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INTERVENTIONAL
Visceral artery aneurysms: Incidence, management, and outcome
analysis in a tertiary care center over one decade
Michael B. Pitton &Evelyn Dappa &Florian Jungmann &Roman Kloeckner &
Sebastian Schotten &Gesine M. Wirth &Jens Mittler &Hauke Lang &
Peter Mildenberger &Karl-Friedrich Kreitner &Katja Oberholzer &Christoph Dueber
Received: 26 June 2014 /Revised: 10 November 2014 /Accepted: 13 January 2015 / Published online: 19 February 2015
#The Author(s) 2015. This article is published with open access at Springerlink.com
Abstract
Objectives To evaluate the incidence, management, and out-
come of visceral artery aneurysms (VAA) over one decade.
Methods 233 patients with 253 VAAwere analyzed according
to location, diameter, aneurysm type, aetiology, rupture, man-
agement, and outcome.
Results VAA were localized at the splenic artery, coeliac
trunk, renal artery, hepatic artery, superior mesenteric artery,
and other locations. The aetiology was degenerative, iatrogen-
ic after medical procedures, connective tissue disease, and
others. The rate of rupture was much higher in
pseudoaneurysms than true aneurysms (76.3 % vs.3.1 %).
Fifty-nine VAA were treated by intervention (n = 45) or sur-
gery (n= 14). Interventions included embolization with coils
or glue, covered stents, or combinations of these. Thirty-five
cases with ruptured VAA were treated on an emergency basis.
There was no difference in size between ruptured and non-
ruptured VAA. After interventional treatment, the 30-day mor-
tality was 6.7 % in ruptured VAA compared to no mortality in
non-ruptured cases. Follow-up included CT and/or MRI after
a mean period of 18.0±26.8 months. The current status of the
patient was obtained by a structured telephone survey.
Conclusions Pseudoaneurysms of visceral arteries have a
high risk for rupture. Aneurysm size seems to be no reliable
predictor for rupture. Interventional treatment is safe and ef-
fective for management of VAA.
Key Points
•Diagnosis of visceral artery aneurysms is increasing due to
CT and MRI.
•Diameter of visceral arterial aneurysms is no reliable pre-
dictor for rupture.
•False aneurysms/pseudoaneurysms and symptomatic cases
need emergency treatment.
•Interventional treatment is safe and effective.
Keywords Visceral aneurysm .False aneurysm /
Pseudoaneurysm .Ruptured aneurysm .Endovascular
procedures .Outcome analysis
Abbreviations
VAA Visceral artery aneurysm
SAA Splenic artery aneurysm
HAA Hepatic artery aneurysm
SMAA Superior mesenteric artery aneurysm
CTRA Coeliac trunc aneurysm
GDAA Gastroduodenal artery aneurysm
PDAA Pancreaticoduodenal artery aneurysm
RAA Renal artery aneurysm
GAA Gastric artery aneurysm
CT Computed tomography
Introduction
Visceral arterial aneurysms (VAAs) are a rare entity; they are
often asymptomatic, incidental findings in computed tomog-
raphy (CT) and magnetic resonance imaging (MRI). VAAs
can present as life-threatening ruptures that require emergency
treatment. However, discriminating between VAAs that are
harmless incidental CT findings which do not require
M. B. Pitton (*):E. Dappa :F. Jungmann :R. Kloeckner :
S. Schotten :G. M. Wirth :P. Mildenberger :K.<F. Kreitner :
K. Oberholzer :C. Dueber
Department of Diagnostic and Interventional Radiology, University
Hospital of Mainz, Langenbeckstr.1, 55131 Mainz, Germany
e-mail: michael.pitton@unimedizin-mainz.de
J. Mittler :H. Lang
Department of Abdominal, Visceral and Transplantation Surgery,
University Hospital of Mainz, Langenbeckstr.1,
55131 Mainz, Germany
Eur Radiol (2015) 25:2004–2014
DOI 10.1007/s00330-015-3599-1
treatment and high-risk aneurysms is not always possible.
Several publications recommend treatment of VAAs >2 cm in
diameter [1–5]. Nonetheless, clinical experience indicates that
the risk of rupture depends not only on the aneurysm diameter,
but also upon VAA localization [3]; underlying disease, such as
congenital defects (e.g., Ehlers-Danlos Syndrome), atheroscle-
rosis, and mycotic/inflammatory aneurysm [6–8]; and the rate
of growth [9,10]. In contrast to true aneurysms, which feature
distension of all three layers of the arterial wall, so-called false
aneurysms or pseudoaneurysms result from a breach of the
inner-wall layers, resulting in bulging of the adventitial layer.
False aneurysms are often caused by iatrogenic trauma, e.g.
after hepatobiliary or vascular surgery.
This retrospective study reviewed all cases of VAA seen at
our university medical centre over a 10-year period. Our ob-
jective was to characterize the incidence of VAA, identify
possible risk factors for aneurysm rupture, and compare sur-
gical and interventional–radiological approaches with respect
to clinical outcome.
Materials and methods
For patient selection, we searched our institutional database
(covering years 2000–2010) for the term ‘aneurysm’, which
yielded 12,588 radiological reports, mostly related to aortic
pathologies. A total of 233 patients were identified as having
VAA. Information about patient age, sex, presenting symp-
toms and signs, diagnostic modalities, risk factors, co-morbid-
ities, recent operations, and medication was obtained from
medical records and office charts. Data were analysed accord-
ing to anatomic features, such as aneurysm location and di-
ameter, true or false aneurysm, and aneurysm status (ruptured
or non-ruptured). The aetiology of each aneurysm was retro-
spectively deduced and analysed from the underlying diseases
documented in the patients’records, previous medical proce-
dures, and from clinical findings at admission.
Clinical management of the patients was investigated in
terms of surgical therapy, interventional treatment and watchful
waiting. The specific type of surgical and interventional tech-
nique was obtained from medical reports and from imaging.
The clinical course of the patients was investigated by
means of a structured telephone survey of all patients or their
relatives and of their general medical practitioners. The survey
included all available information on successive hospital
stays, surgical or interventional treatment, and current clinical
condition.
Results
We identified 233 patients (age 65±13 years [range 17–95
years], 142 men and 91 women) diagnosed with a total of
253 VAAs over the course of a decade (Table 1). In the ma-
jority of cases VAA involved the splenic artery (n=83),
followed by the coeliac trunk (n=47), the renal arteries (n=
44), the hepatic artery (n=40), the superior mesenteric artery
and its branches (n=17), the gastroduodenal artery (n=10),
the pancreaticoduodenal artery (n=8), the gastric artery (n=
4), and combinations of these as listed in Table 2. Thirty-seven
aneurysms in 35 patients presented with rupture; the majority
of aneurysms were detected in a non-ruptured condition (n=
216 aneurysms). Over 90 % of the aneurysms (n=231 in 212
patients) were detected by CT scans, followed by angiography
(n=13in12patients)andMRI(n=9 in 9 patients).
Radiological follow-up was 18.0±26.8 months (range: 1 day
to 109 months).
Sixty-two of the 233 patients (26.6 %) presented with spe-
cific symptoms upon admission to hospital, and all 35 patients
with ruptured aneurysms showed symptoms. A reduced
haemoglobin count of 8.2± 1.6 g/dl in 34 of 62 patients
(54.8 %) was the most frequent sign of rupture. Eleven of 62
symptomatic patients (17.7 %) presented with abdominal
pain. For a summary of the patients’clinical presentation,
see Table 3.
One hundred and seventy-one of the 233 patients (73.4 %)
had no specific symptoms. In 13 asymptomatic patients, a
VAA was already known from previous examinations. Of
the 171 asymptomatic patients, 158 (92.4 %) were incidental-
ly diagnosed with a VAA. Indications for imaging in patients
with incidental findings included follow-up examinations af-
ter tumour treatment or other medical conditions (n=91),
suspected illness unrelated to the VAA (n=44), tumour stag-
ing (n=20), and preoperative imaging (n=3).
According to the retrospective rating described above, the
main aetiology of VAA was degenerative atherosclerosis (197
of 253 aneurysms; 77.9 %), with varying degrees of calcifica-
tion of the arteries. Moreover, there were 13 post-stenotic
aneurysms, with arterial stenosis of the coeliac trunk or its
tributaries and stenosis of the superior mesenteric artery
(Table 2). The second most frequent aetiology was diverse
complications after preceding medical procedures, with 23
iatrogenic false aneurysms of the hepatic artery or its tribu-
taries as well as the renal artery. The remaining VAAs devel-
oped in patients with vasculitis due to connective tissue dis-
eases, hereditary diseases like Ehlers-Danlos syndrome,
fibromuscular dysplasia, and hereditary haemorrhagic telangi-
ectasia. Seven VAAs occurred secondary to inflammatory dis-
eases, such as pancreatitis. Rare causes for VAA included
trauma, tumours and mycotic aneurysms after infection (e.g.,
endocarditis).
A total of 196 pathologies were rated as true aneurysms,
compared to 38 false aneurysms. The remaining 19 aneurysms
could not be clearly assigned to one of these two groups and
were therefore labelled as indeterminable aneurysms. These
aneurysms were caused either by infection or diseases of the
Eur Radiol (2015) 25:2004–2014 2005
connective tissue, which are known to cause both true as well
as false aneurysms (11-20). Since no histological information
was available that would allow us to reliably classify these
aneurysms as true or false, we decided to analyse them sepa-
rately in order to minimize any bias. For an overview of the
incidence and location of true, false and indeterminable aneu-
rysms, see Fig. 1.
Thirty-seven of 253 VAAs (14.6 %) presented with aneu-
rysm rupture (Table 4). The majority of ruptured aneurysms
were pseudoaneurysms (n=29). True VAAs presented with a
rupture rate of 3.1 % (six out of 196 aneurysms). Vice versa,
false VAAs had a significantly higher rupture rate of 76.3 %
(29 of 38 aneurysms). There was evidence of rupture of inde-
terminable VAAs in two cases.
The mean overall size of the VAAs was 16.1± 9.8 mm, with
a wide range of diameters (4.0–111.9 mm), which varied de-
pending upon VAA localization (Table 4). There was no sig-
nificant difference between the diameters of ruptured aneu-
rysms compared to non-ruptured aneurysms (14.8± 8.2 mm
vs. 16.3±10.0 mm, respectively). However, in 18 cases, the
aneurysm size could not be determined, because the aneurysm
rupture prevented delineation and reliable diameter measure-
ment within the haematoma. The greatest diameters were
found in splenic artery aneurysms (SAAs). The overall
maximum diameter was up to 111.9 mm in a non-
ruptured SAA compared to 34.7 mm in a ruptured HAA.
Excluding these outliers of diameters in both groups, the
mean transverse diameter of non-ruptured and ruptured
cases was nearly equal (15.9±7.4 mm vs. 14.3±7.5 mm,
respectively). Moreover, there was no significant differ-
ence between the mean diameters of false aneurysms com-
pared to true aneurysms (15.6± 7.6 mm vs. 16.3 ± 10.3 mm,
respectively) (Table 4).
Specific aneurysm-targeted treatment was applied to 59 of
the 253 VAAs (23.3 %) by means of interventional techniques
(n=45) or open surgery (n=14) (Fig. 2). Thirty-six VAAs with
aneurysm rupture or contained rupture (14.2 %) were treated
on an emergency basis. In one ruptured VAA, a spontaneous
occlusion was observed during emergency angiography,
which was confirmed in a postangiographic CT. An additional
23 non-ruptured VAAs (9.1 %) were treated electively at the
discretion of the interventional radiologist or surgeon based on
individual findings (e.g., aneurysm growth or underlying
disease); 13 by means of intervention and ten surgically.
The remaining 193 cases were rated clinically harmless
without suspicious symptoms and without need for imme-
diate treatment; these cases were followed up by watchful
waiting.
Tabl e 1 Patient characteristics
January 2000–August 2010
Patients (n) 233, 142 men, 91 women
Age (years) 65± 13 (range 17–95)
Aneurysms 253
Ruptured aneurysms 37 in 35 patients
Non-ruptured aneurysms 216 in 198 patients
Diameter (mm) 16.1±9.8 (range 4.0–111.9)
Follow-up via telephone (months) 51.0±32.1 (43 median, Q1/Q3 25/69)
Follow-up imaging (months) 18.0±26.8 (7 median, Q1/Q3 1/19.75)
Co-morbidities n (%)
Arterial hypertension 126 (54.1)
Diabetes mellitus type 2 35 (15.0)
Smoker 41 (17.6)
Coronar heart disease 37 (15.9)
Aortic aneurysm 26 (11.2)
HCC 18 (7.7)
Colon carcinoma 13 (5.6)
Melanoma 8 (3.4)
Rheumatoid arthritis 7 (3.0)
COPD 7 (3.0)
Liver cirrhosis 29 (12.5)
Portal hypertension 12 (5.2)
Chronic renal failure 21 (9.0)
Renal cysts 8 (3.4)
Pregnancy 0 (0)
2006 Eur Radiol (2015) 25:2004–2014
Interventional treatment was applied to 27 aneurysms
with coil embolization, four aneurysms were treated with
glue embolization, five aneurysms with stent grafts, and
another nine aneurysms with combinations of treatments
(i.e., coil embolization+ stentgrafts, coil embolization+ glue
embolization, or coil embolization +Amplatzer plug). The
surgical procedures included ligation of the artery and re-
section of the aneurysm in seven aneurysms, vascular re-
construction and bypass in three aneurysms, and ligation
and en-bloc resection of the adjacent organ (i.e., spleen or
kidney) in two aneurysms. An additional two patients with
aneurysms of the hepatic artery received aneurysm resec-
tion during liver transplantation, in whom the VAA was
only an accompanying pathology (Fig. 2).
There was no periprocedural mortality after radiological
intervention or open surgery. The 30-day mortality after
interventional treatment of VAA was in total 5 % (n=2 of
40 patients), one patient after coil embolization and the
other after stent grafting. Since both deaths occurred in
the emergency setting, the mortality was 6.7 % (n= 2 of
30 patients) in this subgroup. There was no 30-day mortal-
ity in the 11 patients who underwent open surgery; howev-
er, due to the small number of cases, we were unable to
make comparisons with the interventional group or draw
conclusions. For further details concerning the management
of VAA, see Table 5.
The overall rate of periprocedural complications after
interventional treatment was 12.5 % (five complications in
Tabl e 2 Aetiology of visceral
arterial aneurysms
SAA splenic arterial aneurysm,
HAA hepatic arterial aneurysm,
SMAA superior mesenteric artery
aneurysm, CTRA coeliac trunk
aneurysm, GDAA gastroduodenal
artery aneurysm, PDAA
pancreaticoduodenal artery
aneurysm, RAA renal artery
aneurysm, GAA gastric artery
aneurysm
Aetiology VAA
(patients)
Degenerative 197 (186) SAA (79), CTRA (45), RAA (27), HAA(23),
SMAA (11), GDAA (6), GAA (2), PDAA (4)
VAA without calcification 141 (137) SAA (56), CTRA (34), RAA (22), HAA(19),
SMAA (6), GDAA (2), GAA (1), PDAA (1)
VAA with calcification 43 (38) SAA (23), CTRA (8), RAA (5), HAA (4),
SMAA (2), GAA (1)
Post-stenotic VAA 13 (11) GDAA (4), CTRA (3), SMAA (3), PDAA (3)
Medical procedures 23 (23) HAA (15), RAA (6), GDAA (1), PDAA (1)
Operation 14 (14) HAA (11), RAA (2), GDAA (1)
Pancreaticoduodenectomy 5 (5) HAA (5)
Haemihepatectomy 3 (3) HAA (2), GDAA (1)
Liver transplantation 3 (3) HAA (3)
Nephrectomy 1 (1) RAA (1)
Renal cyst enucleation 1 (1) RAA (1)
Biliodigestive anastomosis 1 (1) HAA (1)
Other intervention 9 (9) HAA (4), RAA (4), PDAA (1)
Percutaneous transhepatic biliary
drainage
2 (2) HAA (2)
Renal biopsy 2 (2) RAA (2)
Hepatic biopsy 1 (1) HAA (1)
Nephrostoma 1 (1) RAA (1)
Percutaneous nephrolithotripsy 1 (1) RAA (1)
Selective internal radiation therapy 1 (1) HAA (1)
Gastroduodenoscopy 1 (1) PDAA (1)
Connective tissue disosrder 17 (9) RAA (7), SMAA (5), PDAA (2), GDAA (1),
HAA (1), SAA (1)
Vasculitis 7 (4) SMAA (3), PDAA (2), GDAA (1), RAA (1)
Ehlers-Danlos 6 (1) RAA (3), HAA (1), SAA (1), SMAA (1)
Fibromuscular dysplasia 3 (3) RAA (3)
Osler disease 1 (1) SMAA (1)
Inflammation 7 (6) GAA (2), GDAA (2), SAA (2), RAA (1)
Trauma 5 (5) CTRA (2), SAA (1), PDAA (1), RAA (1)
Tumour 2 (2) RAA (2)
Infection, mycotic aneurysm 2 (2) HAA (1), SMAA (1)
Eur Radiol (2015) 25:2004–2014 2007
40 patients) including one patient with myocardial infarc-
tion (ruptured VAA), two splenic infarctions, one patient
with parenchymal abscesses (liver), and one with intracere-
bral bleeding (ruptured VAA). Four of the five complica-
tions occurred in patients with a ruptured VAA. Secondary
bleeding after interventional treatment occurred in five
cases. After open surgery, two out of 11 patients
(18.2 %) suffered from perioperative complications: one
splenic abscess (ruptured VAA), and one insufficient anas-
tomosis after venous bypass interponate (non-ruptured
VAA). Secondary bleeding occurred in two patients after
open surgery (one in a ruptured and one in a non-
ruptured VAA); Tables 6and 7summarize the complica-
tions that occurred after interventional and surgical treat-
ment, respectively. Patients with VAA who were stratified
for watchful waiting had a 30-day mortality of 6.6 % (12
of 182 patients), without any death caused by verified an-
eurysm rupture.
Cross-sectional imaging was available for 143 of 233 pa-
tients (61.4 %) and comprised CT and/or MRI at a mean
follow-up of 18.0 ± 26.8 months. The current status of the
patients was obtained by a structured telephone survey con-
ducted a mean of 51.0±32.1 months after treatment. The sur-
vey yielded conclusive information for 228 of 233 patients.
The structured interview inquired about the patients’health,
current medication and past hospital stays. Only five patients
were lost to follow-up, resulting in high-quality data with a
completion rate of 97.9 %. Of the 228 patients included in the
follow-up, 161 (70.6 %) were alive and 67 (29.4 %) were
deceased. Causes of death were progressive tumour (n=33),
cardiovascular events (n=12), post-transplantation complica-
tions (n=6), infection (n=5), liver cirrhosis (n=1), renal in-
sufficiency (n=2), complications of insufficient
hepaticojejunostomy (n=1), complications of systemic lupus
erythematosus (n=1), appendicitis (n=1), intracerebral bleed-
ing after double antiplatelettherapy 30 days after insertion of a
stent graft for a ruptured HAA (n=1), and gastrointestinal
bleeding without clinical evidence of VAA rupture (n=1).
Moreover, there were three inconclusive deaths, including
two patients with renal artery aneurysm (RAA) and SAA,
which were conservatively treated. The third patient received
a venous bypass for RAA and died 7 years after the procedure.
Retrospectively, it remained unclear whether any of these in-
conclusive deaths were related to VAA complications.
Seventeen of the 161 remaining patients (10.6 %) suffered
from some sort of abdominal complaint during follow-up;
these were related to cholangitis (n=2), duodenal ulcers (n=
2), gallstones (n=2), splenic infarction (n=2), reflux
Tabl e 3 Specific symptoms at admittance to hospital
Specific signs or symptoms Symptomatic patients Symptomatic patients with ruptured VAA
n (pat) Localization n (pat) Localization
Reduced haemoglobin count 34
*
HAA (15), RAA (8), GDAA (4),
SAA (4), PDAA (2), GAA (1)
33 HAA (15), RAA (7), GDAA (4),
SAA (4), PDAA (2), GAA (1)
Abdominal pain 11 CTRA (4), SMAA (2), GAA (1),
HAA (1), PDAA (1), RAA (1),
SAA (1),
1SMAA(1)
Reduced general condition 4
**
CTRA (3), GDAA (1)
Vomiting 3 SAA (2), HAA (1)
Chest pain 2 RAA (2)
Dyspnoea 2 SAA (2)
Fever 2 CTRA (1), SAA (1)
Cholangitis 1 SAA (1)
Gastrointestinal bleeding 1 SAA (1)
Severe arterial hypertension 1 SMAA (1)
Urinary retention 1 RAA (1) 1 RAA (1)
Total 62 HAA (17), RAA (12), SAA (12),
CTRA (8), GDAA (5), SMAA (3),
PDAA (3), GAA (2)
35 HAA (15), RAA (8), GDAA (4),
SAA (4), PDAA (2), GAA (1),
SMAA (1)
*
17 patients with a combination of symptoms including reduced haemoglobin count +abdominalpain (n= 4), bleeding from drainages after surgery (n=
4), fever (n=2), gross haematuria (n=1), gross haematuria+fever (n= 1), vomiting (n=1), multiple septic infarcts (n =1), cholangitis (n= 1), chronic
anaemia (n=1), melaena (n= 1)
**
1 patient with a combination of symptoms: reduced general condition+melaena (n= 1)
SAA splenic arterial aneurysm, HAA hepatic arterial aneurysm, SMAA superior mesenteric artery aneurysm, CTRA coeliac trunk aneurysm, GDAA
gastroduodenal artery aneurysm, PDAA pancreaticoduodenal artery aneurysm, RAA renal artery aneurysm, GAA gastric artery aneurysm
2008 Eur Radiol (2015) 25:2004–2014
oesophagitis (n=2), colitis (n=1), chronic pancreatitis (n=1),
and chronic type B aortic dissection (n= 1). Four patients had
abdominal complaints due to unknown causes (n=4).
Discussion
The purpose of this study was to investigate the incidence,
aetiology and current management of VAA at our university
medical centre. The overall incidence of VAA was relatively
low, with a total of 233 patients presenting with 253 VAAs over
a 10-year period. The most frequent aetiology was degenerative/
atherosclerotic, which accounted for more than two-thirds of all
cases. The second most frequent aetiology was complications
after preceding medical procedures, with a 9.1 % rate of iatro-
genic false aneurysms. Vasculitis and diverse specific connective
tissue disease were uncommon causes of VAA [11–19].
The prevalence of VAA is reported to be 0.1–2%[20,21];
however, the number of undetected VAAs may be much
higher. The clinical presentation is nonspecific in most cases,
Fig. 1 Incidence and localization
of true, false and indeterminable
aneurysms. SA splenic arterial
aneurysm, HA hepatic arterial
aneurysm, SMA superior
mesenteric artery aneurysm, CT
coeliac trunk aneurysm, GDA
gastroduodenal artery aneurysm,
PDA pancreaticoduodenal artery
aneurysm, RA renal artery
aneurysm, GA gastric artery
aneurysm
Tabl e 4 Transverse diameter of ruptured and non-ruptured visceral artery aneurysms (VAAs)
All VAAs (n = 253 in 233
patients)
True VAAs (n=196 in 186
patients)
False VAAs (n =38 in 36
patients)
Indeterminable VAAs (n= 19 in 11
patients)
n (%) Size (mm) n (%) Size (mm) n (%) Size (mm) n (%) Size (mm)
All 253 (100) 16.1±9.8
(4.0–111.9)
196 (100) 16.3± 10.3
(4.0–111.9)
38 (100) 15.6± 7.6
(6.4–33.2)
19 (100) 15.5± 7.0
(7.3–34.7)
Non-ruptured VAAs 196 (77.5) 16.3±10.0
(4.0–111.9)
190 (96.9) 16.4±10.4
(4.0–111.9)
9 (23.7) 16.3± 6.8
(8.8–27.3)
17 (89.5) 14.3±4.2
(7.3–20.5)
Ruptured VAAs 37 (22.5) 14.8±8.2
(6.0–34.7)
6 (3.1) 9.0± 2.0
(6.0-11.2)
29 (76.3) 15.4± 7.9
(6.4–33.2)
2 (10.5) 22.4± 17.5
(10.0–34.7)
Eur Radiol (2015) 25:2004–2014 2009
and the diagnosis of VAA is often an incidental finding. It is
the general consensus that symptomatic VAA should be treat-
ed immediately, since rupture is associated with a high mor-
tality rate [9,22,23]. A wide range of rupture rates have been
reported [20–22,24,25], and emergency treatment ofruptured
VAA has mortality rates of up to 30 % [26,27]. In our patients,
VAA rupture resulted in intraperitoneal, retroperitoneal and
gastrointestinal bleeding, as well as bleeding into adjacent
organs. A striking number of VAA ruptures occurred after
medical procedures. In our study, the 30-day mortality rate
was comparably low in these cases; however, there was a
considerable complication rate after interventional treatment
and open surgery (12.5 % and 18.2 %, respectively).
The decision to treat or not to treat asymptomatic VAA
poses a challenge in elective cases [24,27–30], and the treat-
ment modality used varies based on location, clinical symp-
toms and co-morbidities [24,28]. There are no evidence-
based data to rely on, and individual treatment decisions are
based on clinicians’experience and the technical facilities of
the interventional radiologist or surgeon. According to the
guidelines, treatment is suggested for VAA with diameters
>2 cm or if the VAA is three times greater in diameter than
the respective normal artery [9,24,29]. However, we did not
find any difference in mean diameters between ruptured and
non-ruptured aneurysms. Therefore, VAA diameter alone ap-
pears to be an inadequate criterion for decision making [24,
31,32]. At our institution, treatment decisions for individual
cases are based on an interdisciplinary discussion including
the aetiology of the aneurysms and all clinical aspects of the
particular case. To determine other possible risk factors, we
tried to identify additional criteria. In our series,
pseudoaneurysms presented with a significantly increased risk
for rupture, with 76.3 % of pseudoaneurysms being ruptured.
By comparison, true VAA presented with a rupture rate of
3.1 %. Whether beta blockers have a preventive effect is still
amatterofdebate[24,31]. Aneurysm calcification indicates a
longstanding and therefore probably more stable aneurysm. In
our series, 27.3 % of non-ruptured VAAs presented with some
calcification, whereas none of the ruptured cases did. Parietal
thrombosis was not associated with rupture risk in our series.
Patients with ruptured VAAs were slightly less likely to be
taking beta blockers compared to those with non-ruptured
VAAs (35.1 % vs. 37.5 %, respectively). Steroid usage was
slightly higher in the group of patients with ruptured VAAs.
The distribution of VAAs in our study was mostly in con-
cordance with the literature. SAAs are reported to be the most
frequent VAA; they account for up to 60 % of all VAAs [5,6].
Bedford et al. [6] discovered 10.4 % SAAs in a routine post-
mortem study of 250 bodies. Our data confirm that SAAs
occurred with the highest frequency; SAAs accounted for
32.8 % of all VAAs, with a female:male ratio of 1.2:1.
Common risk factors for SAA are female gender, pregnancy
and portal hypertension [21,28]. None of our patients were
pregnant, and only one was of reproductive age. Recent re-
ports have suggested an increasing incidence of HAA, which
can be attributed to the more-frequent use of CT imaging after
blunt liver trauma and hepatobiliary intervention [22,33,34].
A total of 17.5 % HAAs had a history of
pancreaticoduodenectomy or biliary tract intervention. With
respect to superior mesenteric artery aneurysm (SMAA) and
aneurysms involving smaller branches of the coeliac trunk
(gastric, pancreaticoduodenal and gastroduodenal arteries),
our data are similar to that of other reports, with a 6.7 %
prevalence of SMAAs ([5,35] and 7.1 % prevalence for an-
eurysms in branches of the coeliac axis [20]. Coeliac trunk
aneurysms (CTRA) have been reported to be associated with
abdominal aortic aneurysms [24], which is consistent with our
data. In contrast to recent reports, we noted a strong predom-
inance of men (95.7 %) in these cases [29]. Also in contrast to
the literature, our analysis detected 18.6 % CTRAs; however,
most of these were characterized as degenerative lesions or
poststenotic dilatation of the coeliac trunk. Only one CTRA
was indicated for treatment. Stenosis is an often-described risk
factor for the development of VAA of the coeliac trunk arteries
Fig. 2 Treatment allocation
2010 Eur Radiol (2015) 25:2004–2014
Tab l e 5 Management of visceral artery aneurysms (VAAs)
Management All Non-ruptured VAAs Ruptured VAAs
nVAA
(n pat)
Complications Re-bleeding Mortality at
30 days
Mortality at
51.0± 21.1
months
nVAA
(n pat)
Complications Re-bleeding Mortality
at 30 days
Mortality at
51.0± 21.1
months
nVAA
(n pat)
Complications Re-bleeding Mortality at
30 days
Mortality
a 51.0± 21.1
months
Intervention 45 (40) 5 5 2 11 13 (10) 1 32 (30) 4 5 2 11
Coil embolization 27 (26) 3 4 1 8 6 (5) 1 21 (21) 2 4 1 8
Glue embolization 4 (3) 1 (1) 3 (2)
Covered stent 5 (5) 1 1 3 1 (1) 4 (4) 1 1 3
Combined methods 9 (6) 1 1 5 (3) 4 (3) 1 1
Surgery 14(11) 2 2 4 10(7) 1 1 3 4(4) 1 1 1
Venous bypass 3 (3) 1 1 3 (3) 1 1
Resection+ ligation 7 (4) 1 1 4 (1) 3 (3) 1 1
Nephrectomy 1 (1) 1 1 (1) 1
Splenectomy 1 (1) 1 1 (1) 1
Liver transplantation 2 (2) 2 2 ( 2) 2
Conservative 194 (182) 12 52 193 (181) 12 52 1 (1)
With follow-up 108 (104) 4 28 108 (104) 4 28
Without follow-up 86 (78) 8 24 85 (77) 8 24 1 (1)
*Nine complications in eight patients, **one patient with two complications (secondary bleeding and myocardial infarction)
Eur Radiol (2015) 25:2004–2014 2011
and SMA [4,23,29,36–39], which is supported by our data.
RAAs also were included in our analysis; the incidence of
RAAs in our study was higher than that reported in the liter-
ature [21]. RAAs seem to be associated with fibromuscular
dysplasia and medial degeneration. Hypertension is reported
to be another risk factor for RAA [8,24,40] and was evident
in 63.6 % of our patients.
The favoured interventional treatment modalities for VAA
include transcatheter embolization and stent grafting [24,41].
In our analysis, embolization was performed with either
pushable coils, detachable coils, glue embolic fluid, or combi-
nations thereof, at the discretion of the investigators. Onyx liq-
uid embolization had not yet been introduced for peripheral
indications at our institution at that time. The stent grafts used
were provided by various companies and were employed based
on the location of the VAA, the size required, and the personal
experience of the investigator. Flow diverter stents might have
served as an alternative in particular cases, but they had also not
yet been introduced at our institution. In contrast to open sur-
gery, interventional procedures are normally performed under
local anaesthesia, with high technical success rates [4,20,23,
34,41], low complication rates, and shorter hospital stays [31,
42]. Reported complications include technical failure to cathe-
terize the artery [43], arterial thrombosis or embolism resulting
in organ infarctions or abscesses, coil migration, aneurysm re-
currence, and a haematoma or a pseudoaneurysm at the arterial
puncture site [24,27,30,41,44]. Our data analysis yielded a
technical success rate of 93.3 % (42 of 45 aneurysms).
Technical failures included one case with migration of a cov-
ered stent in an RAA, which was treated with subsequent coil
embolization. In another case, coil embolization of a false RAA
resulted in an incomplete occlusion, which required
reintervention. In the third case, elective coil embolization of
an SAA presented some coil migration, with consequent is-
chaemia of the spleen and pancreas.
There was a complication rate for interventional treatment
of 13.3 % (four complications in 30 patients) in emergency
cases compared to 10 % (one complication in ten patients) in
elective cases. Rebleeding as a late procedural failure occurred
most frequently after coil embolization. There was no mortal-
ity in elective cases but a 30-day mortality of 6.7 % in emer-
gency cases after interventional treatment, with one case of
intracerebral bleeding and one patient with right heart failure
after rebleeding. This is very low in comparison to other series
published [4,5,34], only Balderi et al. [26]presenteda30-day
mortality comparable to ours. Our data are, however, not suit-
able to achieve a comparative outcome analysis after surgical
and interventional treatment. While most surgical patients re-
ceived an elective operation, the majority of emergency cases
were treated by means of interventional techniques. Moreover,
the number of surgical cases was too small to reliably draw
comparative data with respect to 30-day mortality or compli-
cation rates. The retrospective analysis of the practiced inter-
disciplinary decision making and the acceptable complication
rates as reported above give the impression that the interven-
tional treatment options are the treatment of choice both, in
emergencies as well as in elective cases.
In conclusion, diagnoses of VAA may have increased be-
cause of increasing numbers of cross-sectional imaging stud-
ies; the incidence of SAAs was highest. We also observed
significant numbers of aneurysms of the coeliac trunk arteries
and renal artery, which suggests that these VAAs may be cur-
rently underdiagnosed. The mean diameter of ruptured aneu-
rysms did not significantly differ from that of non-ruptured
aneurysms. Thus, treatment indications should not be based
primarily onthe aneurysm diameter, but in the first instance on
Tabl e 6 Complications of
interventional treatment
* One patient
n VAA (n pat) Complications Re-bleeding 30-d-mortality Re-intervention
Non-ruptured 13 (10) 1 (10 %)
Major splenic infarction 1
Ruptured 32 (30) 4 (13.3 %) 5* (16.7 %) 2 (6.7 %) 2 (6.7 %)
Intracerebral haemorrhage 1 1
Myocardial infarction 1*
Abscess 1
Splenic infarction 1
Tabl e 7 Complications of
surgical treatment n VAA (n pat) Complications Re-bleeding 30-d-mortality Re-intervention
Non-ruptured 10 (7) 1 (14.3 %) 1 (14.3 %)
Insufficient anastomosis 1
Ruptured 4 (4) 1 (25 %) 1 (25 %)
Splenic abscess 1
2012 Eur Radiol (2015) 25:2004–2014
the aneurysm aetiology. Pseudoaneurysms need emergency
treatment. The vast majority of true aneurysms can probably
be managed conservatively; however, there might be some
potential for fatality due to secondary aneurysm rupture.
Acknowledgments This work contains data from the doctoral thesis of
Ms. Evelyn Dappa. The scientific guarantor of this publication is
M.B.Pitton. The authors of this manuscript declare no relationships with
any companies, whose products or services may be related to the subject
matter of the article. The authors state that this work has not received any
funding. No complex statistical methods were necessary for this paper.
Institutional Review Board approval was not required because of the
retrospective and observational nature of the analysis. Written informed
consent was not required for this study because this is a retrospective and
observational analysis. Nostudy subjects or cohorts have been previously
reported. Methodology: retrospective, observational, performed at one
institution.
Open Access This article is distributed under the terms of the Creative
Commons Attribution Noncommercial License which permits any non-
commercial use, distribution, and reproduction in any medium, provided
the original author(s) and the source are credited.
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