AHA Scientific Statement
Vascular Graft Infections, Mycotic Aneurysms,
and Endovascular Infections
A Scientific Statement From the American Heart Association
Vascular Graft Infections
Background
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The use of synthetic material for reconstructive vascular surgery was first reported
during the early 1950s. Infection involving vascular graft prostheses is an infrequent
but devastating complication of reconstructive vascular graft surgery and is associated with a high morbidity and, in some situations, mortality. Improvements in surgical techniques and graft design, including the use of native venous or arterial tissue,
have reduced the frequency of infection and severity of complications from vascular
graft infection (VGI). However, these advances have also led to more frequent vascular graft procedures occurring in a patient population with multiple underlying
comorbidities that would have previously disqualified them as candidates for vascular reconstructive surgery. Underlying comorbidities, such as diabetes mellitus
or immune compromise, increase the risk of infection and serious infection-related
complications. The major complications of VGI include sepsis, amputation, disruption of infected anastomotic suture line with rupture or pseudoaneurysm formation,
embolization of infected thrombi, reinfection of reconstructed vascular grafts, enteric fistulae to the small or large bowel, bacteremic spread of infection to other sites,
and death. VGIs can be categorized broadly into those that occur in an extracavitary
location, primarily in the groin or lower extremities, or in an intracavitary location,
primarily within the abdomen or less commonly within the thorax.
Frequency
The frequency of VGI depends on the anatomic location of the graft. The infection
rate is 1.5% to 2% for most extracavitary grafts and as high as 6% with vascular
grafts in the groin.1–9 For intracavitary grafts, the infection rate is ≈1% to 5%.1–6 Graft
infection is most common after emergency procedures and after reoperation.1–4,10
Aortic graft erosion or fistulous communication into the duodenum or other areas of
the bowel reportedly occurs in 1% to 2% of patients after aortic reconstruction.11,12
Microbiology
The microbiological cause of VGI has evolved over the years.1 In early published
studies, Staphylococcus aureus was the predominant microorganism recovered.1,13
Improvements in surgical technique, administration of prophylactic antistaphylococcal antimicrobial therapy, and other factors have resulted in a changing microbiological epidemiology. Vascular graft surgery performed on patients with multiple underlying comorbidities and the increased frequency of emergency procedures have
contributed to the changing spectrum of infection. Other factors such as changes in
hospital flora, surgery in patients with complicated vascular anatomy, and multiple
revisions of previous vascular surgery have resulted in a more diverse microbioe412
November 15, 2016
Walter R. Wilson, MD,
Chair
Thomas C. Bower, MD
Mark A. Creager, MD, FAHA
Sepideh Amin-Hanjani,
MD, FAHA
Patrick T. O’Gara, MD, FAHA
Peter B. Lockhart, DDS
Rabih O. Darouiche, MD
Basel Ramlawi, MD
Colin P. Derdeyn, MD, FAHA
Ann F. Bolger, MD, FAHA
Matthew E. Levison, MD
Kathryn A. Taubert, PhD,
FAHA
Robert S. Baltimore, MD
Larry M. Baddour, MD, FAHA
On behalf of the American
Heart Association Committee on Rheumatic
Fever, Endocarditis, and
Kawasaki Disease of
the Council on Cardiovascular Disease in the
Young; Council on Cardiovascular and Stroke
Nursing; Council on Cardiovascular Radiology
and Intervention; Council on Cardiovascular
Surgery and Anesthesia;
Council on Peripheral
Vascular Disease; and
Stroke Council
Key Words: AHA Scientific
Statements ◼ aneurysm, mycotic
◼ bacterial infections ◼ vascular
grafting
© 2016 American Heart
Association, Inc.
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Vascular Infections
logical spectrum of infection, which includes multidrugresistant strains, polymicrobial infection, and Candida
species. Gram-positive cocci accounts for at least two
thirds of VGIs.1,13 Infections caused by coagulase-negative staphylococci are more common than those caused
by S aureus. Among S aureus infections, methicillin-resistant S aureus (MRSA) infections are increasing in frequency. Pseudomonas aeruginosa is now the most common cause of gram-negative infections and accounts for
at least 10% of VGIs1,14 (Figure 115).
Pathogenesis and Risk Factors for Infection
Clinical Presentations
The clinical manifestations of VGI are highly variable and
relate to whether the location is extracavitary or intracavitary, the pathogenesis of infection, and the duration
of time since surgery.
Extracavitary
Extracavitary VGI most often occurs in the groin and
much less frequently in the popliteal fossa or more distally in the leg. The clinical manifestations vary depending
on whether the infection occurs early, <2 months postoperatively, or later. Early-onset infections are characterized by fever, chills (especially with S aureus infection),
leukocytosis, and other findings of sepsis. Physical findings can include wound erythema, abscess, sinus tract
drainage, graft occlusion with distal ischemia, peripheral
septic emboli, pseudoaneurysm formation, anastomotic
rupture with hemorrhage (which may be life-threatening),
erosion of the graft through the wound, and poor tissue
incorporation of the graft.
Late-onset infection (>2 months postoperatively) is
less often characterized by signs of systemic sepsis.
In these cases, the infection often is indolent, with local
stigmata of groin erythema, painful swelling, sinus tract
drainage, lack of graft incorporation by surrounding tis-
Figure 1. Microbiology of prosthetic
vascular graft infections.
ICD indicates implantable cardioverter-defibrillator; and PPM, permanent pacemaker.
Reprinted from Sohail et al15 with permission from the American College of Cardiology Foundation. Copyright © 2007, the
American College of Cardiology Foundation.
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Intraoperative bacterial contamination of the vascular
graft is considered to be the most common cause of
VGIs.1,9,10,16,17 The second most common cause of VGIs
is a spread of infection from a contiguous site, such
as a surgical wound infection or an intra-abdominal or
pelvic abscess. As many as 30% of intra-abdominal
VGIs occur as a result of erosion of a vascular graft
into the duodenum and less commonly into the colon, with development of a fistulous communication
between the abdominal aorta and the duodenum or
colon. Other causes of VGI include bacterial colonization of a thrombus or direct inoculation of infection
during an interventional surgical procedure, such as
a percutaneous aspiration or drainage of an abscess
or fluid collection.1,9,10,16,17 Less commonly, VGI results
from a bacteremia.18 The risk of hematogenous infection of VGI is highest in the early postoperative period (<2 months) and decreases over time because
of partial endothelialization of the graft.16,19 Transient
bacteremia from a gastrointestinal, genitourinary, or
dental procedure can also cause VGI but is a much less
common cause than is intraoperative contamination or
wound infection.1,18,19
Vogel and colleagues20 analyzed risk factors in almost
14 000 patients who had undergone abdominal aortic
aneurysm repair. Bacteremia during the index hospitalization for repair was associated (odds ratio [OR], 4.2;
95% confidence interval [CI], 1.5–11.8) with aortic graft
infection. In a separate study conducted over a 21-year
period, groin infection (OR, 4.1; 95% CI, 1.6–10.7) and
wound infection (OR, 5.1; 95% CI, 1.6–16.2) were significant risk factors for VGI.13
Wilson et al
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sue, pseudoaneurysm at the anastomotic site, and erosion of the graft through the skin.
The most obvious sign of a graft infection is a draining sinus tract. The clinical presentation of a pseudoaneurysm is variable. There can be little or no localized
inflammatory response; a palpable, pulsatile mass;
thrombosis of the graft with distal limb ischemia; or
hemorrhage. In approximately half of the patients, a
pseudoaneurysm at the anastomosis site presents with
sudden onset of bleeding or ischemia that can be life- or
limb-threatening.1,21 In patients who have undergone extracavitary lower extremity vascular reconstruction, the
presence of a painful erythematous swelling in the groin,
with or without a draining wound or sinus tract, is highly
suggestive of an underlying VGI.
Szilagyi and colleagues22 first reported a classification of extracavitary VGI, which was refined and modified
by Koenig and von Dongen,23 that shows the widely used
modification proposed by Samson et al.24 The Samson
modification provides guidance for selection of imaging
techniques, options for medical and surgical management, management of complications, and prognosis.
The classification of group I through V infection proposed by Samson et al24 might not always be readily apparent clinically, and these groups often overlap. For example, group I VGI can be indistinguishable from group
II on physical examination. However, an open wound with
drainage of pus or a draining sinus tract strongly suggests
that this is not a group I infection. Contrariwise, the absence of an open draining wound or sinus tract does not
exclude a group III, IV, or V infection. A visible graft with
purulent drainage suggests a group III, IV, or V infection.
Intracavitary
In contrast to extracavitary VGI, intra-abdominal VGI
may have no obvious physical findings to suggest infection. Intra-abdominal VGI can present months to years
after graft placement.1,4–6 Symptomatic patients with intra-abdominal VGI may have abdominal pain, fever, leukocytosis, failure to thrive, and sepsis. The aortic graft
can erode into the third or fourth portion of the duodenum, resulting in intermittent, polymicrobial bacteremia
of fecal flora with a combination of aerobic and anaerobic microorganisms. Some blood cultures will contain
a mix of enteric microorganisms, whereas other blood
cultures contain the same or different microorganisms.
These often include Escherichia coli, enterococci, and
anaerobic microorganisms including Bacteroides species, fusobacteria, anaerobic cocci, and occasionally
Candida species. In a patient who has undergone reconstructive surgery for abdominal aortic aneurysm,
the development of sepsis with otherwise unexplained
polymicrobial enteric bacteremia is highly suggestive
of a VGI with duodenal erosion. Rarely, a VGI can cause
a fistulous communication with the colon, with a similar
presentation and polymicrobial enteric bacteremia.1,4–6
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November 15, 2016
In addition to sepsis, gastrointestinal tract bleeding
can occur, which ranges from minimal to massive with
potential exsanguination. Depending on the location of
the enteric fistula, bleeding can manifest as hematemesis, hematochezia, or melena. A prompt diagnosis of VGI
associated with enteric fistula is critical. If untreated, the
mortality rate is virtually 100%.1,4,11
Intrathoracic VGI often presents differently from intraabdominal VGI. Intrathoracic VGI that involves the aortic root can present with signs and symptoms similar
to those of infective endocarditis (IE) with fever, chills,
heart failure, and disruption of the anastomotic suture
line of the aortic root. Because intrathoracic VGIs are
most often caused by S aureus or coagulase-negative
staphylococci, sepsis with a high-grade sustained bacteremia is common with a high-grade sustained bacteremia. If the VGI is associated with surgery for native
or prosthetic valve endocarditis, the clinical picture reflects the microbiological cause. Patients with viridans
group streptococci or enterococci have a less virulent
course than those with infection caused by S aureus or
coagulase-negative staphylococci. Infection associated
with repair of an aortic aneurysm or aortic dissection
usually occurs within 3 months postoperatively and is
most often the result of intraoperative contamination
with staphylococci or gram-negative microorganisms,
including P aeruginosa. Septic emboli can occur in the
central nervous system (CNS) or peripherally. Anastomotic rupture can result in sudden massive hemorrhage,
which is often fatal.
Diagnosis
General Principles
The principles for diagnosis of VGI include the following:
(1) index of suspicion; (2) recognition of the differences
in clinical presentations of extracavitary or intracavitary
VGI; (3) time of onset postoperatively; (4) physical findings; (5) laboratory test results including cultures of
blood, purulent material from a draining sinus, or aspirates of perigraft fluid and surgical specimens; and (6)
imaging. The choice of an imaging modality depends on
whether the VGI is extracavitary or intracavitary. In some
cases, the diagnosis of VGI requires intraoperative confirmation.
General Laboratory Tests and Culture Results
Elevated peripheral white blood cell count and bioinflammatory markers (such as erythrocyte sedimentation
rate and C-reactive protein) occur commonly but are not
specific for VGI, especially among patients who have
multiple underlying comorbidities. Contrariwise, normal
inflammatory markers are uncommon in patients with
VGI. To assess response to treatment, it can be useful to
monitor biomarker levels over time in patients who have
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Vascular Infections
undergone medical and surgical therapy or who continue
to receive suppressive antimicrobial therapy.
Cultures obtained from ultrasound- or computed tomography (CT)–guided aspiration or from intraoperative specimens usually provide an accurate microbiological diagnosis. These results of cultures guide the choice of a specific
antimicrobial agent or combination of antimicrobial agents
and, when necessary, long-term suppressive therapy. The
results of wound swab cultures from a draining sinus, such
as from the groin, could represent skin flora or colonization and might not accurately reflect the causative microorganism. The microbiological cause can influence the
surgical options. For example, VGIs caused by MRSA, P
aeruginosa, or other multidrug-resistant microorganisms
are managed surgically differently from VGIs caused by
more susceptible microorganisms as discussed below.
perts in vascular surgery, infectious diseases, vascular
medicine, and radiology.
Role of Imaging and Interventional Techniques
for the Diagnosis of VGI
General Principles
The choice of an imaging modality depends in part on
the site of infection. For intracavitary VGI, a combination
of imaging modalities might be necessary. Computed
tomographic angiography (CTA) is most often used for
diagnosis and to define anatomy for subsequent revascularization. Sinograms can be useful in highly selected
patients, but other imaging modalities have diminished
their utility. In addition, there is a risk of introducing
pathogens into a perigraft area with high-pressure instillation of contrast material. Invasive angiography is rarely
useful for the diagnosis of VGI. The choice of an imaging
modality is best determined by consultation among ex-
Clinical Presentation
Local wound swelling; no sinus tract
Open draining wound; sinus tract
Ultrasound
Dermis only
Ultrasound, CT or MRI
Abscess, fluid collection
does not extend to graft
I&D
Samson I
Ultrasound nondiagnostic
Infection involves
Infection involves
Infection surrounds
graft;
graft and
anastomosis not involved
anastomosis;, no
no bleeding
bleeding;
anastomosis;
pseudoaneurysm;
CT/MRI
bleeding;
blood cultures
positive blood
negative
cultures
I&D
No graft involvement
Samson V
Samson III
Samson IV
Figure 2. Extracavitary vascular graft infection: diagnosis using Samson classification.
CT indicates computed tomography; I&D, irrigation and débridement; and MRI, magnetic resonance imaging.
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Extracavitary VGI
Even when clinical or microbiological findings strongly suggest a VGI, imaging, most often ultrasonography or CTA,
is used to support the diagnosis, determine the extent of
the infection, identify a fluid collection for aspiration for
culture, or detect a pseudoaneurysm or bleeding at the
site of the anastomosis. A CTA is useful to define vascular
anatomy to help guide medical and surgical treatment.
Figure 2 shows an algorithm for the diagnosis of Samson
I to V VGIs using a combination of clinical findings, ultrasonography, or other imaging modalities, and surgery.
It is reasonable to consider ultrasonography as the
initial imaging procedure.1,25,26 Ultrasonography is used
primarily, but not exclusively, in patients with extracavitary VGI. Compared with other imaging modalities, ultrasonography is less expensive, can be done quickly,
including at the bedside, and does not expose patients
to the potential risk of contrast-associated kidney injury.
Pseudoaneurysm formation can be detected by ultrasonography. Ultrasonography can also identify a subcutaneous or perigraft fluid collection that could be aspirated
for analysis, culture, cell count, and other studies used
to differentiate a noninfected seroma from bleeding. A
sinogram can demonstrate extension of a sinus tract
to the graft, which might involve an anastomotic site.
A potential risk of sinograms is that an infection can be
introduced during the procedure by the high-pressure instillation of contrast material into the perigraft area.
In selected patients with suspected or established extracavitary VGI and indeterminate findings on ultrasound,
Wilson et al
Gastrointestinal Bleeding
GI bleeding present or
absent
No GI bleeding
Monomicrobial
bacteremia or negative
blood culture
Polymicrobial bacteremia
Enteric fistulae likely
Enteric fistulae less likely
EGD together with CTA
CTA
Nondiagnostic or risk of
contrast kidney injury
Nondiagnostic or risk of
contrast kidney injury
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MRI/MRA; IN scan;
PET/CTA*
Recommendations for Imaging in Diagnosis of
Extracavitary VGI
1. It is reasonable to consider ultrasonography
as the initial imaging procedure of choice
(Class IIa; Level of Evidence B).
2. It is reasonable to consider CTA or MRI when
extracavitary graft infection is suspected and
November 15, 2016
CTA indicates computed tomographic
angiography; EGD, esophagogastroduodenoscopy; GI, gastrointestinal; IN, indium;
MRA, magnetic resonance imaging; MRI,
magnetic resonance angiography; and PET,
positron emission tomography. *Combination of imaging tests is often necessary;
see Table 2 for advantages and disadvantages of the different imaging modalities.
MRI, IN scan;
PET/CTA*
it is reasonable to perform CTA or magnetic resonance imaging (MRI) to identify perigraft fluid collection not attributable to recent (≤3 months) graft implantation; an increase
in the size, location, and the consistency of the fluid; or
an anastomotic pseudoaneurysm.27 CT-guided aspiration
of fluid can be useful diagnostically instead of or in combination with ultrasound-guided aspiration. CT or MRI is
useful to define the extent of infection preoperatively in patients with established extracavitary VGI.1 Positron emission tomography (PET)/CT imaging has been reported in
patients with intracavitary VGI, but there are few reports
regarding its utility. Some studies reported that PET/CT
was useful in the diagnosis of extracavitary VGI.28–32 Until
more data are available with PET/CT for extracavitary VGI
diagnosis, other imaging modalities may be considered
before a PET/CT is obtained. An indium-labeled white
blood cell study can be considered, most often in combination with other imaging techniques in patients with
indeterminate findings on ultrasonography, CTA, or MRI.
Indium scans used alone were not useful to identify VGI in
patients with no findings to suggest VGI.28–32 Indium scans
can be falsely positive in the early postoperative period
and have decreased sensitivity in patients who are receiving current or recent antimicrobial therapy.1,33–36
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Figure 3. Intra-abdominal vascular
graft infection: algorithm for diagnosis.
there are indeterminate findings on ultrasonography (Class IIa; Level of Evidence B).
3. A PET/CT or indium-labeled white blood cell
study scan may be considered when extracavitary graft infection is suspected and
ultrasonography, CTA, or MRI findings are
indeterminate (Class IIb; Level of Evidence B).
Intra-Abdominal VGI
Figure 3 shows an algorithm for the diagnosis of intraabdominal VGI in patients with or without associated
gastrointestinal bleeding. Patients with suspected VGI
and aortoenteric fistula should undergo CTA, an esophagogastroduodenoscopy, followed by vascular imaging
as soon as the patient is stable enough to tolerate the
procedure.1,4,8,11,27 An esophagogastroduodenoscopy
can demonstrate subtle or obvious erosion or a thrombus, which usually is located in the third or fourth portion of the duodenum overlying the abdominal aortic
aneurysm graft. The ulcer or thrombus should not be
manipulated, because this can cause sudden massive
bleeding.
The imaging modalities most widely used for the
diagnosis of intra-abdominal VGI are CT, MRI, indium
scanning, and PET/CT.1,28–32 Invasive angiography is
rarely helpful for the diagnosis and has been replaced by
CTA to determine anatomy for revascularization. Table
1 shows the utility, advantages, and disadvantages of
specific imaging modalities for the diagnosis of intraabdominal VGI.1
It is reasonable to consider CT imaging as the initial imaging procedure in patients with suspected intraabdominal VGI. In the absence of recent manipulations,
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Vascular Infections
Table 1. VGIs: Imaging Advantages and Disadvantages
Advantages
Disadvantages
Ultrasound
Most useful for
extracavitary
Can be performed at
bedside
Inexpensive
No contrast kidney injury
Aspiration for analysis,
culture
Detect pseudoaneurysm
Limited use for
intracavitary VGI
Cannot discriminate
seroma, hematoma,
abscess
CT
Sensitivity 85%–100%;
specificity 85%–94%
Rapid result
Less expensive
than MRI, PET/CT
Aspiration for analysis,
culture
CTA useful for surgical
planning
Contrast kidney injury
Noncontrast with renal
disease less diagnostic
Might not differentiate
hematoma from
inflammation, especially
low-grade inflammation
Images degraded by
metallic clips, spinal
hardware
Magnetic
resonance
Sensitivity 68%–85%;
specificity 97%–100%
Use when CT nondiagnostic
No contrast kidney injury
Differentiate hematoma,
inflammation,
infection
Good soft tissue
resolution
MRI/MRA can detect
mycotic aneurysm,
bleeding, enteric fistula
More expensive than CT
No guided aspiration
Limited use in patients
with intracardiac
devices
Gadolinium fibrosing
dermopathy in renal
disease
Indiumlabeled WBC
scan (In-scan)
Sensitivity 67%–73%;
specificity 87%
No contrast kidney injury
Use when CT, MRI
nondiagnostic
Results take ≥24 h
Decreased sensitivity
with recent
antimicrobial therapy
False-positive result in
early postoperative period
Use in combination with
other imaging
PET
Sensitivity 78%–96%;
specificity 70%–93%
No contrast kidney injury
Less experience than
with other imaging
Does not identify specific
anatomic location
Expensive
Use in combination with
other imaging
CT indicates computed tomography; CTA, computed tomography
angiography; MRA, magnetic resonance angiography; MRI, magnetic
resonance imaging; PET, positron emission tomography; VGI, vascular
graft infection; and WBC, white blood cell study.
Modified from Sohail et al1 with permission from the publisher. Copyright
© 2007, Elsevier.
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Intrathoracic VGI
Imaging studies are necessary to confirm the diagnosis
and define the extent of infection and vascular anatomy.
Diagnostic tests including CTA or MRI with or without an
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Modality
the presence of perigraft air is highly suggestive of
VGI. CT findings often suggestive of infection include
perigraft fluid with fat stranding, lack of fat plane between graft and bowel, and anastomotic leakage or
aneurysm. Perigraft fluid is usually reabsorbed within
3 months postoperatively, and perigraft air is usually
absorbed within the first week or so, although it can
persist for as long as 2 months postoperatively.1,28,37–39
Intra-abdominal VGI can occur many months to years after surgery and might not have the CT findings typically
seen in early infection.28,39,40 In these patients, MRI can
be considered if the CT findings are inconclusive.1,40–42
MRI can be superior to CT to identify subtle perigraft inflammatory changes when CT images are degraded by
metallic clips in the abdomen, and it can differentiate
hematoma from inflammatory changes in the perigraft
area.40 However, the role of MRI used alone for the diagnosis of VGI is not defined. In one study, the sensitivity was relatively low at 68%, but the sensitivity was
high (97%).40 MRI combined with an indium scan can be
considered in patients with inconclusive MRI or CT findings.40 Used alone, indium scans have lower sensitivity
and specificity than other imaging techniques.1,33–35
Several studies have reported that PET/CT is useful
for the diagnosis of intra-abdominal VGI.1,28–32,42–46 Three
recent studies summarized the role of PET/CT for the
diagnosis of VGI.30–32 Although there were variables in
imaging techniques and patient selection among these
studies and other studies, the sensitivity and specificity
of PET/CT were similar to those reported with standard
CT for the diagnosis of VGI28–32,39,43–46 (Table 11). PET/
CT may be less precise than conventional CT to identify
the anatomic location of VGI. A linear, diffuse, homogenous uptake over a blood vessel is not indicative of VGI,
whereas a focal uptake over a blood vessel on PET/CT is
highly suggestive of VGI.32
Sah et al31 reported that the use of a 5-point visual
grading score increased the accuracy of PET/CT for
the diagnosis of VGI. The administration of antimicrobial therapy before PET/CT decreased the sensitivity
and specificity of the diagnosis of VGI.31 There are currently no published studies that demonstrate a clear
benefit of serial PET/CT to follow the response to antimicrobial therapy for VGI.32 The use of PET/MRI for the
diagnosis of VGI is being evaluated.32 PET/CT alone or
in combination with other imaging modalities can be
considered if the results of standard CT studies are
inconclusive for the diagnosis of VGI.28–32,43–46 On the
basis of the published studies, it is reasonable to use
standard CT as the initial imaging modality for the diagnosis of VGI.30–32
Wilson et al
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Figure 4. Extracavitary vascular graft infection: algorithm for management.
I&D indicates irrigation and débridement; MRSA, methicillin-resistant Staphylococcus aureus infection; and VAC, vacuum-assisted
closure device.
indium scan should be used in combination with blood
culture results and echocardiography findings.1 Echocardiography alone cannot diagnose infection but can
define anatomy, valvular dehiscence, graft anastomotic
disruption, fistulae, or aneurysm formation. There are
few published data for the use of PET/CT for the diagnosis of intrathoracic VGI. Angiography is not helpful
for the diagnosis of VGI. It is used rarely to define complex anatomy before resection or revascularization.
Recommendations for Diagnosis
of Intracavitary VGI
1. In patients with gastrointestinal tract bleeding and suspected intra-abdominal VGI, an
esophagogastroduodenoscopy and CTA are
recommended (Class I; Level of Evidence B).
2. In patients with suspected intra-abdominal
VGI, it is reasonable to obtain a CTA as the
initial imaging procedure (Class IIa; Level of
Evidence B).
3. In patients with suspected intra-abdominal VGI
and indeterminate CTA findings, an MRI, PET/
CT, or indium white blood cell study scan may
be considered (Class IIb; Level of Evidence C).
4. In patients with suspected intrathoracic VGI,
echocardiography, CTA, and MRI used in
combination with clinical findings and blood
culture results are recommended for diagnosis (Class I; Level of Evidence B).
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Management of VGIs
General Principles
A multidisciplinary approach that includes specialists in
cardiology, vascular medicine, vascular and cardiovascular surgery, radiology, infectious diseases, and in selected cases, plastic surgery is recommended for the
successful management of VGI. The care team should
also include specialists who assist in management of
diabetes mellitus, smoking cessation, obesity, lower extremity ulcerations, lymphedema, vascular stasis, and
other conditions that impair wound healing and increase
the risk of infection.
The selection and duration of antimicrobial therapy depend on the causative microorganisms, the location and
type of graft infection, and other factors that are discussed
below in the sections on management of specific VGIs.
Recommendation for Management of VGIs:
General Principles
1. A multidisciplinary team approach including specialists in vascular and cardiovascular surgery, vascular medicine, cardiology,
infectious diseases, and radiology is recommended (Class I; Level of Evidence B).
Management
Extracavitary VGI
There is no widely accepted procedure of choice nor
standardized surgical therapy for management of extra-
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Vascular Infections
Figure 5. Antimicrobial therapy
for extracavitary VGI.
IV indicates intravenous; MRSA,
methicillin-resistant Staphylococcus
aureus; PO, oral; and VGI, vascular
graft infection.
Samson I and II VGIs. Antimicrobial therapy alone, with
or without débridement, is reasonable for patients with
Samson class I or II VGI (Figure 5). These infections
should be treated as soft tissue infection that does not
involve the graft. Unless there is recovery of a causative
microorganism from cultures of wound drainage from
purulent material or fluid from ultrasound-guided
aspiration, antimicrobial therapy usually is empiric and
should be directed against staphylococci and gramnegative bacilli.
If a specific microorganism is identified, therapy
should be adjusted accordingly. Antimicrobial therapy
can be administered either intravenously or orally, depending on the susceptibility of the causative microorganism, bioavailability of the antimicrobial agent, absorption
from the gastrointestinal tract, severity of infection, and
response to treatment. A 2- to 4-week duration of antimicrobial therapy is reasonable (Figure 5). Samson class I
infections usually do not require incision, drainage, and
débridement. Samson class II infections are often associated with an open, draining wound. Careful and thorough
débridement of infected tissue is necessary to prevent
extension of infection to the vascular graft. Samson class
II infections may benefit from use of a vacuum-assisted
closure device and occasionally from a muscle flap to
achieve wound coverage, eliminate dead space, and promote healing. In these patients, it is important to achieve
satisfactory wound coverage to prevent deep extension
of infection to involve the graft. Samson II infections have
a higher risk of subsequent involvement of the vascular
graft than do Samson I infections.25,26
Samson III and IV VGIs. Zetrenne and colleagues25,26
proposed a useful and practical guide for management
of patients with Samson III and IV VGIs. O’Connor et al4
Circulation. 2016;134:e412-e460. DOI: 10.1161/CIR.0000000000000457
published a comprehensive meta-analysis of treatment
options. Others reported observations pertinent to
patient selection for specific surgical procedures,
advantages and disadvantages of each procedure,
results of treatment, and recommendation for
management of complications.* Figure 4 illustrates an
algorithm of medical and surgical options for Samson
groups III and IV.
All patients should have meticulous débridement of
all infected material and tissue. Usually, multiple surgical
débridements are necessary to enable wound coverage
with a muscle flap and, in some cases, a vacuum-assisted closure device. Deep surgical specimens should be
sent for culture and susceptibility for general bacteria,
anaerobic microorganisms, and fungi, as well as for mycobacteria in selected patients. Broad-spectrum antimicrobial therapy should be administered until the results
of culture and sensitivity are reported, at which time
therapy should be adjusted appropriately. It is reasonable to administer antimicrobial therapy for a duration of
4 to 6 weeks (Figure 5).
There are insufficient data regarding the use of antibiotic beads or powders to supplement aggressive
surgical débridement and local wound care. Some surgeons use these when there is gross purulence present
in the wound and graft salvage is attempted; however,
there are no published data that demonstrate efficacy of
the use of antibiotic beads for such purpose. The more
important precepts for management of these VGIs are
discussed in this section and on techniques for graft
preservation. Close follow-up and aftercare is imperative
to optimize the chance of successful outcome. The selection of a specific surgical option must be individualized for each patient and may be dependent in part on
the experience of individual vascular surgeons. There is
no widely accepted consensus as to the procedure of
choice for management of Samson class III or IV VGI. A
discussion of the selection of a specific surgical option
*References 1–4, 6, 8–10, 14, 16, 22, 24, 27.
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cavitary VGI. The choice of a specific surgical procedure
should be individualized for each patient.
The Samson classification (Figure 4) helps define the
extent and type of VGI, guides the selection of medical
and surgical options, and determines prognosis.
Wilson et al
(Figure 4), the advantages and disadvantages for each
procedure, and the outcome and management of complications follows.
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Graft Preservation. For Samson group III, reports
indicated better outcomes in selected patients treated
with graft preservation rather than with graft resection in
situ reconstruction.25,26,47–50 Calligaro and colleagues16
reported that patients with early-onset Samson group III
infection (<2 months postoperatively) were more likely
to have successful graft preservation than were patients
with later onset of infection. Late-onset Samson group
III VGI was more likely to have nonpatent grafts or
disrupted anastomosis and could be considered for
graft resection and in situ reconstruction rather than
preservation.16
Successful graft preservation with Samson group IV
depends somewhat on the microorganism causing the
infection and whether there is anastomotic disruption.
Numerous studies suggest that graft preservation or
in situ reconstruction should not be attempted in patients with infection caused by MRSA, P aeruginosa, or
multidrug-resistant microorganisms.25,26,50–53 In these
cases, extra-anatomic revascularization followed by
graft excision is reasonable. With infection caused by
other microorganisms, if the anastomosis is intact,
graft preservation or in situ reconstruction might be
possible.14,25,26,41,47,51,54–56 For common femoral artery
reconstruction, autogenous venous in situ reconstruction may be necessary to preserve the deep femoral
artery. Meticulous, often multiple débridements are
necessary.25,26,57–59 Many authorities suggest adjunctive
wound irrigation therapy with povidone iodine solution,
which may also contain antibiotic drugs.25,26 Suction-irrigation catheters to bathe the exposed prosthetic material with antibiotic-containing solutions have been used
in patients with large abscesses or gross purulence
next to the graft or in patients with infections caused by
a multidrug–resistant microorganism. Zetrenne et al25,26
suggested serial quantitative bacterial cultures should
be performed and that graft preservation should not be
attempted until the colony count of the causative microorganism was <105 colony-forming units per gram
of tissue. If repeated wound débridements, wound irrigation, and systemic antibiotic therapy do not result
in quantitative cultures <105 colony-forming units per
gram of tissue, in situ reconstruction rather than graft
preservation is suggested by these authors.
The wound is then covered by a muscle flap.25,26,55,56,60–63
Meticulous débridement and antimicrobial therapy are
vital to the success of muscle flap coverage.26,59,64,65
Muscle flaps obliterate the dead space, promote healing, increase vascular supply and oxygen tension, augment the effects of antimicrobial therapy, protect the
wound from contamination with other microorganisms,
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sis.26,52,55,56,60,66,67 The choice of a rotational or transpositional muscle flap should be made in consultation
with vascular and plastic surgeons. Some surgeons have
recommended wound coverage with a vacuum-assisted
closure device, either alone or as a possible bridge to
muscle flap.65,66,68 The use of a wound vacuum-assisted
closure device enhances healing by negative pressure
and simplifies wound care by nursing staff but should not
be applied if purulence is present in the wound. The use
of a vacuum-assisted closure device without subsequent
muscle flap should be restricted to selected patients in
whom muscle flap may not be an option.
In Situ Reconstruction. In situ reconstruction methods
include rifampin-bonded or silver-coated synthetic vascular grafts, cryopreserved or fresh arterial allografts,
and autogenous venous grafts3,69–83 (Figure 4). The selection of a specific conduit must be individualized and is
somewhat dependent on the personal experience of the
vascular surgeon. There is no consensus about which
specific material should be chosen for reconstruction.69
There are certain circumstances that favor one material
over the other, and there are advantages and disadvantages of each, as discussed below.
rifampin-bonded or silver-coated synthetic grafts. These
grafts are preferable for patients who might not
tolerate the prolonged surgery that is often required
for arterial allografts or autogenous venous graft in
situ reconstruction. Although the reinfection rates with
rifampin-bonded or silver-coated synthetic grafts are
reportedly low,84 arterial allografts or venous autografts
are more resistant to infection than are rifampin-bonded
synthetic grafts.4 There are insufficient published data to
compare infectious rates with silver-coated grafts.
cryopreserved
or
fresh
arterial
allografts
or
autogenous
superficial femoral venous grafts. These grafts have been
used extensively for in situ reconstruction.4,25,26,69,83Arter
ial allografts and autogenous venous grafts are associated
with a lower infection rate than that which occurs with
synthetic material, such as rifampin-bonded grafts.1,4,14,69
Autogenous venous grafts might have longer patency than
arterial allografts because of graft degeneration that occurs
over time with arterial allografts.69 Venous autografts lack
the HLA class II antigen expression that is found in arterial
allografts.84 Although autogenous superficial femoral
venous autografts might have a higher long-term patency
rate than arterial allografts,69 the disadvantage of their use
is the prolonged operative time required for vein harvesting,
which might not be tolerated in some patients, and the
potential for long-term venous stasis morbidity.
Extra-Anatomic Revascularization Followed by Graft
Excision. This procedure was long considered the
preferred surgical approach for Samson group III or IV
VGI because of a theoretical decreased risk of infection
attributable to avoiding graft preservation or in situ
Circulation. 2016;134:e412-e460. DOI: 10.1161/CIR.0000000000000457
Vascular Infections
Postoperative Antimicrobial Therapy and Follow-up
For patients with Samson I and II VGIs, a duration of
postoperative antimicrobial therapy of 2 to 4 weeks
with a combination of intravenous or orally administered antibiotic drugs is reasonable (Figure 5). Most
do not recommend a longer period of oral therapy
afterward.1,4,15,25–27,49,50,69
For patients with Samson group III and IV VGIs, 4 to
6 weeks of intravenous or oral therapy is reasonable. A
follow-up period of oral antibiotic drugs for 6 weeks to 6
months after completion of the initial course of therapy
can be considered.† The decision to administer an additional course of oral therapy must be individualized for
each patient and should be made in consultation with
vascular surgeons and infectious disease specialists.
For patients with Samson group V VGI, 4 to 6 weeks
of initial intravenous or oral therapy is reasonable. Subsequently, at least 6 months of oral therapy may be considered.
For patients with Samson group III, IV, or V VGI, lifelong suppressive therapy may be considered for the
following: (1) those with MRSA or P aeruginosa infection, multidrug-resistant strains, or Candida species;
(2) those who have undergone multiple surgical procedures; (3) those who have had emergency surgery for
VGI; (4) after graft preservation or in situ reconstruction
in patients who had extensive perigraft infections, especially those patients who had rifampin-bonded synthetic
graft reconstruction; and (5) group III, IV, or V patients
†References 1, 4, 15, 16, 25–27, 49, 50, 69.
Circulation. 2016;134:e412-e460. DOI: 10.1161/CIR.0000000000000457
who are poor candidates for reoperation. In these patients, the benefits of lifelong suppressive antimicrobial
therapy could exceed the risk of adverse reaction to
antibiotic drugs or development of antibiotic resistance.
In fact, this might be the best, if not only, option in these
patients and might not only extend life but also improve
the quality of remaining life, increase mobility, and reduce frequency of readmission to hospital. Patients who
receive lifelong suppressive therapy should be evaluated initially at 2- to 3-month intervals and thereafter at
6-month intervals to ensure that they are tolerating antimicrobial therapy satisfactorily and to monitor control
of infection.1,4,15,16,25–27,49,50,69
Postoperative follow-up is important for patients
with extracavitary VGI regardless of the Samson grade
of infection or the surgical procedure used. Close surveillance of the graft is reasonable during the first 2
years when the risk of recurrence of infection is highest.1,4,25,26,55,86,88 Patients should have a physical examination, laboratory tests including complete blood count
and differential, biomarkers of inflammation such as
erythrocyte sedimentation rate and C-reactive protein,
and an ultrasound examination every 3 to 6 months for
2 years. For patients with Samson group III, IV, or V VGI,
lifelong follow-up with ultrasound every 6 to 12 months
is reasonable.1,4,25,26,55,86,88
Extracavitary VGIs: Recommendations for
Management: Antimicrobial Therapy
1. For patients with Samson class I or II VGI, a
trial of antimicrobial therapy with or without
surgical débridement for 2 or 4 weeks is reasonable (Class IIa; Level of Evidence B).
2. For Samson class III or IV VGI, postoperative antimicrobial therapy for 4 to 6 weeks
is reasonable (Class IIa; Level of Evidence
B). After the initial therapy, a course of
oral antimicrobial therapy for 6 weeks to 6
months may be considered (Class IIb; Level
of Evidence B).
3. For Samson class V VGI, postoperative antimicrobial therapy for 4 to 6 weeks administered
parenterally followed by at least 6 months of
therapy administered orally may be considered (Class IIb; Level of Evidence B).
4. For Samson class III, IV, or V VGI, long-term
suppressive antimicrobial therapy may be
considered for infection caused by MRSA,
Pseudomonas, multidrug-resistant microorganisms, Candida, or other fungal species; for those patients who have undergone
emergency or multiple surgeries; for patients
with graft preservation or in situ reconstruction with extensive perigraft infection; or for
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reconstruction of a new graft in an infected area.54,59,85–87
However, this procedure is associated with significant
morbidity, including persistent infection at the site of
vascular stump ligation blowout of the aortic stump, with
potentially life-threatening hemorrhage, as well as the
risk of infection in the new graft. In addition, thrombosis
can occur within the extra-anatomic graft, resulting in
lower extremity amputation.1,4 For Samson group III
or IV VGI, extra-anatomic revascularization followed
by graft resection is reasonable only for patients with
infection caused by MRSA, P aeruginosa, or multidrugresistant microorganisms or for patients for whom graft
preservation or in situ reconstruction has failed.4,25,26,69,83
For Samson group V VGI, extra-anatomic revascularization followed by graft excision is reasonable4,25,26,69,83
(Figure 4). Graft preservation or in situ reconstruction
should be attempted only in patients who are considered to be unacceptable surgical candidates for extraanatomic revascularization. This includes patients with a
high risk of operative mortality, patients in whom previous surgical procedures have failed, patients who have
no viable anatomic options for revascularization, and patients in whom underlying comorbidities suggest a short
life expectancy.
Wilson et al
patients who are poor candidates for reoperation (Class IIb; Level of Evidence B).
Extracavitary VGIs: Recommendations for
Management: Surgical Therapy
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1. For Samson class III infection, which occurs
early (<2 months postoperatively), it is reasonable to consider graft preservation rather
than graft excision and reconstruction (Class
IIa; Level of Evidence B).
2. For Samson class III infection, which occurs
after 2 months postoperatively, graft excision and reconstruction may be considered
instead of graft preservation (Class IIb; Level
of Evidence B).
3. For Samson class III or IV infection caused by
MRSA, Pseudomonas, or multidrug-resistant
microorganisms, or for patients for whom
graft preservation or in situ reconstruction
has failed, it is reasonable to perform extraanatomic revascularization followed by graft
excision instead of graft preservation or in situ
reconstruction (Class IIa; Level of Evidence B).
4. For Samson class V VGI, extra-anatomic
revascularization followed by graft excision
is reasonable (Class IIa; Level of Evidence B).
5. For Samson class III, IV, or V VGI, ultrasound
examination every 3 to 6 months for 2 years,
followed by lifelong ultrasound examination
every 6 to 12 months, is reasonable (Class
IIa; Level of Evidence B).
Prognosis of Extracavitary VGI
The prognosis depends on many factors, including successful management of underlying comorbidities and
risk factors, the microorganism that caused infection,
the extent of infection according to Samson classification groups I through V, and recurrence of infection.
Samson groups I and II have the best long-term prognosis. Recurrent VGI can develop in these patients, more
often in those with Samson group II than Samson group
I. The major complications for Samson groups III to
V include operative mortality, recurrence of infection,
and lower extremity amputation. Patients with infection
caused by MRSA, P aeruginosa, or other multidrugresistant microorganisms have a worse outcome than
those with infections caused by more susceptible microorganisms.‡ Calligaro et al16 reported that late-onset (>2 months postoperatively) infections were more
likely to develop occluded grafts and require graft
reconstruction. Operative mortality ranges from 0%
to 18%, amputation from 0% to 16%, and recurrence
of infection from 0% to 18%. The higher complication
‡References 1, 4, 7, 16, 25, 26, 48–50, 53, 69, 88–91.
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rates trend upward with increasingly higher Samson
classification.§
Intra-Abdominal
Surgical Options. A number of general principles are
important for the optimal surgical management of intraabdominal VGI. These include (1) drainage of abscess
before definitive surgical management of the VGI,
provided that the patient is stable hemodynamically and
there is no adjacent pseudoaneurysm that can rupture
during drainage of the abscess; (2) bypass of renal or
visceral arteries, which might be necessary to reduce
physiological stress and lower the risk of systemic
inflammatory response; (3) careful débridement of the
devitalized periaortic tissue after explantation of the
infected vascular graft before insertion of a new graft
or extra-anatomic revascularization; (4) the elimination
of dead space and circumferential coverage of the
new graft or aortic stump by omentum, and in some
cases, if technically feasible, a muscle flap for the use
of peritoneum or retroperitoneal fat if omental use
is not possible; and (5) placement of antibiotic drug–
loaded beads in the operative area, although there are
insufficient data that demonstrate their efficacy.
The surgical options for intra-abdominal VGI are
shown in Figure 6. There is no standardized surgical option, and certain circumstances favor one option over
another. Each of these surgical options has advantages
and disadvantages, and the selection of a specific surgical option must be individualized (Table 2). In addition,
the personal experience of the surgical team with a specific option influences the decision to select one procedure over another. The roles for each procedure, advantages, disadvantages, complications, and outcomes are
discussed in the next sections and shown in Figure 6
and Table 2.
Extra-Anatomic Revascularization and Graft Excision. This
procedure, first performed in the 1960s, was accepted
as the standard of care against which other procedures
were measured.5,83,92–99 In selected patients, it is still
considered to be the treatment of choice. However, the
major disadvantages of extra-anatomic bypass followed
by graft excision are lower short- and long-term patency
rates of the bypass graft; a 2-stage, lengthy surgical
procedure; relatively high rate of amputation of the lower
extremity; risk of rupture of the stump at the aortic suture
line, with potentially life-threatening hemorrhage; and
difficulty establishing an extra-anatomic revascularization
route in the inguinal region.2,4,6,74,100
A 2-stage rather than a single-stage procedure is preferred. First, an extra-anatomic bypass is performed and
next, an excision of the infected graft with débridement
is done.4,85,92,93,101 Revascularization by axillobifemoral bypass of the lower extremities is ideally performed before
§References 3, 25, 26, 48–50, 69–77, 81, 82, 92.
Circulation. 2016;134:e412-e460. DOI: 10.1161/CIR.0000000000000457
Vascular Infections
Control Bleeding Sepsis
In situ reconstruction
Extensive perigraft
infection
or
MRSA, Pseudomonas or
multidrug resistance
Arterial allograft
or
Venous autograft
or
Rifampin bonded prosthesis
Extra-anatomic bypass
Graft excision
Antimicrobial Therapy 6 weeks
then
Oral Antimicrobial Therapy 3-6 months
Figure 6. Algorithm for intraabdominal vascular graft infection
management.
MRSA indicates methicillin-resistant
Staphylococcus aureus.
Observe off antimicrobial therapy
In situ reconstruction
in patients with extensive
perigraft infection
Lifelong suppressive therapy
excision of the infected aortic graft to minimize ischemia.
Either during the same procedure or preferably at least
24 to 48 hours after revascularization, a complete excision of the infected graft is performed. The 24- to 48-hour
waiting period before graft excision can reduce lower extremity ischemia and associated limb loss.4,6,85,92,93,101
Reilly et al97 reported 26% mortality when graft excision
was performed during the same procedure.
A 2-stage procedure should be considered only in patients who are stable hemodynamically. In patients who
present with hemorrhage from a ruptured graft, emergency intervention is necessary to control bleeding, and
extra-anatomic revascularization of the lower extremities is performed after bleeding from the aortic stump
is controlled. Most patients who present with sepsis,
such as from an aortoenteric fistula, can be stabilized
by aggressive medical therapy and antibiotic drugs to
allow time for extra-anatomic revascularization before
graft excision.
O’Connor et al4 published a meta-analysis comparing
different surgical procedures for intra-abdominal VGI.
This study compared results of extra-anatomic bypass,
rifampin-bonded synthetic prostheses, cryopreserved
arterial allograft, and autogenous venous grafts. Extra-anatomic bypass procedures had higher amputation rates and early mortality (P<0.05) than rifampinbonded prostheses; higher conduit failure (P<0.05)
than cryopreserved arterial allografts; higher reinfection rate (P<0.05) than autogenous venous grafts; and
overall higher (P<0.05) complication rates, reinfection,
and mortality than any in situ reconstructive surgical
procedure. These and other studies have called into
question whether extra-anatomic bypass and graft exciCirculation. 2016;134:e412-e460. DOI: 10.1161/CIR.0000000000000457
sion is still the surgical treatment of choice for intraabdominal VGI.║
However, the results of a meta-analysis showing inferiority of extra-anatomic bypass and graft resection
must be interpreted with caution. Inclusion or exclusion
criteria in individual studies, referral bias, and the higher
number of patients with aortoenteric fistulae reportedly
treated with extra-anatomic bypass and graft excision
could have adversely impacted results. Selection of a
greater number of higher-risk patients who would be expected to have a higher complication rate and mortality, independent of the type of surgical procedure used,
could also have affected results.
Graft Excision and In Situ Reconstruction.
cryopreserved or fresh arterial allograft. Chiesa et al2
reported 68 patients, 57 with cryopreserved and 11 with
fresh arterial allografts. In this study, there were no
differences observed in outcome with fresh compared
with cryopreserved allografts, although the number of
patients who received fresh arterial allografts was small.
A number of other studies have reported extensive use
of cryopreserved arterial allografts, including in patients
with aortoenteric fistulae.5,76,107
Compared with in situ rifampin-bonded prosthetic reconstruction, the major advantage of arterial allografts
is higher resistance to infection.2,75–77,107,108 The major
disadvantages are as follows: (1) They can be less durable than prosthetic grafts because they degenerate over
time, probably because of prolonged storage before use
and immune rejection of aortic allograft tissue.2,4,76 (2)
║References 4, 6, 8, 14, 51, 76, 77, 102–106.
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MRSA, Pseudomonas
multidrug resistance
Wilson et al
Table 2. Surgical Management of Intra-Abdominal Vascular Graft Infections: Options and Advantages and
Disadvantages
Advantages
Disadvantages
Extra-anatomic bypass, revascularization, graft excision
Theoretical lower risk of infection because excision of infected graft
and no reconstruction in infected area
Two-stage procedure, longer operating time
Can be used for MRSA, Pseudomonas, multiple antibiotic resistance
Conduit failure, lower patency rate
Difficulty in establishing revascularization route
Amputation of lower extremities (20%–30%)
Decreased blood supply to inferior mesenteric and internal iliac arteries
Aortic stump infection, possible blowout (10%–20%)
In situ reconstruction: cryopreserved or fresh arterial allograft
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Can be used in some emergency situations, including aortoenteric
fistula
Long-term patency lower than for rifampin-bonded or venous autografts
because of rejection
Lower infection rate than rifampin-bonded grafts and extraanatomic bypass
Not suitable for MRSA, Pseudomonas, or multiple antibiotic drug resistance
Shorter surgical time than venous autografts
Potential difficulty with appropriate anatomic size and shape of graft
Venous autograft
Lowest infection rate
Longer operating time than arterial allograft
Longer patency rate than arterial allograft
Patients with history of DVT not candidates
Can be used in some aortoenteric fistulae
Not suitable for MRSA, Pseudomonas, or multiple antibiotic drug resistance
Rifampin-bonded synthetic graft
Can be used in emergency surgery
Higher infection rate than arterial allografts or venous autografts
Shorter operating time than for extra-anatomic, arterial allograft,
venous autograft
Not suitable for MRSA, Pseudomonas, multiple drug resistance
Lowest amputation and early mortality rates
Potential long-term development of rifampin resistance
DVT indicates deep vein thrombosis; and MRSA, methicillin-resistant Staphylococcus aureus.
Their use is associated with complication rates of 16%
to 23%, including intraoperative rupture of the allograft
because of friability and anastomotic bleeding.4,76 (3)
They might not be suitable for emergency procedures
because they have to be preordered, and the necessary
length, diameter, shape, and sizing might not be available. In the study by Chiesa et al,2 the presence of an
aortoenteric fistula was a negative predictive factor for
early perioperative mortality. The mortality at 3 years in
patients with aortoenteric fistula was 58% compared with
37% of patients without aortoenteric fistula. In the metaanalysis published by O’Connor et al,4 cryopreserved arterial allografts compared with extra-anatomic revascularization and graft excision had fewer conduit failures,
reinfection rates, and better outcomes (P<0.05).
Most authorities do not recommend the use of lowdose immunosuppressive therapy to prevent rejection in patients with cryopreserved or fresh arterial
allografts.2.4,76 This recommendation is based on the
concern that graft infection could be increased by the
use of immunosuppressive therapy.
autogenous venous grafts. In the meta-analysis by O’Connor
et al,4 reinfection rates were lowest (P<0.05) with the
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use of autogenous venous graft, followed closely by
cryopreserved arterial allografts. Late mortality was also
lowest with autogenous venous and cryopreserved arterial
allografts. Disadvantages of autogenous venous allografts
include the following: (1) A longer operative time is needed
for vein harvest; (2) older patients or those with multiple
comorbidities and higher surgical risks might not be able
to tolerate longer, more extensive surgery; (3) a history
of deep venous thrombosis is a relative contraindication
for use of venous autografts; (4) long-term durability of
venous autografts has not been demonstrated; and (5)
there is a risk of venous morbidity in the lower extremity
on the side of the harvest.
In situ autogenous venous graft replacement might be
most appropriate in younger patients who have a longer
life expectancy. Although venous autografts appear to
be associated with the lowest infection rate, the experience with their use in patients with MRSA and Pseudomonas infections is limited.14,83
rifampin-bonded coated or silver-coated prosthetic grafts. The
use of rifampin-bonded synthetic grafts3,8,11,14,71,106 or
silver-coated grafts70,103,109,110 has been reported.
In a nonconcurrent study, Oderich and colleagues11
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Vascular Infections
Aortoenteric Fistula. The treatment of an aortic VGI with
enteric erosion or fistula is dependent on hemodynamic
stability, comorbidities, and anatomy. It is important
Circulation. 2016;134:e412-e460. DOI: 10.1161/CIR.0000000000000457
to control the risk of bleeding of the supraceliac or
suprarenal aorta above the enteric communication either
by direct surgical exposure or by balloon occlusions.
These steps are critical for patients who are unstable
hemodynamically. After the aorta and iliac arteries are
cross-clamped, a circumferential piece of the prosthetic
graft connected with the bowel is resected so that
the bowel can be packed out of the operative field to
minimize local contamination and to improve exposure
for aortic reconstruction. Large bowel defects can be
quickly and temporarily oversewn. Definitive repair of
the bowel is performed after the aortic reconstruction
has been completed and covered by the omentum.
Aortic reconstruction should be limited to the infected
segment. A limited reconstruction in elective cases has
been associated with lower mortality and fewer major
adverse events and bowel complications than if the
entire aortic graft is removed.8,11,27
In the past, the “gold standard” management of these
patients was extra-anatomic bypass surgery followed by
graft excision.5,83,92–99,111 In selected patients, that might
still be the procedure of choice; however, because of
the high rates of mortality and potential complications,
including limb loss, numerous studies have suggested
that alternative surgical options might be preferable to
extra-anatomic bypass and graft excision. For patients
with aortoenteric fistula caused by methicillin-sensitive
S aureus or less virulent microorganisms, such as coagulase-negative staphylococci, streptococci, susceptible enterococci, or susceptible enteric gram-negative
bacilli, graft excision and in situ reconstruction with
either cryopreserved or fresh arterial allograft, venous
autograft, or rifampin-bonded synthetic graft are reasonable.2,4,11,14,77,106–108 In emergency cases or in patients
with multiple underlying comorbidities, an advantage of
arterial allografts over venous autografts is a shorter
operating time. Potential disadvantages of arterial allografts over venous autografts are the difficulty with
obtaining a suitable size and length and the potential
for arterial degeneration. Although no differences in outcome have been reported with cryopreserved compared
with fresh arterial allografts, there are some differences
and potential advantages with the use of cryopreserved
allografts. Unlike fresh arterial allografts, the use of
cryopreserved allografts increases the availability of suitable size and length of surgical conduits for emergency
use, and blood and human leukocyte antigen compatibility can be matched with allografts, which could reduce rejection compared with fresh arterial allografts.
Finally, cryopreserved arterial grafts might be more
likely than fresh grafts to be virus free and could be less
likely than fresh allografts to develop mid- or long-term
aneurysms, presumably because of less rejection with
cryopreserved than with fresh allografts.2,4,9,76,77,107,108
The preponderance of experience favors the use of cryopreserved arterial allografts over the use of fresh arterial
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compared outcomes in 52 patients who underwent
resection of the infected portion of the vascular
graft and in situ reconstruction with rifampin-bonded
synthetic grafts with those of patients who underwent
axillofemoral reconstruction and excision of the infected
vascular graft. Graft reinfection was 11.5% with in situ
reconstruction compared with 17% in axillofemoral
reconstruction (P=NS). Infection rates were unrelated to
the specific microorganism. The 5-year primary patency
rates with in situ or axillofemoral reconstruction were
89% and 48%, respectively (P=0.01), and limb salvage
rates were 100% and 89%, respectively (P=0.06).
The rates of major complications or procedure-related
deaths with in situ or axillofemoral reconstruction were
30% and 60%, respectively (P<0.04). For patients
with large perigraft abscess, the authors suggested
axillofemoral rather than in situ reconstruction. For other
patients, resection of the infected portion of the grafts
and in situ reconstruction with rifampin-bonded synthetic
graft was a safe, effective alternative to axillofemoral
reconstruction.
Studies compared in situ reconstruction with synthetic silver-coated grafts with cryopreserved arterial homografts and concluded that the use of a silver-coated
graft is a safe, effective, and less expensive alternative
to cryopreserved arterial homografts.70,103,109,110 As with
rifampin-bonded grafts, reinfection rates were higher
with silver-coated grafts than with the use of cryopreserved arterial homografts. The major advantages of
rifampin-bonded or silver-coated synthetic grafts were
lower amputation rates, fewer conduit failures, lower
earlier mortality rates, and the fact that they can be used
in emergency surgery.
Theoretically, because these synthetic grafts contain
antibacterial substances, the risk of reinfection should
be lower; however, in a meta-analysis by O’Connor et al,4
reinfection rates with rifampin-bonded prostheses were
higher than for arterial allografts or venous autografts.
This is most likely the result of in situ interposition of
synthetic material in an infected tissue bed. A potential
disadvantage of rifampin-bonded prosthesis is the development of rifampin resistance, which is not a concern
with silver-coated synthetic grafts.3,70,109,110
Bandyk et al14 and O’Connor et al4 suggested that
rifampin-bonded or silver-coated grafts should be considered for patients with infection caused by less virulent
microorganisms, such as coagulase-negative staphylococci or streptococci. These authors suggested that
rifampin-bonded synthetic grafts should not be used in
patients with aortoenteric fistulae or in infections caused
by MRSA or Pseudomonas or with extensive perigraft
abscess because of the risk of reinfection.
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allografts. Because of lower infection rates, femoral venous autografts might be preferable to aortic allografts
or rifampin-bonded synthetic grafts in hemodynamically
stable patients with extensive perigraft infection or infection caused by MRSA, Pseudomonas, or antibiotic drug–
resistant microorganisms.2,4,14,83
Because earlier studies reported high morbidity, mortality, and reinfection rates, rifampin-bonded grafts were not
recommended for in situ reconstruction of VGI and aortoenteric fistulae; however, recent studies in selected patients reported more favorable results.106 Oderich et al106
reported 54 selected patients treated with rifampin-bonded graft in situ reconstruction. Operative mortality in hemodynamically stable patients was 2%, reinfection rate was
4%, and 5-year graft patency and limb survival rates were
92% and 100%, respectively. The improved outcomes in
this study could have resulted from several factors: (1) patient selection, because those with large perigraft abscess
or extensive purulence and those with infection caused by
MRSA or Pseudomonas species were excluded; (2) resection of only the infected portion, not the entire vascular
graft, which reduced operative time, postoperative physiological stress, and ischemia; (3) circumferential coverage of the graft with omentum; and (4) administration of
long-term suppressive antimicrobial therapy.
The potential advantages of rifampin-bonded grafts
over arterial or venous grafts are their more reliable
availability and ability to be used in emergencies, shorter
operative time, and lower cost. A potential disadvantage
is a possibly higher reinfection rate. However, in the
study by Oderich et al,106 reinfection rates in selected
patients were similar to those of patients with arterial or
venous grafts.
In a small number of patients with aortoenteric fistulae, endovascular therapy (EVT) was used as a bridge
procedure to control bleeding and stabilize hemodynamics. After stabilization, the majority of patients underwent device removal and in situ or axillofemoral reconstruction. The role of EVT in the treatment of vascular
infection is discussed when the management of mycotic
aneurysms (MAs) is discussed in Mycotic Aneurysms.
Extensive Intra-Abdominal Abscess or Gross Purulence Around
the Grafts or Infection Caused by MRSA, Pseudomonas, or
Multiply Antibiotic-Resistant Microorganisms. In these
patients, with or without an aortoenteric fistula,
extra-anatomic bypass grafting followed by graft
excision may be considered.4,92–99,111 The primary
reason for this recommendation is because of the
risk of recurrent infection that can occur with in situ
reconstruction.4,92–99,111 The major disadvantages of
extra-anatomic bypass grafting and graft excision are as
follows: (1) a 2-stage procedure is required; (2) conduit
failure with amputation of lower extremities has been
observed in 20% to 30% of patients; (3) blood supply
is decreased with ischemia to the inferior mesenteric
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and internal iliac arteries; and (4) residual infection of
the aortic stump with blowout occurs in 10% to 20%
of patients.4 Theoretically, the risk of recurrent infection
should be lower with this procedure, because the VGI
is resected with no in situ reconstruction in an infected
tissue bed; however, in the meta-analysis published by
O’Connor et al,4 the infection rate was highest with this
procedure, followed by rifampin-bonded, then arterial
allograft, and lowest with venous autograft.
Summary of Recommendations for Surgical Management
of Intra-Abdominal VGI. There is no consensus about
the procedure of choice for the surgical management
of intra-abdominal VGI infections. The choice of therapy
should be individualized for each patient and depends in
part on personal preferences, experience of individual
surgeons, and availability of equipment and resources.
Figure 6 outlines an algorithm for the management
of intra-abdominal VGI. The importance of a team
approach involving vascular and plastic surgeons,
experts in vascular medicine and infectious diseases,
the microbiology laboratory, and, in selected patients, a
clinical pharmacologist cannot be overemphasized.
For patients who have life-threatening bleeding or
sepsis, emergency surgery is necessary. The most
important goals are surgical control of bleeding, drainage of abscess, control of sepsis, and hemodynamic
stabilization. Patients can be categorized into those who
need emergency surgery to control bleeding and sepsis
and those who do not require emergency surgery. There
could be fewer surgical options available in an emergency. For patients who cannot be stabilized long enough to
select the most appropriate surgical option, endovascular bridge therapy might be the only realistic option.
Recommendations for Surgical Management of
Intra-Abdominal VGI
1. In patients who have no aortoenteric fistula,
graft excision and in situ reconstruction with
cryopreserved, arterial allograft, or venous
autograft or rifampin-bonded synthetic graft
is reasonable (Class IIa; Level of Evidence B).
2. In patients with aortoenteric fistula, graft
excision and in situ reconstruction with either
cryopreserved or fresh arterial allograft or
venous autograft or rifampin-bonded synthetic graft is reasonable (Class IIa; Level of
Evidence B).
3. In patients with infection caused by MRSA,
Pseudomonas, or multidrug–resistant microorganisms or those with extensive intraabdominal abscess or perigraft purulence,
extra-anatomic bypass revascularization followed by graft excision may be considered
(Class IIb; Level of Evidence C).
Circulation. 2016;134:e412-e460. DOI: 10.1161/CIR.0000000000000457
Vascular Infections
Recommendations for Antimicrobial Therapy of
Intra-Abdominal VGI
1. Postoperative parenteral antimicrobial therapy is reasonable for 6 weeks (Class IIa; Level
of Evidence B); an additional 3 to 6 months
of oral antimicrobial therapy may be considered (Class IIb; Level of Evidence C).
2. After the initial course of antimicrobial therapy,
lifelong suppressive antimicrobial therapy may
be considered in patients with extensive perigraft infection or infection caused by MRSA,
Pseudomonas, or multidrug-resistant microorganisms (Class IIb; Level of Evidence C).
Circulation. 2016;134:e412-e460. DOI: 10.1161/CIR.0000000000000457
Prognosis for Intra-Abdominal VGI. Yaeger et al92,93
reported a 15-year experience with 60 patients with
intra-abdominal VGI. The perioperative mortality rate
was 13% of those who survived surgery; the 2- and
5-year survival rates were 97% and 82%, respectively.
The 5-year axillofemoral bypass graft patency rate was
73%. Seeger86 reported an early mortality rate of 19%,
an amputation rate of <5%, and early graft failure or
infection in 20%. In this study, after 30 months, 58% of
patients survived without amputation.
Intrathoracic VGI
These patients can present as an acute surgical
emergency associated with aortic VGI with bronchial
or esophageal erosions or fistulae. There could be
initial herald bleeding similar to that in patients with
abdominal aortoenteric erosion or fistula with intermittent bleeding, or they could present with sudden,
catastrophic hemorrhage. Patients with either type of
bleeding require prompt or emergent evaluation and
treatment depending on their hemodynamic stability. In
patients who are unstable, it is preferable to perform
a CTA to define aortic anatomy and plan treatment
options. These patients usually require in situ graft
replacement, because extra-anatomic reconstruction
is rarely an option. An ascending aorta–to–upper abdominal aortic bypass might be possible in selected
stable patients. In these patients, the infected graft
is removed and the ends of the aorta are debrided
to healthy-appearing tissue and oversewn. Buttress of
suture lines with fascia lata and coverage of the new
graft or the aortic stumps with omentum, a latissimus
dorsi or serratus muscle flap, or a pleuropericardial
vascularized pedicle to separate the graft from the
defect in the esophagus or bronchus are important
surgical adjuncts. Large esophageal defects might require diversion, whereas large bronchial defects might
necessitate a lobectomy.
In patients without an esophageal or bronchial fistula, the majority of these infections involve a synthetic
arterial allograft used to treat aortic aneurysm, dissection, or complications of IE and aortic root abscess or
repair of the aorta damaged from blunt trauma. Unlike
intra-abdominal VGI, there are fewer surgical options
for successful management. The use of a cryopreserved or fresh arterial allograft for treatment of intrathoracic VGI is reasonable.1,2,4 The potential advantages of cryopreserved allografts compared with fresh
arterial allografts are listed in Table 2. If technically
feasible, viable omentum or muscle flap coverage of
aortic allograft is used to promote healing and reduce
infection.1,2,4,5,8,14,106
There are insufficient published data to recommend
the use of venous autografts for the treatment of intrathoracic VGI. The use of a synthetic graft, including
rifampin-bonded graft, is associated with a higher infection
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Postoperative Antimicrobial Therapy for Intra-Abdominal
VGI. Figure 6 shows an antimicrobial therapy strategy
that may be considered. The selection of a specific
regimen for intravenous or oral therapy should be made
in consultation with an infectious diseases specialist and
the microbiology laboratory. Postoperative parenteral
antimicrobial therapy for 6 weeks is reasonable; in
some cases, oral antibiotic drugs can be administered
depending on absorption from the gastrointestinal tract
and whether bioavailability is reasonable.1,2,4,5,8,14,106 A
combination of antimicrobial agents might be necessary,
especially in patients with Pseudomonas or multidrugresistant microorganisms. After completion of the
initial 6 weeks of postoperative antibiotic therapy, an
additional 3 to 6 months of oral antimicrobial therapy
may be considered. The decision to administer 3 to 6
months of additional oral antimicrobial therapy should
be individualized for each patient and could depend
on the microorganism recovered from cultures and
the presence of persistently elevated biomarkers of
inflammation, such as erythrocyte sedimentation rate
and C-reactive protein. In some cases, there may be no
effective or safe oral antimicrobial agent for use in these
patients, and consultation with an infectious diseases
expert will be necessary.
In selected patients, lifelong suppressive antimicrobial therapy may be considered (Figure 6). The most likely
candidates for lifelong suppressive therapy are patients
with rifampin-bonded synthesis grafts in situ reconstruction, in situ reconstruction with arterial or venous grafts
and extensive perigraft infection, or infection caused by
MRSA, Pseudomonas, or multidrug-resistant microorganism, provided that an effective, safe oral antimicrobial
agent is available. In cases in which lifelong oral suppressive therapy is not technically feasible or is ineffective,
intravenous administration of chronic antimicrobial suppressive therapy 2 or 3 times weekly should be considered. These decisions must be individualized for each
patient and made in close consultation with vascular
surgeons, infectious diseases experts, the microbiology
laboratory, and, in some cases, a clinical pharmacist.
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rate, and such use should be avoided unless there are
no other surgical options.4
It is reasonable to administer antimicrobial therapy
postoperatively for 4 to 6 weeks.1,2,4,5,8,14,106 The decision to administer a course of oral antibiotic therapy
thereafter or, in selected patients, chronic suppressive
antibiotic therapy must be individualized for each patient and should be made in consultation with the surgical team, infectious diseases specialists, and the microbiology laboratory. Currently, there are insufficient
data to make a recommendation for longer postoperative courses or for chronic suppressive antimicrobial
therapy. However, because of the risk of recurrence of
infection, the high morbidity and mortality, and the fact
that many of these patients could not tolerate another
extensive surgical reconstruction, the administration
of oral antibiotic therapy for at least 3 to 6 months and
possibly lifelong suppressive therapy may be considered in selected patients.
Recommendations for Management of
Intrathoracic Infected Vascular Graft
1. In situ repair of cryopreserved arterial
allografts is reasonable (Class IIa; Level of
Evidence B).
2. Postoperative parenteral antimicrobial therapy for 4 to 6 weeks is reasonable (Class IIa;
Level of Evidence B).
3. In patients with a high risk of morbidity and
mortality, those who cannot tolerate extensive reconstructive surgery, or those with in
situ repair using a synthetic graft, lifelong
suppressive antimicrobial therapy may be
considered (Class IIb; Level of Evidence C).
Mycotic Aneurysms
Background and General Discussion
As discussed by Peters et al,112 Osler113–115 first described a ruptured aortic aneurysm in a patient with
IE and used the term mycotic endarteritis.112–115
Church116 reported a ruptured middle cerebral artery
aneurysm in a young patient with mitral valve IE. The
term mycotic aneurysm was used to describe all infectious aneurysms and has become common usage
since that time, although the term mycotic is now
used to describe fungal infections. Recently, especially in vascular and neurosurgical literature, the term
infectious aneurysm has replaced the use of mycotic
aneurysm; however, because the term mycotic aneurysm is so widely used and understood, for the purpose of this document we will use this term. MAs can
be characterized by anatomic location as intracavitary
(within the thorax or abdomen), peripheral (primarily in
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the extremity and less often in the carotid arteries),
and intracranial.
Frequency
Although MAs are thought to occur uncommonly, the true
incidence of MA is difficult to determine. Published series probably underestimate the true incidence, because
MAs can be asymptomatic and are diagnosed only at
autopsy. In general, MA occurs in the following order
of frequency: intracavitary, peripheral, and intracranial
arteries, respectively.117 Previous studies reported the
frequency of atherosclerotic aortic aneurysms and intracavitary MA but did not address MAs located elsewhere. In 22 000 autopsies performed at Boston City
Hospital from 1902 through 1951, aortic aneurysms
were detected in 1% to 5% of autopsies, but MAs were
reported in only 1.5% of these.118 At Mayo Clinic, from
1925 through 1954, 178 aneurysms were found among
20 000 autopsies, but only 6 of these were thought to
be MAs.119 MAs are rare in children,120 and a form associated with umbilical artery catheterization in newborns
occurs rarely.121
Pathogenesis
Four mechanisms have been proposed to cause MA122–
125
: (1) Septic microemboli to the vasa vasorum or a
septic embolism that has occluded a blood vessel, often at a branch point. Bacterial infection extends from
the vasa vasorum inward toward the vessel wall, which
results in weakening of the wall and aneurysmal formation. In the latter situation, bacteria escape from
the emboli, infect the intimae, and proceed outward
through the vessel wall. (2) Direct extension from a
contiguous focus to infect the arterial wall. (3) Hematogenous infection of the intimae during bacteremia
originating from a distal site. The bacteria can enter
through an atherosclerotic plaque or infect a preexisting aneurysm. (4) Direct blood vessel contamination or
trauma. This can occur as a result of intraoperative
infection such as with vascular graft surgery, invasive
procedures such as intravascular catheterization and
manipulation, intravenous drug use (IVDU), or traumatic
vascular injury as a result of gunshot wound or other
penetrating trauma.
The risk factors for infection, microbiological cause,
clinical presentation, diagnosis, and management of MA
differ depending on anatomic location and will be considered separately in the following discussion.
Intracranial MA
Intracranial MAs (ICMAs) occur less commonly than intracavitary or peripheral MAs, and they are more difficult to
diagnose. ICMAs can be asymptomatic or can present
with sudden catastrophic, life-threatening, or fatal intracranial hemorrhage. They are managed differently from
MAs located elsewhere in the vascular system.
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Vascular Infections
Pathogenesis
ICMA most often occurs as a result of hematogenous
spread or, less likely, as a result of contiguous spread.
Hematogenous spread results from septic microemboli
to the vasa vasorum, with spread of infection internally
through the vessel wall, or as a result of septic emboli
that lodge at a distal branching point, with spread of
infection through the adventitia through the muscularis
of the vessel wall.122,125,133 ICMAs have a different morphological appearance and anatomic location compared
with congenital berry aneurysms. ICMAs are usually saccular with a poorly defined wide base or absent neck or
fusiform shape with a thin friable wall, are more peripherally located, and can be multiple in number, whereas
congenital berry aneurysms are more often single, more
proximally located, and usually saccular with a well-defined neck.127
Microbiology
The microbiological cause of ICMAs depends on whether
they are associated with IE or are a result of contiguous
spread of infection. S aureus and viridans group streptococci are the most common causes of IE and ICMA.
Less commonly, enterococci, coagulase-negative staphylococci, HACEK group (HACEK indicates Haemophilus
species, Aggregatibacter species, Cardiobacterium
hominis, Eikenella corrodens, and Kingella species), and
other gram-negative bacilli, such as P aeruginosa, can
cause ICMA.112,119,126–128,134,135 Partially treated IE with
negative blood cultures can also cause ICMA, and in
these cases, a specific microbiological cause usually is
not identified.
Circulation. 2016;134:e412-e460. DOI: 10.1161/CIR.0000000000000457
When ICMAs are caused by contiguous extension,
the microbiological cause reflects the underlying condition.125,136 In addition to staphylococci and streptococci,
Streptococcus pneumoniae, Haemophilus species, anaerobic microorganisms, and fungi including Candida,
Aspergillus, and Zygomyces, or mycobacteria may be
recovered. Rarely, ICMA can be caused by a viral infection, such as varicella-zoster. HIV has been reported to
cause ICMA in patients with AIDS.126,127,135,137,138
Clinical Presentation
Because ≈20% of ICMAs are diagnosed at autopsy
and are asymptomatic, the true natural history of patients with ICMA is unknown.135 The clinical symptoms
reflect the underlying associated condition, such as
IE or from contiguous spread from meningitis, cavernous sinus thrombosis, sinusitis, or other underlying
conditions.
Patients with ICMA associated with IE often have
fever, headache, seizures, altered sensorium, or
hemiparesis; however, these same neurological complications commonly occur in patients with IE who do
not have ICMA.128,129,136,139 Salgado et al139 reported
no differences in neurological symptoms in patients
with IE who did or did not have ICMA. Unfortunately,
many ICMAs are not suspected or diagnosed until
sudden, possibly fatal rupture occurs. Accordingly,
any neurological symptom, especially focal, should
raise a suspicion for ICMA in IE patients with underlying risk factors.
Despite the lack of specific clinical or physical findings of ICMA, there are a number of signs and symptoms that should raise an index of suspicion. Severe,
localized, unremitting headache, often in association
with homonymous hemianopsia, has been reported in
patients with ICMA and impending rupture.140 The sudden onset of intracranial hemorrhage in patients with IE
could be the result of rupture of a peripheral MA in the
middle cerebral artery circulation. Hemorrhage results
in severe, sudden-onset headache with rapid deterioration of mental status and loss of consciousness. The
time interval from diagnosis of IE to onset of sudden
hemorrhage is highly variable (0–35 days), with a mean
of 18 days.141 Intracerebral hemorrhage is more common with ruptured ICMA, whereas acute subarachnoid
hemorrhage occurs more commonly in patients with
ruptured congenital berry aneurysms.125,127,135 However,
22% of patients with ruptured ICMA presented with subarachnoid hemorrhage in one study.127 In contrast to
congenital berry aneurysms, the size of ICMAs was not
a reliable predictor of rupture.127 Kannoth and Thomas135 found that small ICMAs were more likely to rupture
than large ICMAs, whereas a larger ICMA grows more
slowly and produces symptoms of mass effect more
often than hemorrhage. Local compression from an
expanding ICMA can cause cranial nerve palsy.112,127,134
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Frequency and Anatomic Location
ICMAs represent 0.7% to 6.5% of all intracranial aneurysms.126,127 Neurological complications are common
among patients with IE and occur in 20% to 55% of
patients with native valve or prosthetic valve endocarditis.128–131 The large majority of cases of ICMA occur
in association with left-sided IE or prosthetic valve
endocarditis. ICMAs occur in 2% to 10% of cases of
IE.112,127,128 Because many cases of ICMA are asymptomatic, the true incidence is probably considerably
higher.127,132
ICMAs associated with IE are more often located
in the distal rather than the proximal cerebral arteries. These are most often located at branching points
of the middle cerebral artery, whereas those resulting
from contiguous spread of infection are located in more
proximal regions of the cerebral circulation where the
artery penetrates through infected meninges, cavernous
sinus, or sinusitis.127 Among cases associated with IE or
prosthetic valve endocarditis, 55% to 77% occur in the
middle cerebral artery and 18% in the posterior cerebral
artery; they occur less commonly in the anterior cerebral artery.112,117,119 Multiple ICMAs occur in up to 25%
of cases.112,127,128
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When ICMA results from septic emboli, patients may initially present with symptoms of ischemic stroke in the
territory of the occluded distal branch vessel, although
such strokes can be silent depending on the eloquence
of the territory affected.
Patients with ICMA resulting from contiguous spread
can also present with hemorrhage from an acute rupture. Other findings in these patients include focal neurological signs, acute exacerbation of meningeal signs as
a result of rupture into the meninges, and, depending on
the location, proptosis, otorrhagia, papilledema, ocular
or facial palsy, epistaxis, or signs of cavernous sinus
thrombosis.125,135,136 Vessel narrowing or vasospasm
can also be a feature of infectious vascular involvement
related to contiguous spread, which results in ischemic
strokes often affecting multiple brain territories because
of the proximal vessels involved.
In summary, the clinical signs and symptoms of patients with ICMA are diverse and can occur commonly in
patients with IE or other CNS127,128,142–147 infections who
do not have ICMA. Accordingly, any patient with these
underlying predisposing conditions who develops severe, localized, unremitting headache; focal neurological
findings; stroke; or acute intracerebral or subarachnoid
hemorrhage should be suspected of having ICMA.
Diagnosis
The diagnosis of ICMA depends on a combination of an
index of suspicion in a susceptible host, clinical signs,
and physical findings and is confirmed by radiographic
imaging or during surgery. Strategies for successful
management of ICMA depend on an accurate diagnosis
and management of the different underlying conditions
and the differentiation of ICMA from congenital berry
aneurysm.
Early diagnosis of an ICMA is critical to optimize
therapy and reduce complications. Table 3 shows
factors important in the differential diagnosis among
ICMAs associated with IE, contiguous spread, and noninfectious congenital berry aneurysm. The medical and
surgical management of patients with ICMA is quite different from that of a berry aneurysm, as discussed in
Treatment.
There are no clinical findings or laboratory tests that
are specific for the diagnosis of ICMA. In patients who
are suspected of having an ICMA, the diagnosis must
be confirmed radiographically or at surgery. Prompt
cerebrovascular imaging should be performed to identify possible ICMA or CNS bleeding in any patient with IE
who develops severe localized headache, neurological
deficits, or meningeal signs and can even be considered in patients without symptoms because of the risk
of ICMA in these patients.127,128,142–148 There is insufficient evidence to recommend dedicated cerebrovascular imaging to detect ICMA in all patients with meningitis, cavernous sinus thrombosis, orbital cellulitis,
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or sinusitis; however, dedicated imaging for possible
ICMA should be performed in these patients if there is
intracranial bleeding, focal neurological abnormalities,
or cranial nerve abnormalities, especially those involving ocular muscles.
Imaging Modalities
For the diagnosis of intracranial aneurysms >5 mm
in diameter, multiple-slice CTA with 3-dimensional reconstruction, magnetic resonance angiography (MRA)
with 3-dimensional reconstruction, and digital subtraction angiography (DSA) appear to be roughly equivalent.¶ Cerebral MRI is reasonable in patients with IE
with CNS signs or symptoms and may be considered
even in those without neurological symptoms to detect
emboli and bleeding. These findings help guide decisions regarding medical and surgical management, especially timing of possible cardiac valve replacement
surgery.144,147,159–162
Some authorities suggest conventional angiography
for the detection of ICMAs, especially those <3 mm in
diameter.132,135,163 Some studies have shown that CTA
could be as effective as DSA in identifying intracranial
aneurysms, but others have reported that CTA had lower
sensitivity, especially in detecting small aneurysms (<3
mm).150,154,156,157,164–167 The sensitivity of MRA is similar
to similar to CTA for the detection of aneurysms, and
MRA is associated with fewer procedure-related risks
than DSA.153,157,158
There is insufficient evidence to recommend a specific imaging modality for the diagnosis of ICMA. DSA
is generally safe but is an invasive procedure that is associated with a small risk (<1%) of complications, including contrast-induced kidney injury or neurological deficits (<0.5%).156,157 In several studies, DSA still offered
diagnostic advantage over CTA or MRA for the detection
of cerebral aneurysms, whereas other studies reported
comparable diagnostic utility. Accordingly, it is reasonable to recommend either CTA with 3-dimensional reconstruction, MRA, or DSA as an initial screening imaging
procedure for ICMAs. If these imaging tests are negative
and there is a high index of suspicion for ICMA, then
conventional angiography may be reasonable.
The selection of a specific imaging technique can
also depend on the availability of specific imaging equipment and the experience and preference of individual
centers with the use of an imaging technique. Because
ICMA can develop during antimicrobial therapy, in selected patients, especially those with focal neurological findings or CNS bleeding, repeat imaging in 2 to 4
weeks after an initial negative procedure may be considered.112,117,126,135,162 The role of imaging to monitor patients with a diagnosis of ICMA to guide medical and surgical therapy is discussed in Diagnosis and Treatment.
¶References 112, 117, 127, 128, 135, 149–158.
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Table 3. Intracranial Mycotic Aneurysm or Berry Aneurysm: Differential Diagnosis
Mycotic
Other Causes: Meningitis, Cavernous
Sinus Thrombosis, Sinusitis, Orbital
Age, y
≤45
Any age
>45
Location
Peripheral:
middle cerebral > posterior, anterior
Proximal:
vertebrobasilar cavernous sinus
Proximal: circle of Willis, posterior
communicating artery
Size, shape; single,
multiple
Variable size; saccular (≥50%) with
poorly defined neck; fusiform (30%–35%)
with friable wall; multiple (25%–40%);
stenosis or occlusion close to aneurysm
Variable size; fusiform > saccular; poorly
defined neck, friable wall; single >>
multiple
Size few mm to ≥1 cm; saccular
with narrow, well-defined neck;
single
Focal neurological
findings
Common (≥50%)
Stroke (≥20%)
Seizures (≥15%)
Less common than with IE; depends on
underlying conditions (ie, meningitis)
Less common (<17%)
Cranial nerve
findings
Ocular palsy (≥25%)
Facial palsy (<25%)
Homogenous hemianopsia,
papilledema (≤10%)
Depends on underlying conditions; with
cavernous sinus thrombosis, ocular palsy
(≥50%)
Uncommon; giant aneurysm can
cause compression of cranial nerve
in ≤10% with ocular palsy
Other clinical
symptoms
Depends on IE: fever, headache, heart
failure
Headache, fever common; meningeal
symptoms in >90% with meningitis
Usually no symptoms until rupture
with bleeding
Bleeding
Intracerebral >> subarachnoid
Depends on location; with cavernous
sinus thrombosis, intraventricular
bleeding in ≤15%
Usually asymptomatic when rupture
occurs, causes sudden subarachnoid
hemorrhage with headache (≥95%),
and meningeal signs (≥80%)
Microbiology
Staphylococci, viridans group
streptococci; less common: enterococci;
other streptococci; HACEK
Depends on underlying conditions.
With meningitis: Neisseria meningiditis;
Streptococcus pneumoniae; Haemophilus
sp. Cavernous sinus thrombosis or sinusitis:
S pneumoniae, staphylococci; Haemophilus
sp, anaerobes; Candida, Aspergillus
Culture negative
Congenital Berry Aneurysm
HACEK indicates Haemophilus species, Aggregatibacter species, Cardiobacterium hominis, Eikenella corrodens, and Kingella species; and IE, infective
endocarditis.
Recommendations for Imaging for the Diagnosis
of ICMA
1. Cerebrovascular imaging should be performed to detect ICMA or CNS bleeding in all
patients with IE or contiguous spread of infection who develop severe localized headache,
neurological deficits, or meningeal signs
(Class I; Level of Evidence B).
2. Cerebrovascular imaging may be considered
in all patients with left-sided IE who have no
CNS signs or symptoms (Class IIb; Level of
Evidence C).
3. Either CTA, MRA, or DSA is reasonable as
the initial imaging test for detection of ICMA
(Class IIa; Level of Evidence B).
4. Conventional angiography for detection of
suspected ICMA is reasonable in patients with
negative CTA, MRA, or DSA imaging results
(Class IIa; Level of Evidence B).
Circulation. 2016;134:e412-e460. DOI: 10.1161/CIR.0000000000000457
Treatment
The management of ICMA is somewhat controversial.
The most important factor in the management of ICMA
is rupture. It is not possible to predict accurately the
natural history of ICMA: which will rupture, and which will
not. Rupture can occur in small or large ICMAs. Although
rupture is more likely in ICMAs that increase in size during antimicrobial therapy, those that remain stable or decrease in size can also rupture, even after completion of
a course of antimicrobial therapy.#
ICMAs are uncommon, and not surprisingly, there are
no published randomized controlled studies to define the
optimal therapy of ICMA. In addition, there are no widely
accepted guidelines or studies comparing antimicrobial
therapy alone with EVT or neurosurgical repair. Proposed
treatment strategies are based on retrospective reviews,
anecdotal experience, and expert opinion.** Recognizing
#References 112, 117, 126, 127, 141–143, 162, 163, 168, 169.
**References 112, 117, 126, 127, 141–143, 162, 168, 169.
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Infective Endocarditis
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the lack of widely accepted guidelines, there are 3 basic
therapeutic options, used alone or in combination: antimicrobial therapy, EVT, and neurosurgery. The principles
of management include evaluation and control of the underlying condition, protection of the brain from damage
from rupture of the ICMA, definitive management of the
ICMA itself, and appropriate follow-up to prevent complications. Therapeutic decisions should be individualized
for each patient, and patients should be managed with
an integrated team approach including but not limited
to specialists in neurology, neurosurgery, neurovascular
radiology, vascular medicine and vascular surgery, cardiology, infectious diseases, and microbiology laboratory.
The discussion that follows reviews published data, with
the results of antimicrobial therapy, EVT, neurosurgical
management, and follow-up, and provides a summary
of what we believe to be a reasonable and prudent integrated strategy for management.
Antimicrobial Therapy
All patients with ICMA should receive antimicrobial
therapy. Although the choice of a specific antimicrobial
regimen is beyond the scope of this document, certain
general principles apply. The underlying condition associated with ICMA influences the choice of therapy. Most
cases of ICMA are associated with IE, and antimicrobial therapy should be directed against the specific microorganism recovered from blood cultures or cardiac
valve tissue culture; if cultures are negative, empiric
therapy should be administered.135,170,171 The choice of
antimicrobial therapy for ICMA associated with contiguous spread of infection should be based on the specific
causative microorganism, or if none is identified, empiric therapy should be chosen based on the underlying
condition.135,172
A minimum of 4 to 6 weeks of parenteral antimicrobial therapy is reasonable. The use of such therapy
alone for the treatment of ICMA has variable success
rates.127,135,162,169,170,172 There are no controlled studies,
but there are numerous anecdotal case reports on the
natural history of unruptured ICMA treated with antibiotic drugs alone.162,169,173–175 Several studies reported
successful healing of ICMA with antibiotic drugs alo
ne.127,135,162,175–177 Corr et al178 reported 18 patients with
ICMA treated with antibiotic drugs alone. Complete resolution occurred in 33%, enlargement in 17%, and a decrease in size in 17%, and 33% remained stable in size.
Bartakke et al132 reported complete disappearance of
ICMA in 29% of patients; 18.5% had a decrease in size,
22% had an increase in size, 15% were unchanged, and
15% developed additional ICMA during treatment. In another study among 20 patients with ICMA, ICMA either
resolved or disappeared in 50%, and 50% showed no
change or enlargement in size during antibiotic therapy.169 Ducruet et al127 published a comprehensive review
of 27 studies comprising 287 patients with ICMA in the
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English language literature. In this review, ≈30% of ICMAs resolved on antimicrobial therapy alone, 20% decreased in size, 20% increased in size, and 15% were
unchanged.127
What is clear from these studies is that the natural history of ICMA and response to antibiotic therapy are highly variable and unpredictable. What is not
clear is which factors predict the likelihood of rupture
of ICMA during antimicrobial therapy and, therefore,
which would prompt early intervention. Disappearance
of the ICMA, a decrease in size or stability in size and
shape, and slow filling of ICMA radiographically during
antimicrobial therapy and on follow-up imaging studies
are generally associated with a lower risk of rupture.127
However, rupture can still occur despite an initial small
size or decrease in size of ICMA during antibiotic therapy.112,129,135 The decision to treat patients with antimicrobial therapy alone must be individualized for each
patient. It is reasonable to monitor patients during antimicrobial therapy with weekly imaging for changes in
the ICMA, such as an increase in size or leaking of the
aneurysm that might suggest risk of rupture. It is reasonable to manage patients in a facility with prompt
availability of experienced endovascular specialists and
neurosurgeons to intervene emergently for impending
or actual rupture of ICMA.
Recommendations for Antimicrobial Therapy in
Patients With ICMAs
1. A minimum of 4 to 6 weeks of parenteral antimicrobial therapy is reasonable (Class IIa;
Level of Evidence B).
2. It is reasonable to image patients weekly
during antimicrobial therapy for changes in
the MA that suggest impending or actual rupture (Class IIa; Level of Evidence B).
3. It is reasonable to manage patients in a
facility with prompt availability of experienced endovascular specialists and neurosurgeons to intervene emergently for
impending or actual rupture (Class IIa; Level
of Evidence C).
Endovascular Treatment
Numerous studies have reported experience with EVT
for the management of ICMA.†† EVT is used to occlude the ICMA by use of detachable coils, preferred
for proximal ICMA, or with liquid embolic agents (N-butyl
cyanoacrylate or Onyx [ev3, Inc]) for more distally located aneurysms. Table 4 shows the advantages and
disadvantages of EVT compared with neurosurgery, as
well as patients who are candidates for either EVT or
neurosurgery. The primary advantages of EVT are as
††References 117, 126, 127, 135, 142, 178–184.
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Vascular Infections
Table 4. Treatment of Intracranial Mycotic
Aneurysms With Endovascular Therapy or
Neurosurgery: Advantages, Disadvantages, and
Selection of Patients
Endovascular therapy
Less invasive than neurosurgery
Option to use sedation, not general
anesthesia
Proximal, distal, single, or multiple mycotic
aneurysms treated with same procedure
Risk of rupture less than with neurosurgery
Does not delay cardiovascular surgery
Can be performed in patients with high risk of
cardiovascular complications
Multiple procedures possible for subsequent
mycotic aneurysms
Disadvantages
Sacrifice parent artery with potential ischemic
complications, especially in eloquent neural
areas
Not suitable with rupture and increased ICP
and mass effect
Theoretical risk of infection with use of foreign
body coil or glue
Selection of
patients
No rupture
Rupture, no mass effect, noneloquent
neural area
Unstable aneurysms in noneloquent
neural area
Patients who require urgent cardiovascular
surgery
Neurosurgery
Advantages
Can be used in cases with rupture, increased
ICP, and mass effect and in patients with no
rupture and eloquent neural area or in cases
of failed EVT
Disadvantages
Delays cardiovascular surgery for 3–4 wk
because of risk of intracranial bleeding
Clipping of aneurysm can result in bleeding
because of friable wall
Technically difficult in distal circulation
Selection of
patients
Rupture with increased ICP with mass effect
No rupture, located in eloquent neural area
EVT failed or not technically feasible
EVT indicates endovascular therapy; and ICP, increased intracranial
pressure.
follows: (1) The procedure is less invasive than neurosurgery and can be performed with sedation rather than
general anesthesia; (2) single or multiple and proximal
or distal ICMAs can be treated during the same procedure; (3) the risk of rupture of a friable aneurysm wall is
low; (4) unlike neurosurgery, EVT does not delay necessary cardiac valve replacement or other cardiac surgery
Circulation. 2016;134:e412-e460. DOI: 10.1161/CIR.0000000000000457
Neurosurgery
Before the development of EVT, neurosurgery was the
standard of care of management of ICMA.112,125,127,135,162
Although improvements in surgical technique, especially
developments in microvascular procedures, have decreased morbidity and mortality, neurosurgery for ICMA
remains a challenging, often technically difficult, and potentially risky procedure. Surgical clipping is technically
more difficult for ICMA than for berry aneurysms. Compared with a berry aneurysm, ICMAs are more friable
and lack a well-defined neck, which increases the risk of
rupture during the procedure. A location of ICMA in distal
branches of the anterior circulation and difficulty in identifying the precise anatomic site pose additional problems
for neurosurgical management. Finally, patients who
‡‡References 112, 127, 135, 142, 162, 171, 181, 184, 185.
§§References 112, 117, 127, 135, 142, 162, 184.
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Advantages
that could be performed shortly after EVT‡‡; (5) EVT
is preferable to neurosurgery in patients considered to
have high risk of cardiovascular complications during
the surgical procedure; and (6) EVT can be repeated in
patients who develop additional ICMAs after the initial
EVT. There are several potential disadvantages of EVT
that could favor neurosurgery: (1) EVT usually results in
partial or complete parent artery occlusion, which could
result in ischemic complications, especially in areas of
eloquent brain function. However, the rate of ischemic
complications is low, possibly because most strokes
occur before EVT is done, and collateral circulation
likely reduces the risk of ischemia. Neurosurgery is considered preferable to EVT if the ICMA threatens eloquent
neural territory.112,127,135,162,186,187 (2) EVT is not appropriate for patients who have had rupture with increased
intracranial pressure and mass effect. Neurosurgery is
necessary in these patients. (3) There is a theoretical
risk of infection associated with the introduction of foreign material, such as a coil or glue, into an infected
blood vessel. Despite this concern, no infectious complications have yet been reported after EVT.112,127,135,162
All patients reported to be treated with EVT were receiving concomitant antimicrobial therapy, which might have
prevented infection.
There are no trials comparing EVT with neurosurgery
for the management of ICMA,180 nor is it likely that such
studies could reasonably be conducted. ICMA is a relatively uncommon condition in a diverse population and
has differences in clinical presentation, course, and
anatomic location. There are too many confounding variables to make a comparative study feasible or even safe
to do. Recognizing these limitations, it is reasonable that
EVT be used in selected patients for the initial management of ICMA.§§ The choice of EVT or neurosurgery, or
in some cases both, should be individualized for these
patients.
Wilson et al
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Figure 7. Algorithm for management of intracranial mycotic aneurysm.
Based on uncontrolled studies; reports of small numbers of patients or expert opinion. AMT indicates antimicrobial therapy; CVS,
cardiovascular surgery; and EVT, endovascular therapy.
undergo urgent neurosurgery might also require cardiac
valve replacement or other cardiac surgery. If possible, it
is reasonable to postpone cardiac valve surgery for a minimum of 2 but preferably 3 to 4 weeks after neurosurgery,
because the use of anticoagulant therapy during cardiovascular surgery can cause intracranial bleeding at the
operative site.125,128,130,170
Neurosurgical intervention for ICMA is reasonable
only in selected patients and depends on the neurological prognosis and the cardiovascular fitness of the
patient to tolerate neurosurgery. Such patients include
the following groups: (1) patients with ruptured ICMA
with a mass effect who require urgent neurosurgery to
evacuate the hematoma, reduce intracranial pressure,
and control bleeding; (2) patients with ICMA involving
an artery that supplies eloquent neural tissue (surgical
techniques that preserve vascular flow offer an advantage over EVT); and (3) patients with ruptured ICMAs in
noneloquent neural tissue with no mass effect for whom
EVT has failed.║║
Improvements in microvascular surgery have increased
the likelihood of preserving blood flow to eloquent neural
tissue. A segment of the MA is excised to ensure healthy,
║║References 112, 117, 127, 135, 142, 162, 184.
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uninvolved arterial vessel margins and end-to-end reanastomosis is possible.112,161 Larger ICMAs may be trapped
and bypassed using a segment of a superficial temporal
artery, a radial artery, or a saphenous vein graft.112,162,188
Reinfection after these procedures is low.
We acknowledge that our strategy for management
of ICMA is based on the collective experience published
in numerous small series, case reports, uncontrolled anecdotal reports, and expert opinion. However, until more
data are available, we believe that the algorithm shown
in Figure 7 may be considered for the management of
patients with ICMA.
Summary of Recommendations for Management
of Patients With ICMA
1. Endovascular therapy is reasonable in
selected patients for the initial management
of ICMA (Class IIa; Level of Evidence B).
Neurosurgical intervention for ICMA is rea2. sonable in patients with
a. rupture of ICMA with a mass effect to
evacuate a hematoma, reduce intracranial pressure, and control bleeding (Class
IIa; Level of Evidence B);
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Vascular Infections
Prognosis
It is difficult to draw valid conclusions concerning the
outcome of patients with ICMA,184 for many reasons:
(1) ICMA is a relatively rare condition, and there are no
controlled studies. (2) Reviews of reported series often
span decades during which radiologic modalities, interventional techniques, microvascular surgery, and management of underlying conditions evolved and improved
over time. (3) The analysis of cases is subject to bias
in uncontrolled studies and variations in management
among individual institutions. (4) Some patients might
have been considered unsuitable candidates for EVT or
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neurosurgery, resulting in higher-risk patients requiring
antimicrobial therapy alone, which could impact mortality rates from antimicrobial therapy alone. (5) Some patients present with sudden, often catastrophic or fatal
hemorrhage from rupture of undiagnosed ICMA that may
have responded to therapy if diagnosed before rupture.
Given the above limitations in analysis of outcome
data, it is clear that ICMA is a serious life-threatening
condition with a high mortality. Reported mortality rates
have ranged widely from 12% to 90% depending on rupture, underlying condition, virulence of the underlying
infection, and other factors.112,117,125,127,135,162
There are certain factors that have consistently influenced outcome. Patients who have rupture of an ICMA have
worse outcomes than those who do not.112,117,125,135,162,184
Patients with multiple ICMAs have worse outcomes than
those with a single ICMA.135,174 Mortality was significantly
higher for older people and for those with meningitis and
ICMA located in the vertebrobasilar territory.112,125,135 Mortality of ICMA is reportedly higher in association with meningitis than with IE.135,174 This higher mortality with meningitis could be because ICMAs are more often located
in the vertebrobasilar territory with higher frequency of
stroke, are more proximal, and are more likely to bleed.
In contrast, ICMAs associated with IE are more often in
the carotid territory, are more often distal and probably
less likely to bleed, and are more likely to respond to antimicrobial therapy.135 Fungal ICMA, especially aspergillus,
is associated with a high mortality rate that approaches
90% to 100%.112,117,125,127,135 In most series, the size of
the ICMA did not influence outcome, nor did it predict the
likelihood of rupture.
Because of the small number of diverse patients in
uncontrolled noncomparative studies, it is not possible
to draw valid conclusions about outcomes comparing
results of antimicrobial therapy alone with EVT or with
neurosurgery. There appears to be a trend among published studies that shows lower mortality with EVT-treated patients (7%–61%) than with antibiotic therapy alone
(20%–83%).¶¶ Mortality after neurosurgery is higher
than with antibiotic drugs alone or with EVT, but this
likely reflects the selection of patients for neurosurgery
who more often had rupture with increased intracranial
pressure from mass effect, or that the neurosurgery was
performed as the last option in a desperately ill patient
with a predicted high mortality independent of the neurosurgical procedure.
Finally, patients with ICMA usually have serious underlying infections that independently are associated with a
relatively high mortality. Control of the underlying infectious disease must be the first objective for successful
management of ICMA. Cardiac failure associated with severe native valve or prosthetic valve infection, multiorgan
failure, and multiple comorbidities are common in patients
¶¶References 112, 125, 127, 135, 142, 174, 184.
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b. an ICMA involving an artery that supplies
eloquent neural tissue to preserve vascular
flow (Class IIa; Level of Evidence B); and
c. ruptured ICMA in noneloquent neural tissue
with no mass effect in patients for whom EVT
has failed (Class IIa; Level of Evidence B).
3. If no rupture occurs and cardiac valve
replacement or other cardiovascular surgery is necessary, it is reasonable that EVT
should be performed first (Class IIa; Level of
Evidence B). If no cardiovascular surgery is
necessary and the ICMA has decreased in
size or has disappeared on imaging, it is reasonable to continue antimicrobial therapy to
complete a 4- to 6-week course (Class IIa;
Level of Evidence B).
4. Serial imaging is reasonable at 1- to 2-week
intervals for at least the first 6 weeks of
therapy to ensure proper response to treatment, to ensure there are no signs to suggest
impending rupture, and to evaluate for development of additional ICMAs during therapy
(Class IIa; Level of Evidence B).
5. In patients with IE and focal neurological deficits who have initial imaging studies that do
not demonstrate an ICMA, repeat imaging
may be considered at least once during therapy to ensure that an ICMA did not develop
during therapy (Class IIb; Level of Evidence B).
6. In stable patients who undergo neurosurgery,
it is reasonable to wait at least 2 but preferably 3 to 4 weeks before they undergo cardiac
valve replacement or other cardiovascular
surgery because of the risk of intracerebral
bleeding caused by anticoagulant therapy
during cardiovascular surgery (Class IIa;
Level of Evidence B).
The use of a bioprosthetic cardiac valve
7. instead of a mechanical valve may be considered because of the long-term requirements
for anticoagulant therapy with mechanical
prostheses and the risk of CNS bleeding
(Class IIb; Level of Evidence C).
Wilson et al
with ICMA, and these factors could be the most important
determining factors in the outcome of patients with ICMA.
Thoracic and Abdominal Aortic MAs
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Thoracic and abdominal aortic MAs are relatively uncommon and account for 0.7% to 4.5% of all aortic aneurys
ms.8,26,72,90,125,189–191 The most common locations are in
the abdominal aorta (≈70%) and thoracic aorta (≈30%);
visceral MAs are rare (accounting for <1%).8,72,125,189,190
Because most intra-abdominal MAs occur in patients with
severe atherosclerosis, men predominate over women
by 3:1. The average age is >65 years, and there is a
strong association with cigarette smoking and diabetes
mellitus. Eight-five percent of atherosclerotic aortic aneurysms are located in the infrarenal segment,148,192–195
whereas most aortic MAs are located in the suprarenal
portion of the aorta.148,192–195 Thoracic MA is often associated with recent reconstructive aortic surgery, IE, or
prosthetic valve endocarditis.
Renal transplant recipients can develop MA related to
perinephric infections.148,192–195 Among 640 renal transplant recipients over 8 years at the University of Minnesota, 8 (1%) developed MAs, and 6 of these 8 occurred
in the external iliac artery.105
Pathogenesis
The pathophysiology of aortic MA is somewhat different
from ICMA or peripheral MA. The 5 mechanisms for the
development of aortic MA are as follows: (1) The normal
intima of the aorta is quite resistant to infection. If the intima is damaged by atherosclerosis or the development
of plaques or ulcers, the damaged endothelium can be
colonized and infected during bacteremia with the development of an infected atherosclerotic aneurysm. (2)
Infection can occur as a result of either bacteremic or
contiguous spread of infection to the vasa vasorum. The
infection then proceeds inward toward the vessel wall,
causing a localized infection with thinning of the vessel
wall and the development of an MA. (3) Infection can
result from contiguous spread from a gastrointestinal
source, such as gastroenteritis, especially caused by
Salmonella nontyphoidal species or by extension from
vertebral osteomyelitis. This leads to the development
of a primary abdominal aortic MA or, less commonly,
a secondary MA involving a preexisting atherosclerotic
aneurysm. (4) Infection of the ascending or descending
aorta can develop as a result of damage to the endothelium resulting from a congenital abnormality, such as
cystic necrosis or coarctation, which makes the blood
vessel more susceptible to infection from bacteremia or
contiguous spread. (5) MA in the sinus of Valsalva or
the aortic arch may be associated with reconstructive
surgery, IE, or prosthetic valve endocarditis. A sinus of
Valsalva MA is most common in the right or noncoronary sinus and can rupture into the right ventricle, right
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atrium, or pericardial sac with tamponade or cause coronary artery occlusion.196
Microbiology
The microbiological spectrum of aortic MA is evolving
and may depend on geographic conditions. Staphylococci, including S aureus and coagulase-negative staphylococci, in recent years have emerged as the most common cause of aortic MA and account for roughly 50%
to 60% of cases.125,190,197–199 Previously, gram-negative
bacilli, especially nontyphoidal Salmonella, were more
common than staphylococci, but now they account for
at least 30% to 40% of cases.125,200–202
Salmonella enteritidis, Salmonella choleraesuis, and
other nontyphoidal strains are more common causes
of abdominal aortic MA in Asia. Salmonella nontyphoidal strains have a special predilection to infect vascular
tissue.200–203 The mechanism for this is poorly understood. The presumed portal of entry is the gastrointestinal tract. Translocation of Salmonella species or
transient bacteremia is thought to gain access to the
aorta through plaques associated with atherosclerotic
disease. Lumbar spine osteomyelitis has been reported
to be present in up to one-third of patients with aortic
MAs caused by Salmonella species.201 S enteritidis was
recovered in 40% of cases and S choleraesuis in 32%.
Approximately 25% of patients aged ≥50 years with
Salmonella species bacteremia have an endovascular
focus of infection.200–203
Other gram-negative bacilli can also cause aortic MA.
Arizona species, especially A hinshawii, cause gastroenteritis and other infectious diseases similar to those of
Salmonella species and can infect the abdominal aorta,
especially in elderly diabetic men with a history of cigarette smoking and atherosclerotic peripheral vascular
disease.204 Many other species of gram-negative bacilli,
anaerobic microorganisms, and occasionally Candida
and other fungi have been reported to cause infection
of atherosclerotic aneurysms.205,206 Listeria monocytogenes is a cause of gastroenteritis and has been reported to cause endovascular infections, including aortic MA.207,208 Mycobacterium tuberculosis rarely causes
aortic MA, probably as a result of erosion of the aortic
wall from a contiguous focus, most often from vertebral
osteomyelitis.209
Clinical Presentation
The clinical findings associated with intra-abdominal aortic MA are nonspecific. The classic triad of fever, pain,
and a pulsatile abdominal mass reported in previous
studies is actually rather uncommon.8,125 In patients with
intra-abdominal MA, fever is present in ≥70% of patients
and is uncommon in patients with uninfected atherosclerotic abdominal aneurysms. Back pain is present in at
least 65% to 90% of cases and less commonly occurs
in patients with uninfected atherosclerotic aneurysms. It
can be difficult to differentiate inflammatory, noninfected
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Vascular Infections
Diagnosis
The diagnosis of aortic MA depends on an index of suspicion in a susceptible host; recognition of the clinical presentations and physical findings; laboratory test results,
including blood cultures; and imaging. The susceptible
history, clinical, and physical findings are discussed in
Clinical Presentation.
Laboratory Findings
There are no laboratory test results that are specific
for aortic MA. Patients with aortic MA usually have leukocytosis (65%–85% of cases) and elevated inflammatory markers such as erythrocyte sedimentation rate
or C-reactive protein (75%–80%); however, noninfected
inflammatory abdominal aortic aneurysms also have
these findings. Unlike noninfected inflammatory abdominal aortic aneurysms, MAs have positive blood cultures
in 50% to 90% of cases; however, many patients with
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MA have received recent antibiotic therapy, and blood
cultures are negative in 25% to 50% of these patients.
Blood cultures can remain positive in patients with
aortic MA despite antibiotic therapy. Sustained bacteremia is characteristic of endovascular infection. In a
patient with gastrointestinal bleeding, sustained polymicrobial bacteremia caused by aerobic and anaerobic microorganisms, often with Candida, that persists despite
appropriate antibiotic therapy suggests a fistulous communication between the abdominal aorta and the third
portion of the duodenum.94,213,218
Sustained bacteremia caused by certain microorganisms has a high association with endovascular infection,
including MA. The mere presence of these microorganisms in multiple positive blood cultures suggests that
endovascular infection must be excluded before an alternative source of bacteremia is considered. Sustained
Salmonella nontyphoidal bacteremia in a patient with abdominal aortic aneurysm is highly suggestive of arteritis
or MA.200–203 Sustained Salmonella nontyphoidal bacteremia can cause distal site infection, including vertebral
osteomyelitis, septic arthritis, hepatic abscess, or other
infection, but these distal infections are usually the result
of Salmonella endovascular infection, not the cause of
the endovascular infection. In addition to positive blood
cultures, stool cultures can also be positive for nontyphoidal Salmonella.
Multiple positive blood cultures for Streptococcus
abiotrophia (nutritionally variant viridans streptococci)
or HACEK microorganisms are highly suggestive of endovascular infection.169 Patients with sinus of Valsalva
aneurysm or thoracic aortic aneurysm and multiple positive blood cultures for these microorganisms should be
considered to have IE with MA until proven otherwise.
Imaging
Because clinical findings and routine laboratory test results are nonspecific, imaging plays a critical role in the
rapid diagnosis and management of aortic MA. Among
imaging modalities, CTA is reasonable as the initial imaging procedure of choice for aortic aneurysm.9,102,105,163,191
Findings on CTA are important to differentiate abdominal
MA from a noninfected bland atherosclerotic aortic aneurysm.9,102,125,163,191,219
CTA allows for rapid examination in a patient who may
be unstable and require urgent surgical intervention.
CTA defines the precise location, can detect impending
rupture, defines vascular anatomy for reconstructive
surgery, identifies associated complications, and provides serial imaging to monitor expanding or unstable
aneurysms. The major disadvantage is the potential for
contrast-induced kidney injury in patients who often have
multiple underlying comorbidities for renal disease.
Table 5 shows findings on CTA that are helpful for the
diagnosis and management of aortic MA.148,163,191,192,219
The typical appearance is a saccular aneurysm with an
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abdominal aortic aneurysms from an MA. Inflammatory
abdominal aortic aneurysms account for 5% to 10% of
all abdominal aortic aneurysms.210,211 Inflammatory abdominal aortic aneurysms usually occur in older men
with a history of cigarette smoking or diabetes mellitus,
but fever is less common than with MA. An aortoenteric
fistula and MA should be suspected in patients with a recent or remote abdominal aortic aneurysm repair. These
patients can have a long asymptomatic period before
the onset of the current illness.212 Up to 4% of patients
who have undergone repair of abdominal aortic aneurysm develop aortoenteric fistulae.213
Intrathoracic MAs usually present with fever, chest
and interscapular pain, and findings commonly seen
in patients with IE, prosthetic valve endocarditis, or infection involving an ascending or descending thoracic
aorta.9,125,191
Superior mesenteric aneurysms account for only 8%
to 10% of visceral artery aneurysms, but when they occur, they are usually an MA.214 They often cause abdominal pain that can be acute, and they can be associated
with fever and, rarely, a palpable pulsatile mass in the
epigastrium. Gastrointestinal hemorrhage can occur and
can be catastrophic.163,214,215 Hepatic artery MAs are
less common than visceral artery aneurysms and can
present with fever, colicky upper abdominal pain, hemobilia, jaundice, and gastrointestinal hemorrhage.215 Renal
artery MAs are uncommon and usually present with fever, hematuria, and elevated blood pressure.216
A complete or contained rupture of an intrathoracic
or intra-abdominal MA occurs in at least 50% to 75% of
patients. These MAs rupture into the retroperitoneal or
peritoneal space (50%), duodenum (12%), pleural cavity
(10%), esophagus, mediastinum, or pericardium in 3%
to 5% of cases.9,125,163,217 An impending or contained rupture can be associated with severe pain, hemodynamic
instability, or a sudden, catastrophic rupture with shock
and a high mortality.9,125,163
Wilson et al
Table 5. Computed Tomographic Imaging
Characteristics of Aortic Mycotic Aneurysm
Compared With Atherosclerotic Aneurysm
Mycotic
Atherosclerotic
30–40
15–20
Location, %
Aortic
Suprarenal
5–15
5–7
Infrarenal
15–25
75–90
Shape
Lobular, irregular,
saccular
Fusiform >
saccular
Intimal calcifications
Less common, but
can occur
Common
Uncommon
Common
Rapidly changing
Chronic, stable
Common
Uncommon
Mural thrombosis
Evolution
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Periaortic findings
Stranding, encasing or
contiguous mass
Concentric inflammation
Hematoma, gas*
*Presence of gas is uncommon, but if visible, it is highly suggestive of
mycotic aneurysm.
Data derived from Chen et al,148 Lee et al,163 Macedo et al,191 Colin et
al,192 and Lin et al.219
irregular lobular contour. Absent or minimal calcification
is suggestive of MA.162,191,220–222 Others, however, have
reported that calcium was frequently present and was
not helpful to differentiate an MA from an atherosclerotic aneurysm.191,219 However, the majority of studies
suggest that absence of calcium is more often seen in
MA than in atherosclerotic aneurysms.9,125,163,192 Mural
thrombi were reported more frequently with atherosclerotic aneurysms than with MAs.
Periaortic soft tissue stranding, fluid, a concentric
inflammatory response, and contiguous mass are commonly seen in aortic MAs. Although uncommon, the
presence of periaortic gas confirms the diagnosis of
MA.191,220–222 The association of adjacent vertebral body
abnormalities was reported by McHenry et al,223 who
viewed 70 cases of vertebral osteomyelitis and MA.
Rapid enlargement of MAs and an enlarging periaortic
inflammatory mass or hematoma are ominous signs of
contained or impending rupture. These findings suggest
urgent surgical intervention.
There are a limited number of published studies using MRI, MRA, DSA, PET/CT, or nuclear medicine scans
for the diagnosis of aortic MA.## Compared with CTA,
MRA requires longer examination time, is susceptible
to motion artifact, has lower spatial resolution, and has
smaller volume imaging cover. These imaging modalities
##References 9, 125, 163, 191, 219, 224–226.
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may be useful in selected patients, but there are insufficient published data to recommend their routine use for
diagnosis. Conventional arteriography is rarely useful diagnostically.9,11,106,163,191,192 Ultrasonography has limited
utility for aortic MA. Transesophageal echocardiography
is reasonable in patients with MA of the sinus of Valsalva
and thoracic aortic MA.7,125
Recommendations for Imaging and Diagnosis
of Aortic MA
1. CT or CTA is reasonable as the initial imaging modality for diagnosis (Class IIa; Level of
Evidence B).
Transesophageal echocardiography or car2. diac MRI is reasonable for diagnosis of sinus
of Valsalva or thoracic MA (Class IIa; Level of
Evidence B).
Management of Patients With Intrathoracic or IntraAbdominal MA
There are no published randomized prospective studies for the medical management of patients with intrathoracic or intra-abdominal MA, nor is it likely there will
be. There are a number of reasons why such studies
would be difficult to accomplish. (1) Intrathoracic and
intra-abdominal MAs are rare diseases. (2) Randomized,
multicenter controlled studies would require many years
to accrue sufficient patients and would likely require participation of multiple centers throughout the world. (3)
Standardization would be difficult if not impossible in a
population of patients that is highly diverse, who have
multiple underlying comorbidities, and for whom there
are global and regional differences in microbiological
cause, variable availability of technical equipment for diagnosis, and differences in experience and expertise of
medical and surgical subspecialties. (4) During the long
time period necessary to complete such a study, new
techniques and innovations would likely be introduced
that could make the treatment options obsolete or possibly even hazardous.
Not surprisingly, there is no consensus among authorities on the optimal management of these patients. Most
published studies contain a relatively small number of
patients and a review of the literature or are expert opinion or single-case reports. The few studies that contain
relatively larger numbers of patients might span 2 decades or longer and contain diverse patient populations
without standardized therapy. The following represents
what we believe may be considered for the management of patients with intrathoracic or intra-abdominal MA
and is based on our review of published literature and
the collective opinion and personal experience of this
writing group. Intrathoracic or intra-abdominal MAs are
life-threatening infections with a high morbidity and mortality. We believe the choice of medical and surgical manCirculation. 2016;134:e412-e460. DOI: 10.1161/CIR.0000000000000457
Vascular Infections
*Experience limited with use of cryopreserved arterial allograft or venous autograft.
EVT indicates endovascular therapy; and GI, gastrointestinal.
agement should be individualized for each patient and
should be executed via a team approach that involves
experts in vascular diseases and surgery, cardiology and
cardiovascular surgery, diagnostic and interventional radiology, critical care medicine, infectious diseases, and
microbiology in a facility with access to these experts
and services on an emergency basis.
The therapeutic options include a combination of
antimicrobial therapy, open vascular surgery, EVT, and
a combination or hybrid technique of open surgery together with EVT.
Antimicrobial Therapy
The choice of antimicrobial therapy should be based on the
identification and susceptibilities of the specific microorganism, and if possible, bactericidal therapy should be administered. The choice of a specific antimicrobial agent is
beyond the scope of this document. Depending on whether these patients have received prior antimicrobial therapy,
blood cultures may be positive in only 40% to 50% of patients, and intraoperative tissue cultures may be negative
in one-third of patients; therefore, empiric therapy is often
necessary. Most authorities believe at least 6 weeks to 6
months of antimicrobial therapy postoperatively may be
considered. In some cases, lifelong suppressive antimicrobial therapy may be considered and individualized for each
patient. The selection of patients for 6 weeks to 6 months
or lifelong suppressive therapy is discussed in Treatment.
Antimicrobial therapy used alone for the treatment of
aortic MA has been reported to have an associated morCirculation. 2016;134:e412-e460. DOI: 10.1161/CIR.0000000000000457
tality rate of 60% to 100%.125,163,170,217,227–231 The use of
antimicrobial therapy alone may be considered only in
patients who are unfit for surgery or who refuse surgery
or EVT, or for palliative care.
Recommendations for General Principles of
Management and Antimicrobial Therapy for
Patients With Aortic MA
General Principles
1. Patients should be managed by a team of
experts in vascular diseases and surgery,
cardiology and cardiovascular surgery, critical care medicine (intensivists), radiology,
infectious diseases, and microbiology in a
facility with emergency access to these services (Class I; Level of Evidence C).
Antimicrobial Therapy
1. A duration of 6 weeks to 6 months of antimicrobial therapy may be considered (Class
IIb, Level of Evidence B); in some cases, lifelong suppressive therapy may be considered
(Class IIb; Level of Evidence B).
2. Antimicrobial therapy alone may be considered only for patients who are unfit for
surgery or who refuse surgery or EVT, or
for palliative care (Class IIb; Level of
Evidence B).
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Figure 8. Algorithm for management of intra-abdominal aortic mycotic aneurysms.
Wilson et al
Table 6. Management of Aortic Mycotic Aneurysm: Comparison of Resection and Extra-Anatomic
Reconstruction, In Situ Reconstruction, or Endovascular Device Repair
Procedure
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Potential Indications*
Advantages
Disadvantages
Extra-anatomic
reconstruction
Infrarenal location with gross purulence,
psoas or retroperitoneal dosing,
vertebral osteomyelitis, inadequate
response to antibiotic therapy, selected
aortoenteric fistulae
Avoids placement of foreign body in infected area
Not technically feasible for
thoracic, suprarenal, or visceral
location or for emergency use
Long operating time
Long-term patency rates low
Stump blowout
Limb is ischemic, amputation
Reinfection rate higher than for in
situ reconstruction
Ischemic colitis
In situ
reconstruction
Thoracic, suprarenal, infrarenal, or
visceral location
Selected aortoenteric fistulae
More versatile than extra-anatomic: Fewer longterm complications, higher patency rates, lower
recurrent infection rate, shorter operating time
Polyester grafts† available for emergency surgery
Selected aortoenteric fistulae
Theoretical risk of infection
because of interposition of
foreign material in infected site
Endovascular
device repair
Bridge procedure‡: hemodynamic
instability, uncontrolled bleeding, rupture
or impending rupture, selected patients
with aortoenteric fistulae, patients who
are not fit for open surgery
Emergency stabilization
Low early morbidity, mortality
Less invasive
No cross-clamping of aorta: spinal cord injury,
reperfusion injury
Persistent infections and device
infections
Higher long-term morbidity,
mortality with device retention
Requires device explantation,
reconstruction
*Potential indication; must be individualized for each patient.
†Polyester grafts, rifampin soaked or silver coated; less experience reported with cryopreserved arterial allografts or venous autografts.
‡Bridge procedure, used to stabilize patients until device explantation and arterial reconstruction.
Options for Management
The choice and timing of an optimal procedure should
be individualized and depend on a number of factors.
These include rupture or impending rupture, presence of
an enterovascular fistula, response to initial antimicrobial
therapy, single or multiple MAs, location of MA (intrathoracic or intra-abdominal), presence of gross purulence
surrounding the MA or adjacent vertebral infection, and
underlying comorbidities.
The options for management include open surgical resection with extra-anatomic revascularization or
in situ reconstruction, EVT, or a combination of these
procedures. For MAs located in the thoracic or suprarenal aorta, extra-anatomic revascularization and resection of the MA are usually not technically feasible.
In these patients, the options are resection of the MA
and in situ reconstruction, EVT, or a combination of
these procedures. An algorithm that may be considered for the management of intra-abdominal MAs is
shown in Figure 8.
Open Surgical Resection With Extra-Anatomic Revascular­
ization. Numerous studies have reported results
of resection and extra-anatomic revascularization
compared with in situ reconstruction in patients primarily
with infrarenal aortic MA, which was once considered
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to be the surgical procedure of choice for patients
with aortic MA.*** There are no published randomized
controlled studies that compare in situ with extraanatomic reconstruction. Although in selected patients,
resection and extra-anatomic revascularization may
be appropriate, for the majority of patients, resection
and in situ revascularization rather than extra-anatomic
reconstruction are reasonable.††† Table 6 shows the
advantages and disadvantages of in situ versus extraanatomic reconstructions.
For the surgical management of infrarenal aortic MA,
extra-anatomic revascularization followed by resection
may be considered only for the following selected patients: (1) those with the presence of gross pus in the intraoperative field, (2) those with retroperitoneal or psoas
abscess, (3) those with adjacent vertebral osteomyelitis,
(4) those with inadequate response preoperatively to antimicrobial therapy with persistence of fever and signs of
sepsis, and (5) selected patients with aortoenteric fistula. One study201 suggested that patients with nontyphoidal Salmonella infection should be treated with resection
and extra-anatomic reconstruction. In this report of 92
patients, the survival rate was 71% for patients treated
***References 102, 163, 189, 195, 212, 217, 227, 232–234.
†††References 9, 11, 27, 102, 106, 125, 189, 195, 217, 227, 235.
Circulation. 2016;134:e412-e460. DOI: 10.1161/CIR.0000000000000457
Vascular Infections
with resection and extra-anatomic reconstruction compared with 51% of those treated with in situ reconstruction.201 Nontyphoidal Salmonella infection occurs more
commonly in Asian and southeast Asian countries than in
Western countries.
The disadvantages of extra-anatomic reconstruction are the relatively high rate of vascular complications outlined above. Extra-anatomic revascularization
is usually not technically feasible with suprarenal or
thoracic MA or in patients with rupture or impending
rupture.9,11,27,106,125,189
‡‡‡References 9, 11, 27, 102, 104, 106, 189, 190, 217, 227,
231, 236.
§§§References 9, 11, 27, 106, 189, 217, 227, 236.
Circulation. 2016;134:e412-e460. DOI: 10.1161/CIR.0000000000000457
Endovascular Treatment. EVT of abdominal aortic
aneurysm was first reported in 1986 and is now widely
used for noninfected aortic aneurysms.238 Semba et al239
were the first to report successful EVT of thoracic aortic
MA in 1998. Since that initial report, numerous studies
║║║References 9, 11, 27, 106, 189, 217, 227, 236.
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Open Surgical Repair With In Situ Reconstruction. Many
studies have reported results of resection of an infected
aortic MA with in situ reconstruction, and this has
become the procedure of choice for most patients with
aortic MA.‡‡‡
The major advantages of in situ over extra-anatomic reconstruction are the following: (1) Rifampin-soaked polyester or other conduits are readily available, especially in
patients with rupture or impending rupture who require
urgent surgical intervention. (2) For technical reasons, in
situ reconstruction is more versatile than extra-anatomic
reconstruction for thoracic, suprarenal, or visceral artery
MA; the latter requires renal and visceral artery revascularization. (3) There are fewer long-term complications,
such as limb amputation, aortic stump rupture, and recurrent infection. (4) Selected patients with aortoenteric
fistulae have a lower risk of complications. (5) Higher
long-term survival rates have been achieved. The major
theoretical disadvantage of in situ reconstruction is the
potential risk of reinfection because a foreign body material is used as an interposition graft in infected vascular
tissue, often with surrounding purulence (Table 6).
In numerous studies, recurrence or persistence of
infection after in situ reconstruction is low.§§§ The
relatively low rate of infection could be related to a
number of factors. Polyester grafts are often coated
in rifampin or are silver impregnated, which can decrease the risk of infection. The use of autogenous
venous grafts or cryopreserved arterial allografts can
reduce the risk of infection in patients with VGI surgery. Although there are limited data, the use of these
grafts could also reduce the risk of infection in patients with MA and in situ reconstruction. In addition,
the operative bed is meticulously debrided and the
in situ graft wrapped with omentum, which increases
the vascular supply, eliminates dead space, and protects the graft from the infected bed.66,102,237 Finally,
the relatively low rate of infection associated with in
situ reconstruction may in part reflect patient selection. Extra-anatomic reconstruction is often preferred
in patients who would be expected to have a higher
risk of recurrent infection.
It is difficult to compare accurately the postoperative
reinfection rates associated with in situ compared with
extra-anatomic reconstruction because of the relatively
small number of patients in comparative noncontrolled
studies, nonstandardized antimicrobial therapy, patient
variables, and selection bias. Reported reinfection rates
associated with in situ reconstruction have ranged
from 0% to 22%.║║║ In a literature review, Kyriakides
and colleagues105 reported that 20% of patients with in
situ reconstruction eventually required reoperation and
extra-anatomic revascularization because of infection.
However, the majority of studies suggest a trend toward
higher infection rates associated with extra-anatomic
compared with in situ reconstruction.125,189,236
It is difficult to draw valid conclusions regarding
complications and outcomes in patients treated with in
situ versus extra-anatomic reconstruction. Most studies
comparing in situ with extra-anatomic reconstruction
contain a preponderance of patients treated with either
in situ or extra-anatomic reconstruction. There is considerable selection bias, the study period was often >2
decades long, and the patient populations were quite
diverse. Recently reported studies of patients with infrarenal MA offer the best opportunity to compare outcomes, because there are relatively larger numbers of
patients in each treatment group. Lee et al189 reported
28 patients with infrarenal MA; 13 had in situ repair, and
15 had extra-anatomic reconstruction. Perioperative
mortality among in situ and extra-anatomic reconstruction was 8% and 27%, respectively (P=NS). Early or late
vascular complications occurred in no patients with in
situ reconstruction and in 53% of patients with extra-anatomic surgery (P=0.44). Among patients who survived
initial hospitalization, the long-term results were similar
in both groups. Other studies have reported complications associated with extra-anatomic reconstruction that
include stump disruption (8%–19%), limb amputation
(17%–27%), and reinfection (8%–22%).125,189,195,217,227,236
In summary, a strategy of resection and in situ reconstruction is reasonable for most patients with thoracic,
suprarenal, or visceral artery MA and in selected patients with infrarenal MA. For patients with infrarenal MA
with gross purulence, retroperitoneal or psoas abscess,
adjacent vertebral abscess, and possibly Salmonella
nontyphoidal infection, extra-anatomic revascularization
and resection may be considered.
Wilson et al
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have reported the use of EVT for aortic MA. Kan et al197
reported 41 cases of abdominal aortic MA; 20 patients
were treated with EVT and 21 with open surgical therapy.
Mortality at 1 month was 5% in both groups of patients;
however, mortality at 2 years was 10.5% in the EVT group
compared with 45% in the open surgical group (P<0.05).
At 24 months, among survivors, the aneurysm-related
event-free rates were 78% and 80%, respectively, in the
EVT and open surgical groups. Risk factors that predicted
poor outcome with EVT were persistent signs of sepsis
preoperatively despite appropriate antimicrobial therapy
and the presence of an aortoenteric fistula. In this study,
EVT itself was not a predictor of a poor outcome.
In an earlier meta-analysis of 22 reports of 48 patients
with thoracic or abdominal aortic MA, these authors observed a 30-day survival rate of 90% and a 2-year survival rate of 82% with EVT.199 Risk factors that predicted a
poor outcome were persistent preoperative sepsis, aortoenteric fistula, and rupture, which were similar to those
observed in the later study by Kan et al.198 Factors that
were associated with favorable outcome were antibiotic
therapy administered for at least 1 week preoperatively
and the placement of image-guided drains to treat infection before EVT.198,199,240
Razavi and Razavi241 reported a literature review of 52
articles concerning 91 patients with aortic MA treated with
open surgical repair or EVT. Among patients treated with
open surgical treatment, the 30-day mortality rate was
11% to 43% compared with 5.6% after EVT. However,
late mortality and complication rates were higher with EVT
(20%) than with open surgery (3%–14%). Factors that were
associated with unfavorable outcome were similar in both
groups: aortoenteric fistula, rupture, persistent signs of
sepsis, and undrained periaortic infection preoperatively.
Vallejo et al190 reported 19 aortic MAs in 17 patients;
12 of them had thoracic MAs, and 5 had abdominal
MAs. In situ reconstruction can be technically difficult
in patients with thoracic or suprarenal MA. In patients
with acute rupture, EVT can be a life-saving bridge procedure to later open in situ repair in the thoracic or infrarenal position. Management of thoracoabdominal MA
is complicated by renal and visceral arteries. In these
patients, Vallejo and others reported that a combination
(hybrid) of in situ reconstruction and EVT might be necessary.190,228,241–248 Subsequent explantation of EVT devices is especially challenging in patients with hybrid procedures and might not be technically feasible. Vallejo and
colleagues190 recommended EVT or hybrid procedures
only in selected patients and concluded that open in situ
repair remains the surgical management of choice.
The major concern with EVT is the placement of a
foreign body in an infected area that is not debrided or
drained. It is difficult to determine accurately the frequency
of recurrence or persistent infection associated with EVT
and whether this infection rate is higher or lower than that
associated with open surgical repair. In patients with thoe442
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racic MA, Szeto et al248 reported that all 10 patients who
had EVT had persistence of infection if the device was not
removed; 2 of 10 patients died if the device was not removed, and 3 of 8 who had explantation for infection died.
Kan et al197 reported persistence of infection in 23 of 41
patients (56%) who did not have explantation of the device.
The lack of specific comparative infection rates could be
related to the fact that many patients with retained EVT
devices receive long-term, often lifelong antibiotic therapy, whereas patients treated with surgical repair usually
receive antibiotic drugs for 6 weeks to 6 months. The
use of lifelong antibiotic drugs might suppress infection
in patients with EVT-retained devices, which could result
in underreporting or recognition of persistent infection.248
Szeto et al248 reported that endograft devices can be successfully removed surgically if complicated by infection.
On the basis of the collective published experience
with EVT, EVT may be considered as bridge therapy
to later open surgical treatment in patients with aortic MA who have the following complications: rupture
with unstable hemodynamics, uncontrolled bleeding associated with aortoenteric or aortobronchial fistula, or
concurrent comorbid conditions associated with a high
operative risk of morbidity and mortality, which makes
them unfit for open surgical repair. In these 3 groups
of selected patients, EVT may be a life-saving procedure to stabilize patients and serve as a bridge to open
surgical treatment. After initial placement of the EVT
device, explantation of the device and open surgical
resection of the aortic MA and reconstruction may be
considered in patients who can tolerate an open procedure.189,227,228,241–248 There are insufficient data to recommend EVT as the procedure of choice for patients
with aortic MA (Figure 8).
Recommendations for Surgical or Endovascular
Management of Patients With Aortic MA:
Open Surgical Resection With Extra-Anatomic
Revascularization
1. For the majority of patients with aortic MA,
resection and in situ revascularization rather
than extra-anatomic revascularization and
resection is reasonable (Class IIa; Level of
Evidence B).
2. Extra-anatomic revascularization followed by
resection may be considered for patients with
infrarenal MA only for the following (Class IIb;
Level of Evidence C):
a. gross pus in the operative field,
b. retroperitoneal or psoas abscess,
c. adjacent vertebral osteomyelitis,
d. inadequate response to preoperative antimicrobial therapy, or
e. aortoenteric fistula.
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Vascular Infections
3. Endovascular therapy
a. EVT may be considered as a bridge therapy
to later open surgical management in these
patients (Class IIb; Level of Evidence C):
i. those with rupture with unstable
hemodynamics,
ii. those with uncontrolled bleeding with
aortoenteric fistula or aortobronchial
fistula, or
iii. those who are unfit for open surgical
repair because of underlying comorbid conditions.
b. After initial placement of the endovascular
device, removal of the device, resection
of the aortic MA, and aortic reconstruction may be considered (Class IIb; Level of
Evidence C).
Rupture. Rupture is the most serious life-threatening
complication of aortic MA and has been reported to occur
in 50% to 85%.¶¶¶ Free rupture occurs less commonly
than a contained rupture, and either free or contained
rupture has been associated with a higher mortality rate
than unruptured MA in numerous reports.### Weis-Müller
et al reported a 90-day mortality rate among 66 patients
treated for aortic MA.217,227 All patients with free rupture
died, and the mortality rate (42%) for free or contained
rupture was significantly higher (P<0.05) than for patients
whose aneurysms did not rupture. This experience was
similar to that observed in numerous other studies.****
Free rupture with hemodynamic instability represents
a surgical emergency. There may not be sufficient time
or the patient may be too unstable for open surgery. In
patients with free or contained rupture, EVT may be considered to stabilize hemodynamics and as a bridge to
subsequent open in situ repair (Figure 8).190,227,228,241–248
Recommendation for Management of Rupture
or Contained Rupture of Aortic MA
1. Endovascular device therapy may be considered in patients who are unstable hemodynamically or who are unable to tolerate an
open surgical procedure as a bridge procedure to later open surgical repair (Class IIb;
Level of Evidence C).
¶¶¶References 2, 5, 8, 11, 27, 69, 94, 190, 195, 217, 219, 227.
###References 2, 5, 8, 11, 27, 69, 94, 190, 195, 217, 219, 227.
****References 2, 5, 8, 11, 27, 69, 94, 190, 195, 219.
Circulation. 2016;134:e412-e460. DOI: 10.1161/CIR.0000000000000457
Aortoenteric Fistulae With Duodenum. Primary aortoenteric
fistulae into the duodenum associated with aortic MA
are less common than are secondary aortoenteric
fistulae, which result from erosion of an aortic vascular
graft placed for repair of abdominal aortic aneurysm or
occlusive disease. Aortoenteric fistula, which occurs
at the suture line, occurs in up to 4% of patients after
repair of abdominal aortic aneurysm.8,11,27,106,213,217,227
Aortoenteric fistula was first reported by Brock in
1953.249 Herberer250 reported the first successful repair.
Since that initial report, numerous authors have reported
treatment with either open surgical repair or EVT.††††
Patients with aortoenteric fistulae present with sepsis
and polymicrobial bacteremia with blood cultures containing bowel flora and may have acute, potentially life-threatening gastrointestinal bleeding. Imaging procedures for
the diagnosis of aortoenteric fistula are discussed in the
section on VGI. Aortoenteric fistulae are a life-threatening
condition requiring emergency intervention with either
open surgical reconstruction or EVT. The immediate goals
for management are control of gastrointestinal bleeding
to stabilize hemodynamics, maintenance of distal arterial
perfusion, and control of infection. Open surgical reconstruction can achieve these goals but is associated with a
high morbidity and mortality and with VGI.217,229,244,253 EVT
for treatment of aortoenteric fistula was first described
by Oliva et al254 and Summar and colleagues.255
The selection of open reconstructive surgery, EVT, or
a combination of both must be individualized for each
patient. In a multicenter study with a small number of
patients, Kakkos et al253 compared EVT (8 patients) and
open surgical repair (17 patients). In this study, there
were no in-hospital deaths after EVT, compared with a
35% in-hospital mortality rate among patients who underwent open repair (P=NS). Morbidity was significantly
(P<0.028) higher after open repair (77%) than with EVT
(25%). Morbid complications included recurrence of
gastrointestinal bleeding, ischemic limb, and limb loss.
Among surviving patients, the early advantages of EVT
over open surgery were not sustained after surgery.
Among EVT-treated patients compared with open surgery, the postprocedure rates of events were recurrence
of fistulae 49% and 22%, sepsis 72% and 30%, reoperation 70% and 36%, and survival 15% and 38%, respectively. The number of preoperative symptoms (2 versus
1) was the most important factor in predicting outcome.
††††References 8, 11, 27, 106, 197–199, 213, 217, 227, 228,
241–248, 251, 252.
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Additional Factors in Management of Aortic MA
There are a number of specific circumstances that should
be considered in the management of selected patients.
These include rupture, aortic fistulae (enteric, bronchial,
or esophageal), visceral artery MA, and removal of the
endograft device after EVT.
Fistulous Communication. Aortofistulous communications
are uncommon or rare life-threatening complications
of aortic vascular surgery and vascular infections. In
decreasing order of frequency, fistulous communications
occur with (1) the bowel lumen, usually the third portion
of the duodenum; (2) bronchus; and (3) esophagus.
Wilson et al
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These authors concluded that EVT may be useful as
bridge therapy to open surgical repair to control acute
complications such as gastrointestinal bleeding and hemodynamic instability. The morbidity and mortality were
higher in patients when the EVT device was not removed
and open reconstruction was not performed. Similar experience with short- and long-term outcomes associated
with EVT and open repair for aortoenteric fistula were
reported by Lew et al244 and Antoniou and colleagues.243
EVT may be considered as a bridge to open surgical repair of aortoenteric fistula. The advantages of EVT
over open surgical repair in select patients may include
lower early morbidity and mortality, emergency control
and stabilization of gastrointestinal bleeding and hemodynamics, its reduced degree of invasiveness and better tolerance in older patients with multiple underlying
comorbidities, and avoidance of aortic cross-clamping
with its physiological consequences, including potential
spinal cord injury and reperfusion injury. The major disadvantages of EVT are persistence of infection and higher
long-term morbidity, including limb loss and mortality.
Figure 8 shows an algorithm that may be considered
in patients with aortoenteric fistula.
There are insufficient published data in a small number of patients with aortoenteric fistulae to draw valid
conclusions regarding the duration of postoperative antibiotic therapy with either in situ repair or EVT. In either
case, a foreign body is placed in an area of high-grade
infection at the site of aortoenteric fistula. Because the
risk of recurrent infection and morbidity and mortality
are high, after an initial period of 6 weeks to 6 months
of parenteral antibiotic therapy, lifelong antibiotic suppressive therapy may be considered.213,248,253 Infections
of transcutaneous aortic valve or transpulmonary valve
replacements are considered prosthetic valve infections.
The diagnosis and management of these infections are
outside the scope of this statement and are addressed
in another scientific statement170 or guideline.171
Recommendations for Management of
Aortoenteric Fistula With Duodenum
1. Endovascular therapy may be considered as
a bridge to open repair (Class IIb; Level of
Evidence C).
2. After an initial period of 6 weeks to 6 months
of antimicrobial therapy, lifelong suppressive
therapy may be considered, especially in
patients with a retained EVT device (Class IIb;
Level of Evidence C).
Aortobronchial Fistula. Aortobronchial fistula is a rare
condition with a fistulous communication between
the thoracic aorta and the adjacent tracheobronchial
system.213,256–258 Aortobronchial fistula can occur in
association with MA, atherosclerotic aneurysm, trauma,
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or other causes.256–258 Clinically, these patients present
with sepsis and hemoptysis that may be intermittent
or massive with possible exsanguination. There are
no specific diagnostic tests, but aortobronchial fistula
should be suspected in patients with underlying
risk factors, sepsis, and hemoptysis. CTA may not
demonstrate a definite fistulous communication, but
the presence of periaortic gas bubbles in an at-risk
patient is suggestive of the diagnosis. Angiography or
bronchoscopy may demonstrate a fistula but must be
performed with extreme caution, because the procedure
could potentially dislodge a clot overlying a fistula and
induce massive, possibly fatal hemorrhage.213,259,260
A high index of suspicion is vital for an accurate and
prompt diagnosis of aortobronchial fistula.
If untreated, the mortality rate is virtually 100%. Despite
the advantages in surgical techniques, open in situ repair
has a high mortality, ranging from 15% to 41%.213,257 The
high mortality rate associated with in situ repair is related
to thoracotomy in a critically ill patient, cross-clamping
of the descending aorta with possible spinal cord injury
or reperfusion injury, and complications including rupture
from in situ repair or attempts at arterial bypass.213,257,259
Chuter et al261 first reported thoracic endovascular
aortic repair (TEVAR) in 1996. Bailey et al257 reported 11
patients with TEVAR, which represents the largest series
of patients treated with TEVAR for aortobronchial fistula.
Of these 11 patients, 10 (91%) had successful repair.
One patient developed endoleak and required reintervention with another device replacement. No other patients
required additional intervention. In this study, TEVAR was
not considered as bridge therapy but was considered a
definitive surgical treatment option. Although this was a
small series of patients, TEVAR represents a promising
alternative to in situ repair for a rare condition associated with a high mortality rate. Riesenman et al258 published a review of 67 patients from 32 separate reports
of aortobronchial fistula treated with TEVAR. The 30-day
mortality rate was 1.5%. Aortobronchial fistula recurred
in 6 patients (9%); 3 of them were successfully re-treated, and 3 died. The frequency of successful device explantation was not specifically reported in the review.
There are insufficient data to make a definitive statement regarding postprocedure antibiotic therapy. In the
report by Bailey et al,257 only 2 of the 11 patients received long-term antibiotic therapy, and there were no recurrences of infection. However, because TEVAR places
a foreign body in an infected area, after an initial period
of 6 to 8 weeks of antibiotic therapy, lifelong suppressive antibiotic therapy may be considered.213,248,253,256,258
Although a relatively small number of patients with aortobronchial fistula have been treated with TEVAR on the
basis of published data thus far, we believe that TEVAR
may be considered as preferable to open surgical therapy
for aortobronchial fistula. TEVAR may be considered as
an emergency procedure to control potentially massive
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Vascular Infections
exsanguinating hemorrhage, stabilize hemodynamics, and
lower morbidity and mortality compared with open surgical treatment of aortobronchial fistula. Unlike patients with
aortoenteric fistula, in whom EVT is considered as a bridge
procedure to later open repair and device explantation, in
selected patients with aortobronchial fistula, TEVAR retention of the endovascular device may be considered. This
approach may be considered instead of in situ reconstruction because of the associated high surgical risks. Aortobronchial fistula is a rare condition, and more data are
needed to clarify the short- and long-term risks of TEVAR.
Recommendations for Management of
Aortobronchial Fistula
Aortoesophageal Fistula. Aortoesophageal fistula is a
very rare condition and is more often secondary to
esophageal cancer, trauma, presence of a foreign body,
or erosion of a vascular graft into the esophagus, or
less commonly primarily caused by a thoracic artery
MA or thoracic artery infection.256,262 These represent
<10% of all aortoenteric fistulae and occur in 1.9% of
patients who undergo TEVAR for treatment of thoracic
artery aneurysm.213,231,241,244,256,262 Either primary
or secondary aortoenteric fistula is a highly lethal
condition with a 100% mortality rate if not diagnosed
and treated promptly. These patients present with
a sepsis syndrome, hemodynamic instability, and
hematemesis.256,262 CTA usually does not demonstrate
a fistulous communication, but the presence of
esophageal wall thickening and periesophageal gas
bubbles together with the clinical syndrome in an at-risk
patient is highly suggestive of aortoenteric fistula.
Because this is such an uncommon condition, there
are no definitive guidelines for optimal management,
and therapeutic options must be individualized for
each patient. The goals of management are the same
as for aortoenteric fistula or aortobronchial fistula:
control of bleeding, hemodynamic stabilization, repair
of the fistula, and control of sepsis. The three options
for management are open surgical repair, TEVAR, or a
combination of these procedures. There are a number
of reports of single cases or small numbers of cases
and multicenter retrospective reviews.213,253,256 Chiesa
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Recommendations for Management of
Aortoesophageal Fistula
1. Thoracic EVT may be considered to control
bleeding and stabilize hemodynamics and
as bridge therapy to device explantation
and open surgical repair (Class IIb; Level of
Evidence C).
2. After an initial period of 6 to 8 weeks of antimicrobial therapy, lifelong suppressive antibiotic therapy may be considered with EVT or
in situ repair (Class IIb; Level of Evidence C).
Visceral Artery MA. Visceral artery MAs are a rare
complication of a rare infection; they account for ≤1% of
intra-abdominal MAs.263–269 They most often involve the
superior mesenteric artery but have been described in
the liver, spleen, and kidney. Clinically, they can cause
fever and (rarely) a pulsatile abdominal mass, and
depending on the location, they may be associated with
acute gastrointestinal bleeding, hemobelia, or hematuria.
Because visceral artery MA is rare, there are no large
published studies for diagnosis. The imaging modalities
appear to be similar to those for other intra-abdominal
MAs. CTA has been reported to have a 95% sensitivity
for the diagnosis of visceral artery MA.189
Because the number of patients with visceral artery MA is so small, there are no consensus guidelines
for optimal management. A number of studies outline
the management of patients with visceral artery aneurysm.189,263–270 Because the risk of rupture of visceral
artery aneurysm is high and is associated with a high
mortality, either open surgical intervention or EVT may
be considered.263–270 Open surgical treatment usually involves ligation and resection of the aneurysm with or
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1. Transthoracic endovascular repair may be
considered as preferable to open surgical
repair because of the high operative risk with
open surgical repair as a temporizing measure or in patients who cannot tolerate open
repair (Class IIb; Level of Evidence C).
In patients with a retained endovascular
2. device, after an initial period of 6 to 8 weeks
of antimicrobial therapy, lifelong suppressive
therapy may be considered (Class IIb; Level
of Evidence C).
et al256 published the largest series from multicenter
studies in Italy and included 14 cases. The consensus
opinion of these authors and other published reports is
that TEVAR can be a lifesaving emergency procedure to
control bleeding and help stabilize hemodynamics, but
it should be a bridge to subsequent device explantation
and open in situ surgical repair of the aortoesophageal
fistula. The recurrence rate of infection after TEVAR
ranges from 33% to 60% without explantation, and the
mortality rate ranges from 40% to 60%. The number
of patients is too small and the population too diverse
to draw valid conclusions. In summary, in patients with
aortoesophageal fistula, we believe that TEVAR may be
considered as an initial procedure to control bleeding
and stabilize hemodynamics and as bridge therapy for
subsequent device explantation and open surgical repair
of the fistula. Long-term, possibly lifelong suppressive
antibiotic therapy may be considered in patients with
TEVAR or in situ repair.213,248,253,256,258
Wilson et al
tion of coil embolization of branching arteries for stent
placement in the aneurysm. Künzle et al264 reported 3 patients with visceral artery MA treated with EVT; 1 patient
died of underlying cancer, and the other 2 survived with
retained devices and no recurrence of infection. Stone et
al263 reported 2 MAs among 306 patients with visceral
artery aneurysms (0.6%). Both of these patients were
treated successfully with ligation and excision of the MA.
There are no published data on optimal antimicrobial
therapy. If EVT therapy is selected, a foreign body is
placed in an infected vascular field. The long-term risk of
potentially fatal hemorrhage or other complications after
EVT therapy is unknown. On the basis of experience with
EVT for retained devices for MAs located in other anatomic locations, long-term suppressive antibiotic drugs
may be considered.
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Recommendations for Management of Visceral
Artery MA
1. Either open surgical resection or EVT may be
considered for visceral artery MA (Class IIb;
Level of Evidence C).
2. After EVT, if there is a retained device, lifelong suppressive antimicrobial therapy may
be considered (Class IIb; Level of Evidence C).
Endovascular Device Infection. Endovascular
device
treatment of aortic aneurysms was initially developed as
an alternative management tool for patients who were
considered to be unfit for traditional open surgical repair
because of underlying comorbidities or high risk for
surgical complications, or for emergency temporizing
control of rupture or impending rupture of aortic
aneurysm. However, as more experience was gained
with this procedure, many authorities considered EVT as
the procedure of choice for the management of aortic
aneurysms in patients with suitable anatomy.171,238,271–273
EVT has a number of advantages over open surgical repair,
including lower perioperative morbidity and mortality. EVT
may be used for emergency management of rupture, may
result in a shorter hospitalization, and may have outcome
measures similar to those of traditional open procedures.
However, infection of an EVT device used for TEVAR or
endovascular abdominal repair of aortic aneurysms or
other conditions may be more complex and difficult to
manage than infection associated with open procedures.
Chalmers et al274 reported the first case of EVT graft
infection in 1993. The incidence of infection associated
with EVT is low (0.2%–5%) and is similar to that for open
surgical repair.8,213,256,275–278
Infections associated with endovascular abdominal
repair are reportedly lower, ≈1%, than for TEVAR (up to
5%).8,213,256,275–278 The higher TEVAR infection rates could
relate to the complexity of thoracic compared with aortic
EVT, higher patient comorbidity, and a small increased
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risk of fistulous communication with the bronchus or
esophagus. Infection of endovascular devices falls into
2 broad categories: those that occur in association with
repair of uninfected aortic aneurysms and those that
are used for treatment of MA, including MAs associated
with aortic, enteric, or aortobronchial fistulae. Infections
are more likely with repair of MAs because the device is
placed in vascular tissue that is already infected.
Among patients with EVT for uninfected aortic aneurysm, the cause of infection is thought to be related to
several factors. The endovascular device can become
infected because of intraoperative contamination. These
infections are usually caused by staphylococci or streptococci and less commonly by gram-negative bacilli, including P aeruginosa.213,256,275,279 An endograft is more
susceptible to infection until endothelialization of the
device occurs, usually 2 months after placement.280
Endothelialization makes the device less susceptible to
hematogenous infection from a distal focus. Other factors include placement of the device under emergency
conditions or in a procedure room instead of an operating room, secondary infection of unevacuated thrombus
around the device, the presence of an endoleak, and erosion of the device through the aorta with development of
a fistulous communication to the bronchus, esophagus,
or bowel.5,213,256–258,262
The onset of infection is usually within 2 to 3 months
after the procedure. Infections that occur later are more
often caused by coagulase-negative staphylococci or
other less virulent microorganisms, including Candida
species. Infections associated with a fistulous communication depend on the location of the fistula. The clinical and physical findings are nonspecific. Patients usually have a sepsis syndrome with or without abdominal
pain, and blood cultures may be positive in only 20% to
30% of patients. The diagnosis requires a combination
of index of suspicion and imaging findings. CTA findings
suggestive of infection include enhancing perigraft fluid
or soft tissues or visible gas bubbles.275 Indium-labeled
white blood cell studies or PET/CT studies have also
been reported to be helpful for diagnosis.275,277 The number of reported cases is too small to make a strong
recommendation for the imaging procedure of choice.
A number of studies reported results of explantation of
infected EVT devices and reconstruction.213,251,256,275–279
A small number of patients with infected EVT devices
did not undergo explantation because they were considered medically or surgically unfit to undergo explantation
and reconstruction. The mortality rate in these patients
ranged from 36% to 100%.275–279 Cernohorsky et al277
reported no difference in mortality between patients with
device explantation versus retention, but the number
of patients in each group was too small to draw valid
conclusions. Fatima et al275 published data on the largest number of patients treated in a single center. In this
study, there were 24 patients, 21 with endovascular abCirculation. 2016;134:e412-e460. DOI: 10.1161/CIR.0000000000000457
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Circulation. 2016;134:e412-e460. DOI: 10.1161/CIR.0000000000000457
Recommendations for Management of
Endovascular Device Infection
1. For abdominal or thoracic endovascular
device infection, device explantation and in
situ reconstruction may be considered (Class
IIb; Level of Evidence C).
2. For the treatment of infected endovascular
devices after explantation, at least 6 weeks
of antimicrobial therapy may be considered
(Class IIb; Level of Evidence C).
3. For retained infected endovascular devices,
lifelong suppressive antimicrobial therapy may be considered (Class IIb; Level of
Evidence C).
Prognosis of Aortic MA
Aortic MA is a serious, life-threatening infection. The
prognosis of intrathoracic or intra-abdominal MA varies substantially and depends on many factors, including location, rupture or impending rupture, presence of
aortoenteric or aortobronchial fistula, underlying comorbidities, and other factors. The prognosis of aortic MA is
discussed in the individual sections.
Peripheral MA
Compared with intracranial or aortic MA, patients with
peripheral MAs have a more consistent and recognizable clinical presentation. The diagnosis is more straightforward, and the morbidity and mortality are lower. The
majority of patients with peripheral MAs are IVDUs. Accordingly, unlike patients with ICMAs or aortic MAs, for
whom long-term follow-up data to measure outcome are
often available, the population of patients who are IVDUs
are often lost to follow-up or continue to inject drugs into
the same peripheral artery that was treated surgically
for MA. These and other factors complicate the management of these patients.
Frequency
The overall frequency of MAs, in decreasing order, is
aortic, peripheral, cerebral, and visceral. The most common anatomic location for peripheral MAs in decreasing order of frequency is femoral, humeral, and axillary.
MAs involving the popliteal or external carotid artery are
rare.125,163,281
Pathogenesis, Risk Factors, and Microbiological Cause
The anatomic location reflects the sites that are
most readily accessible to IVDUs. It is estimated that
peripheral MAs occur in ≈0.14% of those who inject
drugs.281,282 Maliphant and Scott282 estimated that the
average duration of continuous intravenous injection of
drugs is 7.7 years until the user exhausts the accessible peripheral veins and begins to inject drugs intraarterially.281,282 Femoral arteries are more readily accessible to IVDUs than are humeral or axillary arteries.
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dominal repair and 3 with TEVAR; 4 of these patients had
aortoenteric fistulae, and 1 had aortobronchial fistula
complicating device infection. In this study, development
of an aortobronchial fistula as a result of EVT placement
occurred in only 0.3% of all endograft procedures performed at Mayo Clinic.275 The authors postulated that
the development of EVT graft enteric fistula occurred as
a result of graft migration or severe angulation causing
repetitive friction wear and mucosal tear.
Although there is no consensus regarding optimal surgical management, the general principles for device removal and vascular reconstruction are essentially the same as
for patients with infected vascular grafts discussed in the
section on VGI. There is more published experience with
device infection in endovascular abdominal repair than
with TEVAR. The management differs for these 2 groups
of patients. For an endovascular abdominal repair device
infection, device removal and extra-anatomic revascularization, especially in patients with gross intraoperative
purulence, was once considered to be the preferred option, but now explantation and in situ reconstruction may
be considered.213,275,276,279 In situ reconstruction has been
reported using rifampin-bonded polyester graft, venous
autograft, or cryopreserved arterial allografts, but the
number of patients is too small to draw valid conclusions
about whether one material is preferable. The choice of
a polyester graft, venous autograft, or cryopreserved allograft should be individualized for each patient, and the
advantages and disadvantages are discussed in detail
under Treatment of VGI. The risk of infection after device
explantation and in situ reconstruction is low (≈4%) and is
similar to the infection rate after open surgical resection
and reconstruction for VGI.8,11,27,106,217,227,275
There are only a few reported cases of device infection for TEVAR,251,256,275,277 and device removal and in situ
repair may be considered for these patients.251,256,275,277
Device extraction and extra-anatomic revascularization
are usually not technically feasible.
The management of infected endovascular devices
in these situations is discussed in Endovascular Device
Infection. TEVAR is considered to be an emergency, potentially life-saving procedure to control bleeding and
stabilize a patient hemodynamically and is a bridge,
temporizing procedure until definitive open in situ reconstruction and device explantation can be performed.
There is no consensus agreement about the duration
of antimicrobial therapy. The number of patients is too
small to draw valid conclusions. Endovascular devices
that are inserted into a vascular bed that is infected
are by definition infected. On the basis of the limited reported experience, at least 6 weeks of initial parenteral
therapy may be considered.256,275–279 For patients with
retained devices, lifelong suppressive antimicrobial therapy may be considered in those who are not candidates
for device extraction and open surgical repair.213,251,256,275
Wilson et al
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The injection of drugs and the nonsterile liquid used
to suspend the illicit drugs causes local tissue necrosis
and damage to the arterial wall and can cause arterial
thrombosis. This results in an environment highly favorable to bacterial infection. The bacteria may be injected
directly into the arterial wall and bloodstream or into the
surrounding soft tissue. Either way, infection causes
weakening of the arterial wall and the development of
the MA and, in some cases, an infected thrombus with
peripheral septic emboli. IVDUs may also have IE, which
results in continuous bacteremia. The localized tissue
necrosis caused by drug injection creates a favorable
environment for infection caused by IE-related bacteremia. The infection can extend to the arterial wall and
result in the formation of an MA.
Less commonly, peripheral MAs can occur in nonIVDUs, such as patients with IE and bacteremia, vascular
surgery, percutaneous arterial puncture or catheterization, or trauma such as from a gunshot wound.125
The most common microorganisms causing peripheral
MA are S aureus, which are frequently MRSA.125,163,281–285
Less commonly, coagulase-negative staphylococci,
gram-negative bacilli, Candida, and other microorganisms have been recovered, and in IVDUs, infection can
be polymicrobial.125
Clinical Presentation
Patients often present with an erythematous, painful, pulsatile mass. Fever is absent in 50% to 60% of patients
and is not a reliable predictor of peripheral MA. Cellulitis
or soft tissue abscess in the site is common. Septic embolization may occur. Some IVDUs can have significant
gangrenous changes and critical limb ischemia caused
by the infection, localized tissue necrosis from injection
of foreign material, or arterial thrombosis.125,163
Diagnosis
Clinical findings in an IVDU are highly suggestive of the
diagnosis of peripheral MA. Elevated white blood cell
count and inflammatory biological markers occur frequently but are nonspecific laboratory findings. Blood
cultures are reportedly positive in 30% to 60% of patie
nts.125,163,286,287 Many patients with peripheral MAs have
received antibiotic drugs before presentation, which can
render blood cultures negative.
The diagnosis of peripheral MA is most often confirmed by imaging. Ultrasonography or CTA may be
considered for the diagnosis.162,281,288 Ultrasonography
is useful to distinguish cellulitis or abscess from MA.163
To-and-fro filling of a pseudoaneurysm demonstrated
by Doppler ultrasonography is suggestive of an MA in
susceptible patients.163,287 Doppler ultrasonography has
a reported 94% sensitivity and 97% specificity of pseudoaneurysm but does not distinguish an infected from a
noninfected aneurysm. The ultrasound or CTA findings
should be correlated with findings on physical examination and laboratory test results for the diagnosis.
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November 15, 2016
Recommendation for Imaging for the Diagnosis
of Peripheral MA
1. Ultrasonography or CTA or both may be considered for the diagnosis of peripheral MA
(Class IIb; Level of Evidence B).
Management
There are no published, randomized prospective studies that define the optimal management of patients with
peripheral MAs. Because of the risk of rupture with potential exsanguinating hemorrhage or limb loss, prompt
surgical intervention is necessary. In addition to antimicrobial therapy, surgical options include ligation only,
resection and in situ reconstruction, or resection with
extra-anatomic revascularization.
A number of studies report ligation without revascularization.240,281,288–291 Postoperative ischemia and
claudication occurred in 33% to 97% of patients, hemorrhage in 18% to 44%, and limb amputation in 5% to
33%.240,281,288–291 Ligation only of an MA involving the
femoral artery is associated with a higher risk of postoperative claudication or amputation than with ligation of
MA in the superficial femoral or tibial arteries.163,281,285
Popliteal artery ligation carries a risk of amputation or
severe chronic ischemia.
Devecioglu et al281 reported 33 cases of peripheral
MA; 20 had ligation and in situ reconstruction, and 6
had ligation and extra-anatomic revascularization. In situ
reconstruction with an autogenous vein was preferred
in the study. Other studies reported in situ reconstruction with cryopreserved arterial allografts75,269,283,292
Postoperative complications occurred in at least 24%
to 39% of patients and included suture line rupture and
hemorrhage, recurrent infection, thrombosis of graft,
claudication, or limb amputation in 6% to 33% of patients.281,283,293 These authors did not recommend in situ
reconstruction with synthetic graft material because of
high infection rates, including some studies that had a
100% rate of reinfection after in situ reconstruction with
synthetic material.281,293–295
The third surgical option is ligation and extra-anatomic
revascularization.281,285 In these studies, extra-anatomic
revascularization was performed because of extensive
necrosis or purulence in the operative field, which made
in situ reconstruction technically not possible. Complications included persistent infection, stump rupture, failure to maintain long-term patency of the extra-anatomic
graft, and limb claudication or amputation.
It is difficult to compare complication rates among
these 3 surgical options, because many of these patients are IVDUs who continue to inject drugs into the
ligated or reconstructed area. There are insufficient data
to recommend a specific surgical procedure, and the
choice must be individualized for each patient. There are
no prospective studies that define the optimal duration
of postoperative antibiotic therapy. Like the choice of a
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Vascular Infections
surgical procedure, the duration of antimicrobial therapy
must be individualized. A 6-week postoperative course
of antibiotic therapy may be considered. In selected patients with gross purulence intraoperatively treated with
in situ reconstruction or extra-anatomic revascularization, after the initial 6-week course of antimicrobial therapy, an additional 6-month period of therapy or, in some
cases, lifelong suppressive therapy may be considered.
Recommendations for Postoperative Antimicrobial
Therapy for Patients With Peripheral MA
Prevention of Infections of Vascular
Grafts or Endovascular Devices and
Stents
The administration of antimicrobial agents for the prevention of infection of vascular grafts, endovascular devices,
or stents may be considered as primary or secondary prophylaxis. Primary prophylaxis refers to the administration
of antimicrobial prophylactic therapy to prevent perioperative infections. Secondary prophylaxis refers to the administration of antimicrobial therapy intended to prevent infection as a result of transient bacteremia associated with an
invasive procedure, such as a dental procedure.
Primary Prophylaxis
Perioperative or intraoperative antimicrobial therapy for
patients who undergo vascular graft surgery or intravascular device placement is a longstanding, widely accepted expectation and standard of care. However, there are
few randomized, prospective, placebo-controlled blinded
studies that demonstrate clear efficacy of prophylactic
therapy to prevent graft or endovascular device infections. The frequency of vascular graft or endovascular
device infection ranges from 0.2% to 5%.1–9,213,256,275–278
Because of the low frequency of infections, a large
number of patients would be required to demonstrate
efficacy of primary prophylaxis. In addition, because primary prophylaxis is such a long established standard of
care and infections are associated with a high morbidity
and mortality, patients and healthcare providers might
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Recommendations for Primary Antimicrobial
Prophylaxis Perioperatively for Clean Vascular
Graft Surgery or Placement of an Endovascular
Device
1. Perioperative administration of a β-lactam
antibiotic to prevent wound infection is reasonable for patients who undergo clean
vascular graft surgery (Class IIa; Level of
Evidence B).
2. Perioperative administration of a β-lactam
antibiotic may be considered for patients
who undergo placement of an endovascular
device (Class IIb; Level of Evidence C).
Secondary Prophylaxis
There is a longstanding perception that dental procedures
can cause distal infection as a result of transient bacteremia that occurs commonly during the procedure. In the
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1. In patients with peripheral MAs, a 6-week
course of antimicrobial therapy may be considered (Class IIb; Level of Evidence B).
2. In patients with gross intraoperative purulence, MRSA, or infection caused by a multidrug-resistant microorganism or Candida
species, a 6-month course of antimicrobial
therapy may be considered. In selected
patients, lifelong suppressive therapy may be
considered (Class IIb; Level of Evidence B).
understandably be reluctant to participate in placebocontrolled studies.
Kaiser et al296 reported a controlled, randomized,
prospective, double-blinded study in patients undergoing clean vascular graft surgery that compared placebo
(237 patients) with perioperative cefazolin (225 patients). There was a significantly (P<0.001) higher rate
of wound infections among the placebo group (6.8%)
than among the cefazolin recipients (0.9%). The 2 infections that occurred in the cefazolin recipients were class
II groin wound infections without involvement of the vascular graft. Among the 16 wound infections in the placebo group, 4 had class III groin infection with involvement
of the vascular graft; 2 of them died, and 2 underwent
above-the-knee amputation. Patients in both the placebo
group and the cefazolin group had perioperative skin application of topical antibacterial substances, most often
povidone-iodine.
Hopkins297 reviewed published studies in English language literature that compared placebo with antimicrobial therapy. Although the number of patients reported
was relatively small, the wound infection rates among
patients in the placebo group ranged from 16.7% to
22.6% compared with 0% to 5.8% among those who
received perioperative antimicrobial prophylaxis.
On the basis of these studies, the use of a β-lactam
antibiotic for perioperative prophylaxis to prevent wound
infection is reasonable for patients who undergo clean
vascular graft surgery.296–298 There are insufficient published data to recommend vancomycin for perioperative
prophylaxis. It is unlikely that placebo-controlled, blinded studies will be published for primary prophylaxis in
patients who undergo endovascular device placement;
however, the administration of a perioperative β-lactam
antibiotic may be considered.
Wilson et al
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post–antibiotic drug era, antimicrobial prophylaxis for dental procedures has been suggested for >25 medical conditions (eg, valvular heart disease or in patients who have
implanted devices, such as a joint arthroplasty).297–301 The
efficacy of secondary prophylaxis for dental procedures is
unproven and is based largely on the potentially devastating
consequences of infections in these patients rather than
on scientific evidence.302–304 The rationale for secondary
prophylaxis for patients who undergo a dental procedure
to prevent a vascular graft or endovascular device infection is based largely on case reports, textbook chapters,
or expert opinion.7,304,305 There are no published evidencebased studies that document the efficacy of antimicrobial
therapy to prevent these infections in patients who undergo
a dental procedure. The American Heart Association does
not recommend antimicrobial prophylaxis for prevention of
vascular graft or endovascular graft infection in patients
who undergo a dental procedure or in uninfected patients
who undergo a urologic or gastrointestinal tract procedure.7,304,305
FOOTNOTES
The American Heart Association makes every effort to avoid
any actual or potential conflicts of interest that may arise as a
result of an outside relationship or a personal, professional, or
business interest of a member of the writing panel. Specifically,
all members of the writing group are required to complete and
submit a Disclosure Questionnaire showing all such relationships
that might be perceived as real or potential conflicts of interest.
This statement was approved by the American Heart Association Science Advisory and Coordinating Committee on Sep-
tember 16, 2015, and the American Heart Association Executive
Committee on February 23, 2016. A copy of the document
is available at http://professional.heart.org/statements by
using either “Search for Guidelines & Statements” or the
“Browse by Topic” area. To purchase additional reprints, call
843-216-2533 or e-mail [email protected].
The American Heart Association requests that this document
be cited as follows: Wilson WR, Bower TC, Creager MA, AminHanjani S, O’Gara PT, Lockhart PB, Darouiche RO, Ramlawi B,
Derdeyn CP, Bolger AF, Levison ME, Taubert KA, Baltimore RS,
Baddour LM; on behalf of the American Heart Association Committee on Rheumatic Fever, Endocarditis, and Kawasaki Disease
of the Council on Cardiovascular Disease in the Young; Council
on Cardiovascular and Stroke Nursing; Council on Cardiovascular Radiology and Intervention; Council on Cardiovascular Surgery and Anesthesia; Council on Peripheral Vascular Disease;
and Stroke Council. Vascular graft infections, mycotic aneurysms, and endovascular infections: a scientific statement from
the American Heart Association. Circulation. 2016;134:e412–
e460. doi: 10.1161/CIR.0000000000000457.
Expert peer review of AHA Scientific Statements is conducted
by the AHA Office of Science Operations. For more on AHA
statements and guidelines development, visit http://professional.
heart.org/statements. Select the “Guidelines & Statements”
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Permissions: Multiple copies, modification, alteration,
enhancement, and/or distribution of this document are not
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Disclosures
Writing Group Disclosures
Employment
Research
Grant
Other
Research
Support
Speakers’
Bureau/
Honoraria
Expert
Witness
Ownership
Interest
Consultant/
Advisory
Board
Other
Mayo Clinic
None
None
None
None
None
None
None
University of Illinois
at Chicago
None
None
None
None
None
None
None
Mayo Clinic
None
None
None
None
None
None
None
Yale University
School of Medicine
None
None
None
None
None
None
None
UCSF
None
None
None
None
None
None
None
Thomas C. Bower
Mayo Clinic
None
None
None
None
None
None
None
Mark A. Creager
Brigham & Women’s
Hospital
None
None
None
None
None
None
None
Infectious Disease Section
and Center for Prostheses
Infection, Veterans Affairs
None
None
None
None
None
None
None
Writing Group
Member
Walter R. Wilson
Sepideh Amin-Hanjani
Larry M. Baddour
Robert S. Baltimore
Ann F. Bolger
Rabih O. Darouiche
(Continued )
e450
November 15, 2016
Circulation. 2016;134:e412-e460. DOI: 10.1161/CIR.0000000000000457
Vascular Infections
Writing Group Disclosures Continued
Employment
Research
Grant
Other
Research
Support
Speakers’
Bureau/
Honoraria
Expert
Witness
Ownership
Interest
Consultant/
Advisory
Board
Other
University of Iowa
None
None
None
None
None
None
None
Matthew E. Levison
Drexel University College
of Medicine
None
None
None
None
None
Merck†
None
Peter B. Lockhart
Carolinas Medical Center
None
None
None
None
None
None
None
Patrick T. O’Gara
Brigham & Women’s
Hospital
None
None
None
None
None
None
None
Valley Health System,
Heart & Vascular Center
None
None
None
None
None
Sorin Inc*;
Medtronic*
None
American Heart
Association
None
None
None
None
None
None
None
Writing Group
Member
Colin P. Derdeyn
Basel Ramlawi
Kathryn A. Taubert
Reviewer Disclosures
Research
Grant
Other
Research
Support
Speakers’
Bureau/
Honoraria
Expert
Witness
Ownership
Interest
Consultant/
Advisory
Board
Other
Reviewer
Employment
James H. Black
Johns Hopkins
University
None
None
None
None
None
None
None
Bambino Gesù
Children`s Hospital
IRCCS (Italy)
None
None
None
None
None
None
None
Matteo Trezzi
This table represents the relationships of reviewers that may be perceived as actual or reasonably perceived conflicts of interest as reported on the
Disclosure Questionnaire, which all reviewers are required to complete and submit. A relationship is considered to be “significant” if (a) the person receives
$10 000 or more during any 12-month period, or 5% or more of the person’s gross income; or (b) the person owns 5% or more of the voting stock or
share of the entity, or owns $10 000 or more of the fair market value of the entity. A relationship is considered to be “modest” if it is less than “significant”
under the preceding definition.
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Circulation. 2016;134:e412-e460. DOI: 10.1161/CIR.0000000000000457
Downloaded from http://circ.ahajournals.org/ by guest on November 16, 2016
Vascular Graft Infections, Mycotic Aneurysms, and Endovascular Infections: A Scientific
Statement From the American Heart Association
Walter R. Wilson, Thomas C. Bower, Mark A. Creager, Sepideh Amin-Hanjani, Patrick T.
O'Gara, Peter B. Lockhart, Rabih O. Darouiche, Basel Ramlawi, Colin P. Derdeyn, Ann F.
Bolger, Matthew E. Levison, Kathryn A. Taubert, Robert S. Baltimore and Larry M. Baddour
On behalf of the American Heart Association Committee on Rheumatic Fever, Endocarditis, and
Kawasaki Disease of the Council on Cardiovascular Disease in the Young; Council on
Cardiovascular and Stroke Nursing; Council on Cardiovascular Radiology and Intervention;
Council on Cardiovascular Surgery and Anesthesia; Council on Peripheral Vascular Disease;
and Stroke Council
Circulation. 2016;134:e412-e460; originally published online October 13, 2016;
doi: 10.1161/CIR.0000000000000457
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