently
reported has been the implantation of gentamicin-methyl-
methacrylate-methylmethacrylate beads in the bed of the
in situ prosthetic graft in 4 patients with infected aneurysms
of the carotid, innominate, ascending, and infrarenal
aorta.[214]
Review of this largely antecdotal experience highlights
several principles which should guide the clinician con-
templating in situ replacement of an infected aneurysm with a
prosthetic conduit. Aggressive soft tissue debridement is
absolutely necessary, and the graft anastomoses must be
performed to uninvolved vessels.[81] Gross purulence,
rupture, and gram-negative infection are relative contra-
indications to attempting in situ reconstruction.[33,53]
An alternative strategy for performing in situ reconstruction
which is being increasingly undertaken today is the use of
freshly harvested or cryopreserved homograft vessels.[215 – 221]
682 Part Five. Aneurysms
This approach is based upon the cardiac surgical experience
utilizing homograft tissue in managing patients with valvular
infection and associated problems.[222,223] This represents a
more theoretically appealing approach than placing a synthetic
conduit in the bed of the infected artery. While freshly harvested
vessels might avoid some of the potential long-term
degenerative complications associated with cryopreserved
vessels, the limited number of organ donors and the frequently
urgent or emergent nature of these infectious problems makes
cryopreserved conduits, which are more readily available,
appealing. Preliminary experience has been favorable, and it is
speculated that more refined techniques of homograft
preparation and preservation will reduce the incidence of
long-term graft calcification and aneurysmal degeneration.[220]
Endovascular Repair
The most innovative, and perhaps controversial, approach
to the management of patients with infected aortic aneurysms
has utilized currently evolving stent-graft technology. Semba
and colleagues[224] recently reported 3 patients with infected
thoracic aortic pseudoaneurysms who underwent placement
of polyester fabric-covered Z stents delivered from the
femoral artery under fluoroscopic control. There were no
periprocedural deaths. One patient suffered a cardiac arrest 25
months later, without evidence of recurrent infection. The
other 2 patients were alive and without signs of recurrent
infection at 4 and 24 months, respectively, following the
procedure.
Visceral Arteries
The relatively small size and frequency of multiple visceral
aneurysms emphasizes the importance of arteriography for
diagnosis and preoperative planning (Fig. 47-2).[16] The
surgical approach required for treatment depends upon the
size and location of the lesion, as well as the adequacy of
collateral development. Goals of operative management are to
prevent rupture of the aneurysm while preserving adequate
distal perfusion.
Superior Mesenteric Artery
DeBakey and Cooley[225] performed the first successful
resection of a mycotic aneurysm of the SMA in 1949. By
1987, a total of 19 patients with infected SMA aneurysms had
been successfully treated by ligation with or without
aneurysm excision.[71,226] Attempts to excise these aneurysms
completely may be hazardous, since they are usually densely
adherent to important adjacent structures. With adequate
drainage and long-term antibiotic therapy, recurrent infection
should not be a problem even with only partial excision and
endoaneurysmorrhaphy.[227]
Following ligation of the vessel, the bowel should be
observed for 30 minutes to assess viability. Use of the sterile
Doppler probe or injection and detection of sodium
fluorescein dye may prove useful in assessing bowel
viability.[228,229] These two techniques are clearly superior
to using clinical parameters of mesenteric arterial pulsations,
peristalsis, and color to assess viability. Short segments of
apparently nonviable intestine must be resected. If long
segments of bowel appear compromised, mesenteric revas-
cularization will be required, preferentially utilizing auto-
genous artery or vein conduits through noninfected tissue
planes if possible.[227] The use of synthetic graft material has
been associated with persistent infection and anastomotic
disruption;[47,230] it is therefore contraindicated.
Endoaneurysmorrhaphy, another method of treating
arterial aneurysms, has proven successful in managing
infected SMA aneurysms.[69,70,227] Restorative endoaneur-
ysmorrhaphy requires obtaining proximal and distal control of
the involved artery, opening the aneurysm, and oversewing
the aneurysm orifice; that is, performing an arteriorrhaphy
which preserves the vessel lumen. An intraluminal shunt
facilitates vessel repair by maintaining bowel circulation and
provides a stent around which the arteriorrhaphy is
performed. The shunt is removed before placing the last
few sutures. If the aneurysm is not saccular and involves both
afferent and efferent vessels, obliterative endoaneurysmor-
rhaphy may be performed by oversewing the orifices of these
vessels from within the open aneurysmal sac. By limiting
dissection and working from within the aneurysm, maximum
collateral circulation is preserved. Use of intraluminal balloon
occlusion of the inflow and outflow vessels facilitates
endoaneurysmorrhaphy because the extensive dissection
required for proximal and distal clamp occlusion is not
required.
Hepatic Artery
Most infected hepatic arterial aneurysms can be success-
fully managed by ligation or ligation with aneurysm
excision.[231] When the aneurysm involves the proper hepatic
artery (the segment distal to the gastroduodenal branch) or
when preoperative angiography documents poor collateral
development, an attempt at arterial reconstruction should be
made to prevent liver ischemia.[169] Saphenous vein or
autogenous hypogastric arterial segments are the preferred
bypass materials.
Infected aneurysms of intrahepatic arteries have, until
recently, been considered curable only by hepatic lobectomy.
Porter and colleagues[32] describe a 29-year-old man with
staphylococcal endocarditis who developed a mycotic
aneurysm in a posterior intrahepatic branch of the right
hepatic artery. The vessel was selectively catheterized, and
several methicillin-soaked pieces of Gelfoam were embolized
into the aneurysm, resulting in occlusion. Arteriography
performed 2 months following embolotherapy confirmed
obliteration of the aneurysm. It is suggested that transcatheter
arterial embolization may prove useful for treatment of
infected visceral arterial aneurysms when surgical interven-
tion is not advisable or technically possible.
Other Visceral Vessels
Mycotic or infected aneurysms involving the celiac,
splenic, or inferior mesenteric arteries (IMA) have been
successfully treated by the surgical options described.[232]
Most splenic arterial lesions may be ligated or excised, with
or without splenectomy. Likewise, rich mesenteric collateral
circulation may permit IMA ligation and aneurysm
resection.[233] Measurement of IMA stump pressure or use

of a sterile Doppler helps document adequacy of colonic
collateral blood flow, permitting safe IMA ligation.[234]
Carotid Artery
Infected aneurysms of the carotid artery are very
uncommon. In a 1995 review only 27 cases of extracranial
carotid artery infected aneurysms were reported.[235] The
principals of management of infected aneurysms of the
extracranial carotid arteries are the same as those for infected
arterial lesions elsewhere, namely excision, wide debridement
and drainage, and intensive antibiotic therapy. The necessity
for and optimal methods of restoring carotid arterial
continuity have provoked debate. Risks of neurologic deficit
after ligation must be balanced against risks of recurrent
infection, arterial disruption, and potentially fatal hemorrhage
following arterial reconstruction in a contaminated field.
Sir Astley Cooper performed the first common carotid
artery ligation for an extracranial aneurysm in 1805. This
patient became hemiplegic and died. However, he performed
a second common carotid arterial ligation 3 years later and the
patient survived for 13 years.[236] Mont Reid[237] reported on
10 patients treated by ligation; 4 died and 2 of the 6 survivors
developed hemiplegia. Moore and Baker[238] recorded
mortality and morbidity rates of 17 and 28%, respectively,
among 104 patients undergoing carotid ligation associated
with head and neck tumors. In contrast to these disastrous
results, Rogers[239] reported transient hemiplegia developing
in only one of 19 patients undergoing carotid ligation. Also,
James and colleagues[240] recorded only one transient deficit
among 13 patients after common carotid ligation performed
using local anesthesia. Monson and Alexander[57] reported the
first successful autogenous saphenous vein interposition graft
after resection of an infected carotid arterial aneurysm in
1980. Several other workers[61 – 63] have also reported
successful saphenous vein bypass grafts after resection of
infected carotid aneurysms. Successful primary end-to-end
anastomosis following excision of an infected carotid
aneurysm has also been reported.[241]
The question of arterial reconstruction versus ligation for
infected carotid artery aneurysm remains unsettled. Histori-
cally, most workers have favored ligation.[242,243] Conversely,
in a recent review of patients with infected carotid artery
aneurysms, Jebara and colleagues noted a 25% mortality
among 12 patients who underwent ligation, and reoperation
was required for recurrent cerebral ischemia in one survivor
of ligation.[55] As an index of adequacy of collateral cerebral
blood flow, Ehrenfeld and his colleagues[244] have success-
fully employed measurement of carotid stump pressure when
ligation was required. After analysis of data obtained from 24
patients in whom carotid ligations were performed, they
concluded that patients whose stump pressure exceeds 70 torr
systolic tolerated acute carotid ligation, especially if systemic
blood pressure was maintained at the same levels as when
stump pressure measurements were obtained. Those with
intermediate stump pressures of 52–68 torr were vulnerable
to post-ligation stroke. It appeared, however, that safety of
carotid ligation in these patients was enhanced by systemic
anticoagulation with heparin sodium and maintence of
high systemic blood pressures. Furthermore, 7 patients also
had preoperative stump pressure estimates using ocular
Chapter 47. Infected Aneurysms 683
pneumoplethysmography (OPG-Gee) with common carotid
compression. Close correlations of all operative and
preoperative measurements were observed in all cases.
Another alternative to ligation historically has been the
application and progressive tightening of a Selverstone clamp
around the common or internal carotid arteries. Avellone
et al.[245] described a 24-year-old woman in whom the clamp
was applied to the internal carotid artery proximal to the
aneurysm and progressively tightened over a 72-hour period.
This procedure proved successful. If, however, neurologic
symptoms had developed, the clamp would have been opened.
If the patient does not tolerate carotid occlusion—as
documented by EEG changes, stump blood pressure measure-
ments, or neurologic instability while awake—a possible
alternative for cerebral revascularization is extracranial–
intracranial bypass using autogenous saphenous vein.[246]
Extremity Vessels
The subclavian or axillary artery between the thyrocervical
and supscapular branches can usually be safely ligated
because of profuse protective collateral circulation around the
shoulder. Resection of lesions involving the distal axillary
artery, however, may require reconstruction. When recon-
struction is required, autogenous tissue should be used and the
grafts should be placed through clean tissue planes.[14,247] The
brachial artery distal to the profunda branch may be safely
ligated. Aneurysms of the radial and ulnar arteries can usually
be excised without reconstruction. Documentation of
adequacy of collateral circulation through the superficial
and deep volar arches by Allen’s test or Doppler assures safe
ligation of these vessels.
The femoral artery is the most common site of infected
peripheral aneurysms, and today the incidence may be
increasing as a result of iatrogenic trauma as well as the
prevelance of drug abuse in our society. The management of
these lesions continues to generate debate. The most
conservative approach, especially in the setting of gross
purulence, is excision and arterial ligation. In young
individuals common or superficial femoral artery ligation
usually results in a viable extremity, although these patients
will often experience claudication. If these symptoms are
disabling, subsequent reconstruction, after infection has
resolved, is appropriate. In one series of 18 infected femoral
pseudoaneurysms secondary to intravascular drug injections,
no deaths and no complications occurred among 6 patients
who underwent ligation alone. The mean ankle-brachial
index after ligation in this group was 0.63.[244] There were 12
patients who underwent revascularization procedures, and
among this group there were 13 reoperations for vascular
complications and 3 (25%) major amputations.[248] When
aneurysm resection also requires sacrifice of the profunda
femoris artery, arterial reconstruction will often be necessary
to maintain limb viability, although this is not always the
case. For example, in one recent report the mean ankle-
brachial index was 0.41 among patients undergoing ligation
of the common femoral, superficial femoral, and profunda
femoris arteries and 0.58 among patients in whom only single
vessel ligation was required for management of infected
femoral pseudoaneurysms secondary to drug abuse.[249] In the
largest series reported to date the mean ankle-brachial index
684 Part Five. Aneurysms

was 0.43 and 0.52 among those undergoing triple and single
vessel ligation, respectively.[250] It is clear that ligation and
extensive debridement offers the best chance of controlling
the septic process and minimizing the risk of subsequent
hemorrhage. Intraoperative documentation of an audible
Doppler signal at the ankle is highly predictive of limb
viability after arterial ligation.[240] Among patients in whom
limb perfusion is inadequate, a number of reconstructive
options exist.
An anatomic reconstruction may be performed through the
bed of the resected aneurysm in the absence of gross
purulence and if the proximal and distal anastmoses can be
performed in clean tissue planes to vessels not directly
involved in the septic process. The use of an autogenous
conduit, usually saphenous vein, is mandatory. There is some
evidence that coverage of the graft with a sartorius muscle
flap may reduce the likelihood of recurrent infection in this
setting (Fig. 47-6).[251 – 253] In the presence of gross
contamination or if a prosthetic graft must be placed, an
extraanatomic route for the bypass should be selected. Several
authors[254,255] advocate the lateral circumflex iliopopliteal
bypass. Since this graft by definition must pass through a
portion of the femoral triangle, secondary graft infection by
contiguous spread is a possible complication and represents a
shortcoming of this approach. Therefore, most workers
advocate placing the iliopopliteal or ilioprofunda graft
through the obturator foramen (Fig. 47-7).[256 – 259] Alter-
natively, recent studies have suggested that in situ
reconstruction may be successfully performed, even with a
synthetic conduit, by covering the graft and closing the wound
with a formal rotational muscle flap. Rotating a muscle from a
separate bed, based upon a pedicled blood supply that is
independent of the site of infection, ensures maximum
vascularity of the rotated muscle. A well-vascularized muscle
bundle will deliver a high level of antibiotics and
immunocompetent cells to the wound and will raise the
oxygen tension within the wound, which may promote
eradication of residual infection through stimulation of
leukocyte function and thus promote healing.[260] For these Figure 47-6. Sartorius muscle has been transposed to cover
reasons and others, it has been suggested that performance of interposition sapheneous vein graft, after resection of infected
a formal rotational muscle flap procedure is a superior femoral artery aneurysm. (From Reddy DJ, et al.[265] Reproduced
approach when compared to local sartorious transfer.[261,262] by permission.)

POSTOPERATIVE MANAGEMENT reasonable in dealing with fungal infections, its necessity

in bacterial infection has not been conclusively established.

Regardless of the surgical procedure performed, prolonged

postoperative antibiotics are mandatory to protect arterial
suture lines and vascular grafts from potential reinfection.
Although the duration of antibiotic coverage required has
not been firmly established, most authors[34,47] recommend
at least 6 weeks of intravenous organism-specific antibiotic
treatment. When prosthetic grafts are placed in situ, some
have advocated life-long antibiotic therapy.[263] Conver-
sely, Malone has suggested that 6 weeks of intravenous
followed by 6 months of oral antibiotic therapy is most
appropriate.[264] This recommendation is predicated on the
observation that graft surface coverage stabilizes at 6
months.[264] Although long-term chronic therapy seems
RESULTS OF TREATMENT
Prior to the advent of antimicrobial drugs, mycotic or infected
aneurysms were invariably fatal. The natural history of these
lesions was one of rapid enlargement and early rupture. It has
been estimated that the average time from diagnosis to death
was approximately 3 months.[135] With the introduction of
antibiotics, better understanding of the pathophysiology of
these lesions, and greater appreciation of the proper
therapeutic principles, survival has improved.

Figure 47-7. Bypass graft placed from right external iliac
artery to superficial femoral artery through obturator canal.
(From Patel KR, et al.[256] Reproduced by permission.)
Peripheral Aneurysms
Infected aneurysms of peripheral vessels are more easily
diagnosed; consequently, mortality is less than for lesions in
the aorta or the visceral circulation. Mundth and his
associates[34] recorded a 25% operative mortality for patients
with infected peripheral aneurysms. In the report of Anderson
et al.,[47] of 14 patients with infected peripheral aneurysms, 5
were treated by ligation alone and all survived, although 1
required amputation. Of the 14 patients, 9 underwent
aneurysm resection and arterial reconstruction. Only 2 of
these patients were cured. The other 7 developed bleeding or
recurrent sepsis within 1 week. Of these patients, 2 expired
and leg amputation was required in another 2 after
reoperation.
Recent studies of infected peripheral aneurysms have
reflected increasing number of lesions secondary to parenteral
drug abuse. Reddy et al.[265] performed selective revascular-
ization in 54 patients with no mortality and an 11%
amputation rate. In another report,[256] routine revasculariza-
tion was carried out with prosthetic grafts in 15 patients, with
1 postoperative graft infection and no operative mortality.
Padberg et al.[248] reported 18 patients with infected femoral
pseudoaneurysms secondary to ilicit drug abuse, including 6
patients who underwent ligation alone, with no deaths and no
amputations. Among 12 patients who underwent attempted
reconstruction, there were 3 (25%) amputations and 13
reoperations for arterial complications.
Chapter 47. Infected Aneurysms 685
Aortic Aneurysms
Infected aortic aneurysms present a much greater risk to life
than peripheral aneurysms, although results are improving.
In one early report, among 13 patients undergoing operation
for an infected aortic aneurysm, 60% died.[34] A 67%
operative mortality was reported among patients with
Salmonella-infected aortic aneurysms.[35] In a 1983 review
of the English literature,[115] only 34 survivors were
identified after operation for infected abdominal aortic
aneurysms. In 89% of the successfully treated patients, the
diagnosis was made before operation. Likewise, in 88% of
these patients, operation was performed prior to rupture. In
Mundth’s study[34] of infected aortic aneurysms, 67% of
patients with nonruptured aneurysms survived, whereas none
with ruptured aneurysms did so. It appears that accurate
preoperative diagnosis, before rupture has taken place, is
crucial to successful results. In addition, bacteriology has an
important impact on survival with gram-negative organisms
portending a more omnious prognosis.[43]
There is less agreement today, however, concerning the
optimal method of revascularization, namely, in situ versus
extraanatomic bypass. In the earlier experience,[115] the
majority of survivors had undergone extraanatomic bypass.
Clearly, surgical outcome continues to improve among
patients who undergo the conventional management of
aneurysm excision and extraanatomic bypass. In a 1997
report 5 (83%) of patients who underwent extraanatomic
bypass for infected infrarenal aortic aneurysms survived,[266]
and in a 1998 review of 10 cases, survival was 90% after
extraanatomic reconstruction.[53] In another center 5 patients
underwent extraanatomic reconstruction following resection
of an infected aortic aneurysms without mortality.[95]
Nevertheless, it is clear that even in the most
experienced hands the conventional managment of aortic
infection is still associated with considerable morbidity.
Operative mortality is not insignficant, and survivors
continue to be at risk of aortic stump rupture and
extraanatomic bypass graft thrombosis.[33,106] In view of
this, there has been increasing enthusiasm in recent years
for performing in situ revascularization following resection
of infected aortic aneurysms. While experience with in situ
revascularization is largely anecdotal, preliminary reports
suggest a reduced operative mortality when compared to
historical series of patients undergoing extraanatomic
bypass (Table 47-7). Furthermore, reinfection has been
noted infrequently, even when prosthetic conduits have
been utilized. It is clear that careful patient selection is
crucial in undertaking in situ reconstruction. For example,
in one study reinfection occurred three-times more often
among patients with gram-negative infection.[115] Presently,
it appears that in situ repair is most appropriate among
patients with gram-positive arterial infection and minimal
contamination at operation, and clearly for patients with
suprarenal aortic involvement. If available, homograft
conduits, at least theoretically, should be preferable to
prosthetic grafts. In each case, the risk of subsequent
graft infection must be weighed against the operative
morbidity, risk of aortic stump blowout, and morbidity of
recurrent graft thrombosis when extraanatomic bypass is
performed.
686 Part Five. Aneurysms

Table 47-7. In Situ Reconstruction for Aortic Infection: Acute and Long-Term Results

Author Year No. Cases Conduit % Mortality % Recurrent infection Follow-up

Fichelle[106] 1993 21 P 14 0 12 – 172 ð
x ¼ 53 mÞ

Pasic[204] 1993 6 P 33 25 7 m – 9 yr ð
x ¼ 5:5 yrÞ
Yokoyama[206] 1994 1 P 0 N.A. N.A.
Ahad[219] 1995 1 CH 0 0 2m
Vogt[217] 1995 2 CH 0 0 6 m/12 m
Knosella[221] 1996 8 CH 12 0 ,1 – 40 m ð
x ¼ 13 mÞ
Illuminati[208] 1996 2 P 0 N.A. N.A.
Codero[207] 1996 3 P 33 0 2 yr
Pagamo[218] 1996 1 H 0 0 18 m
Moriyana[205] 1998 1 P 0 N.A. N.A.

P = prosthetic graft; H = homograft; CH = cryopreserved homograft, yr = year, m = month.

Visceral Artery Aneurysms bowel resection. Of the 24 patients, 9 were successfully

Results of treatment of infected visceral artery lesions are
unclear, since individual experiences are limited and only
anecdotal reports are available for study. In 1981, Howard and
Mazer[226] collected 24 patients from the literature who had
survived operative treatment for an infected SMA aneurysm.
In 10 patients, ligation of the SMA without arterial
reconstruction was performed, and 6 of these underwent
aneurysm resection. Only 30% of this group required
treated by aneurysmorrhaphy alone and 5 underwent
aneurysm resection with some form of revascularization. In
2 of these patients, a prosthetic graft was used, and recurrent
infection developed in 1, necessitating replacement with a
vein graft. Although the incidence of infected and non-
infected lesions was not defined, Stanley and coworkers[66]
reported an operative mortality of 32% for hepatic artery
aneurysms, of which 85% were ruptured at the time of
operation.

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