Radiol med (2015) 120:50–72

DOI 10.1007/s11547-014-0459-z

EMERGENCY RADIOLOGY

MDCT distinguishing features of focal aortic projections (FAP)

in acute clinical settings
Tullio Valente · Giovanni Rossi · Francesco Lassandro ·
Gaetano Rea · Maurizio Marino · Salvatore Urciuolo ·
Giovanni Tortora · Maurizio Muto 

Received: 27 May 2014 / Accepted: 14 August 2014 / Published online: 24 September 2014
© Italian Society of Medical Radiology 2014

Abstract  Focal aortic projections (FAP) are protrusion Keywords  Aorta · MDCT · Diagnosis · Intimal tears ·
images of the contrast medium (focal contour irregular- Ulcer-like lesion
ity, breaks in the intimal contour, outward lumen bulging
or localized blood-filled outpouching) projecting beyond Abbreviations
the aortic lumen in the aortic wall and are commonly seen FAP Focal aortic projections
on multidetector computed tomography (MDCT) scans of TEVAR Thoracic endovascular aortic repair
the chest and abdomen. FAP include several common and EVAR Endovascular aortic repair
uncommon etiologies, which can be demonstrated both in CM Contrast medium
the native aorta, mainly in acute aortic syndromes, and in MPR Multiplanar reconstruction
the post-surgical aorta or after endovascular therapy. They MIP Maximum intensity projection
are also found in some types of post-traumatic injuries VR Volume rendering
and in impending rupture of the aneurysms. The expand- AD Aortic dissection
ing, routine use of millimetric or submillimetric collima- AAS Acute aortic syndrome
tion of current state-of-the-art MDCT scanners (16 rows IMH Intramural hematoma
and higher) all the time allows the identification and char- PAU Penetrating atherosclerotic ulcer
acterization of these small ulcer-like lesions or irregulari- ULPs Ulcer-like projections
ties in the entire aorta, as either an incidental or expected IBP Intramural blood pool
finding, and provides detailed three-dimensional pictures BAP Branch arteries pseudoaneurysm
of these pathologic findings. In this pictorial review, we AA Aortic aneurysm
illustrate the possible significance of FAP and the discrimi- ILT Intraluminal thrombus
nating MDCT features that help to distinguish among dif- PSA Pseudoaneurysm
ferent types of aortic protrusions and their possible evolu- MAI Minimal aortic injury
tion. Awareness of some related and distinctive radiologic BAI Blunt aortic injury
features in FAP may improve our understanding of aortic CPB Cardiopulmonary bypass
diseases, provide further insight into the pathophysiology PTFE Polytetrafluoroethylene
and natural history, and guide the appropriate management EL Endoleak
of these lesions.

Introduction

T. Valente (*) · G. Rossi · F. Lassandro · G. Rea · M. Marino · Knowledge about aortic diseases has grown consider-
S. Urciuolo · G. Tortora · M. Muto  ably and continues to evolve with ongoing research into
Section of General Radiology, Department of Diagnostic
pathophysiology, technological advances in detection, and
Imaging, Azienda Ospedali dei Colli, P.O. Monaldi,
80131 Naples, Italy improved therapeutic options [1]. Focal aortic projections
e-mail: tullio.valente@gmail.com (FAP) are protrusion images of the contrast medium (focal

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Radiol med (2015) 120:50–72 51

contour irregularity, breaks in the intimal contour, outward
lumen bulging or localized blood-filled pouch) projecting
beyond the aortic lumen in the aortic wall and are commonly
seen on multidetector computed tomography (MDCT) scans
of the chest and abdomen. They include several common
and uncommon etiologies, which can be demonstrated both
in the native aorta, mainly in acute aortic syndromes, and
in the post-surgical aorta or after endovascular therapy (tho-
racic endovascular aortic repair, TEVAR/EVAR). They are
also found in some types of post-traumatic injuries and in
impending rupture of aneurysms (Table 1). Multiple advan-
tages, including ready availability, rapid examination times,
Table 1  Main etiologies of focal aortic projections (FAP)
Native aorta
 IMH-related FAP
  Tiny ulcers acute IMH-associated (at initial imaging)
  New ulcer-like projections (ULPs)
  PAU (PAU-associated IMH)
  Intramural blood pool (IBP) or branch arteries pseudoaneurysm
(PSA)
 IMH non-related FAP
  AD variant FAP: limited intimal tear (Svensonn’s class III)
  AA FAP: fissured thrombus in unstable aneurysm
  Saccular and mycotic aneurysm
  Aortic trauma FAP
Post-surgical aorta related-FAP
  Infected, dehiscence and traumatic PSA
Post-endovascular aortic repair (TEVAR/EVAR)procedures related-
FAP
  Endoleaks type I/III
Mimics
IMH acute intramural hematoma, PAU penetrating atherosclerotic
ulcer, AD aortic dissection, AA aortic aneurysm
isotropic spatial resolution and full anatomic evaluation
of the thoracoabdominal aorta and branch vessels, make
MDCT the preferred imaging modality for the diagnostic
evaluation of FAP in acute clinical settings.
MDCT technique
Current MDCT equipped with state-of-the-art tube and
detector technology and optimal temporal and spatial res-
olution have become widely available. It can provide iso-
volumetric, three-dimensional information without loss of
spatial resolution, during a single breath-hold. The MDCT
protocol should include triphasic CT angiography: unen-
hanced, early and delayed post-contrast medium (CM)
scans [2, 3]. No oral contrast agent should be administrated
unless gas is identified in the endovascular or perivascu-
lar soft tissue or if bronchial/esophageal-vascular fistula
is suspected. The images, acquired from software-assisted
centerline reconstructions, can be used either to gener-
ate reliable and reproducible measurements or to carefully
assess changes in luminal diameter and contours. A con-
trast-enhanced thoracic acquisition should be obtained with
retrospective electrocardiographic (ECG)-gating (Table 2)
when feasible and in cases of suspected complications
involving the aortic valve or aortic sinus, valve plane, aor-
tic root and proximal ascending aorta. The higher temporal
resolution of ECG-gated MDCT angiography dramatically
improves the detectability of some typical findings such as
the primary intimal tear in thrombosed aortic dissection
(AD) or ulcerative plaque in penetrating atherosclerotic
ulcer (PAU) [2, 3]. Since ECG gating is associated with
significant increase in radiation dose, various dose reduc-
tion techniques may be used such as prospective ECG trig-
gering, ECG-based tube-current modulation, automatic

Table 2  Contrast-enhanced CE spiral CT CE ECG-gated CT

(CE) multidetector computed
tomography (CT) acquisition Section thickness (mm) 0.5–0.625 0.5–0.625
parameters (64-section MDCT)
Increment (mm) 0.4 0.4
Tube potential (kV) 100–120 100–120
Collimation 64 × 0.5–0.625 64 × 05–0.625
Pitch About 1 BPM dependent
Rotation time (s) 0.5 Minimum
Field of view (mm) 210–260 210–260
Matrix 512 × 512 512 × 512
Non-ionic CMa 50–120 (plus saline chaser) 50–120 ml (plus saline chaser)
Polyphasic injection protocol Yes Yes
Injection rate (ml/s) 3–6 (18–20G preferably 3–6 (18–20G preferably
in right arm) in right arm)
a
 High-concentration Region of interest (ROI) Distal AA/Arch (bolus triggering) Distal AA/Arch (bolus triggering)
(≥350 mgI/ml) contrast
Study plan Lung apices to the groin Lung apices to diaphragm
material (CM)

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52
Fig. 1  The multidetector computed tomography (MDCT) report
of a focal aortic projection (FAP) always includes its measurements
(depth, width and height), its location on the aorta and maximal
diameter of the aortic lumen at the site of the FAP. Diagrams show
FAP measurements on (a) axial and (b) orthogonal images: depth
(a, blue arrow), height (b, green arrow), and width (c, black line);
exposure control, lower peak kilovoltage (kVp), and itera-
tive reconstruction algorithms. Various postprocessing
techniques such as multiplanar reformation (MPR), maxi-
mum intensity projection (MIP), and volume rendering
(VR), help to facilitate understanding of complex aortic
pathology and to expedite communication with the sur-
geons and the attending physicians. The MDCT report of a
FAP always includes its whole measurement (depth, width
and height), its location on the aorta and the maximal diam-
eter of the aortic lumen at the site (Fig. 1).
Native aorta
FAP in acute aortic syndrome
Acute aortic syndrome (AAS) is a modern term to describe
a spectrum of acute, life-threatening interrelated emer-
gency aortic conditions with similar clinical characteristics
and challenges, which share a common set of signs and
symptoms, the most important of which is aortic (abrupt,
severe, sharp chest or back or abdominal) pain. These con-
ditions include AD, intramural hematoma (IMH), and PAU
as well as traumatic aortic rupture and impending rupture.
The common pathological denominator of AAS is mainly
disruption of the media layer of the aorta with bleeding
(IMH), along the aortic media resulting in separation of the
wall layers (dissection), or transmurally through the wall
in the case of ruptured PAU or trauma [4, 5]. At the initial
diagnosis, 30 % of AAS are still missed, with the conse-
quence that the initial outcome is strongly affected [1–4].
Among the AAS, IMH is characterized by a higher inci-
dence of FAP at initial diagnosis with MDCT or along its
course.
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Radiol med (2015) 120:50–72
a, b and c correspond to the biometry of the focal aortic projection.
Contrast-enhanced MDCT (c) axial and (d) sagittal maximum inten-
sity prjection (MIP) reconstructions show an example of FAP meas-
urements (proximal descending aorta fissured thrombus in unstable
aneurysm). The lines correspond to the FAP measurements
Acute IMH
Acute IMH is classically defined as a localized separa-
tion of the aortic wall layers, with partially or totally clot-
ted blood (hematoma) in the aortic wall. It is distinguished
from classic double-barrel AD by the absence at imaging
of any evident demonstrable intimal tear or intima-medial
flap (as an aortic dissection without an intimal tear). The
rupture of the vasa vasorum in the media is the presumable
reason why intramural hematoma occurs [1–8].
Intramural hematoma, commonly classified according to
the Stanford classification used for AD, has been found in
5–20 % of patients who present clinical signs suggestive of
AAS, and may, however, be asymptomatic [4–8]. Most IMH
(50–85 %) are located in the descending aorta and are typi-
cally associated with hypertension; patients with IMH lim-
ited to the arch or the descending aorta (type B IMH) and
who are without complications on admission, present the
greatest challenge. IMH may not be a homogeneous con-
dition but rather a heterogeneous array of pathologies with
various potentialities [9]. The etiology of IMH remains con-
troversial, but four major different pathophysiological pro-
cesses can lead to intramural hematoma formation [10]:
(a) In patients with mild or no atherosclerosis, spontane-
ous rupture of the vasa vasorum may initiate aortic
wall degeneration, which leads to hematoma formation
in the aortic wall, splitting of the medial layer, with
no blood flow within the media (not PAU-associated
IMH). Cases of IMH observed without an intimal tear
at autopsy or during surgery support this theory;
(b) IMH may be an AD with intimal defect and early
closed and thrombosed false lumen without re-entry
tear. This type was defined as ‘thrombosed-type acute
Radiol med (2015) 120:50–72 53
aortic dissection’, such as in an otherwise classic AD
with an entry tear without flow in the false lumen
(early thrombosed false lumen-type acute AD or dis-
section variant IMH or IMH with intimal tear) [11–13].
Some recent reports suggest that most IMH result from
an entry tear similar to classic AD [10–12];
(c) Bleeding associated with an atherosclerotic ulcer that
penetrates into the internal elastic lamina and allows
hematoma formation within the media of the aortic
wall, a penetrating atheromatous ulcer or PAU (PAU-
associated IMH) [13];
(d) More rarely, IMH can occur secondary to blunt or
iatrogenic traumatic aortic injury, to incomplete wall
involvement (trauma-induced IMH).
Nonetheless, at imaging a definitive distinction cannot
be made between PAU-associated IMH and re-entry sites of
IMH, because of the lack of radiological-pathological cor-
relation studies. Pure IMH, originating from ruptured vasa
vasorum in medial wall layers, is otherwise considered a
precursor of dissection, resulting in an aortic wall infarct.
This may provoke a secondary tear, causing a classic overt
AD (in 28–47 % of patients).
The natural IMH evolution, described in the literature,
includes various remodeling patterns: (1) spontaneous
healing (10–40 % of cases); (2) saccular aneurysm forma-
tion (ulcer-like projections, ULPs); (3) fusiform aneurysm
Fig. 2  Main MDCT findings of aortic acute intramural hematoma
(IMH). A 67-year-old man presented with sudden onset of substernal
chest pain and dyspnea. a Unenhanced MDCT axial scan shows inti-
mal calcifications in a curvilinear configuration (black arrow) and a
formation; (4) progression to classic open acute dissection
(16–47 %); (5) rebleeding; (6) proximal or distal IMH aor-
tic progression; (7) aortic rupture (in 20–45 %) [1–15].
This variable natural history and remodeling processes,
even during the chronic phase, indicate that IMH is a more
vulnerable or dynamic condition than classic AD, suggest-
ing the absolute need for close imaging surveillance to
avoid progressive dilatation and rupture, especially within
the first 30–60 days [5].
In addition, increased permeability of the aortic wall
may lead to pericardial or pleural effusions or a mediastinal
hemorrhage. Most effusions will resolve, however, large
and progressive fluid accumulations are an ominous sign.
At the initial MDCT performed in the acute phase, a diag-
nosis of acute IMH (not PAU-associated) is made accord-
ing to the following main (a–c) and ancillary (d–e) criteria
[4–7, 13–22] (Fig. 2):
(a) The “crescent-sign” is the hallmark of IMH: a subinti-
mal crescent-shaped (or rarely ring-shaped) thickening
(>5–7 mm) of the wall of the aorta that shows higher
attenuation values (60 ± 15 HU) than those of the aor-
tic lumen on the unenhanced CT image (using a narrow
window; e.g., width 200–300 HU; level 25–35 HU);
(b) Having no contrast enhancement in the intramural
hyperdense area on the MDCT image obtained after
CM enhancement;
crescentic hyperattenuating intramural fluid collection (white arrow).
b Contrast-enhanced MDCT axial scan depicts a smooth, non-
enhancing, crescentic region of aortic wall thickening (black arrow)
without a spiraling intimal flap
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Fig. 3  Ancillary MDCT findings of aortic acute IMH. A 63-year-old
man presented with sudden onset of substernal chest pain and dysp-
nea. a, b Contrast-enhanced MDCT axial later scans show enhance-
(c) Longitudinal extension over a greater distance, having
smooth lumen-wall interface, with possible visualiza-
tion of the dislocation of subintimal semicircular or
curvilinear calcifications;
(d) Having no intimal flap, no overt false lumen, no ulcer-
like projections (ULP), or no penetrating atheroscle-
rotic ulcer at initial MDCT. In the acute phase, how-
ever, there may be small ulcers associated with IMH;
(e) In our experience, intense enhancement of the aortic
wall external to the hematoma and of the surrounding
mediastinal fat, can be seen mainly in the later post-
contrast phase; it may reflect adventitial inflammation
or vasa vasorum congestion or their greater density
(Fig. 3).
It has been argued that reliable MDCT findings for dis-
tinguishing a closed and thrombosed false lumen of dissec-
tion from acute IMH are:
–– The wall thickness of IMH is usually less than a quarter
of the aortic diameter, rarely less than one-half, while
most thrombosed false lumens extend over one-quarter
to one-half of the aortic diameter;
–– A mural hematoma involving the entire aortic circum-
ference is an uncommon IMH finding but it is a reliable
sign for distinguishing it from AD thrombosed false
lumen;
–– The spiral shape of thrombosed false lumens in AD is a
common feature, described as a change in the appear-
ance of the true and false lumens on serial transverse
MDCT sections of the aorta, but not present in IMH,
which maintains a constant circumferential relationship
with the aortic wall [14].
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Radiol med (2015) 120:50–72
ment of the aortic wall external to the type B IMH due to adventitial
inflammation (arrows)
In IMH it is important to report:
–– The absolute maximal axial thickness of the hema-
toma (>11–16 mm identifies patients at increased risk,
while <10–11 mm predicts a lower risk of complica-
tions within 30 days and a greater chance of IMH reso-
lution),
–– The thickness ratio in relation to aortic diameter (less
than a quarter, one-quarter to one-half, and more than
one-half),
–– Transverse extension of the lesion, defined according to
the extent to which the lesion involved the circumfer-
ence in a cross-section of aorta (one-quarter, one-half,
or three-quarters of the circumference),
–– The minimum and maximum transverse diameters of
the aortic lumen, at the level of the hematoma to stratify
the risk of progression (Table 3) [7, 14].
The mortality from proximal IMH is higher than that
of distal IMH (34–55 versus 14–19 %) and most deaths
tend to occur within the first 24–72 h after hospital admis-
sion. The importance of initial maximal aortic diameter in
the prediction of outcomes has also been documented in
patients with proximal and distal IMH and classic AD. This
suggests the clinical importance of abnormal aortic dis-
tensibility or wall stress, associated with initial aorta size.
Predictors of early mortality or adverse outcome include an
initial maximal aortic diameter (cutoff value of 40 mm or
greater) in patients with distal IMH, an IMH thickness of
greater than 11 mm and ascending aortic involvement [5,
6, 8].
Unlike Stanford type A aortic dissection (for which sur-
gical management is standard), controversy remains in the
 Table 3  MDCT distinguishing features in diagnosis/management of main focal aortic projections
FAP MDCT distinguishing Management Prognosis Main therapeutic Alternative therapeutic Alternative Alternative Poor prognostic
features option option therapeutic option therapeutic option factors

New ulcer-like A new developed local- Close imaging Poor Optimal treatment Surgical management if Located in the ascending
projections (ULPs) ized outpouching of follow-up for type A IMH is poor prognostic factors aorta and arch cutoffs
in IMH CM with a >3 mm not well estab- for ULPs diameter
neck with aortic lumen lished (10–20 mm) and depth
as intimal tears (5–10 mm)
Penetrating ather- Focal mushroom-like Close imaging Poor Early surgical or Endovascular repair if In the absence of Width >2 cm and
Radiol med (2015) 120:50–72

omatous ulcer outpouching com- follow-up endovascular high risk patients with complications is depth >1 cm PAUs in
(PAU) municating with aortic especially repair if poor prog- comorbidities usually medically the ascending or arch
lumen on the initial within the first nostic factors managed
scan; extensive plaque 30 days
elsewhere
Branch arteries Pooling of CM isodense Imaging follow- Usually In asymptomatic If symptoms and isolated If enlarging BAP
pseudoaneurysm with the aortic lumen up good patient, needs no enlarging BAP, emboli- and associ-
(BAP) in IMH, along the specific treatment zation ated ULP,
aorta circumfer- (medically man- TEVAR/EVAR if
ence, ± branch artery aged) B-IMH
communication
Limited intimal tear Eccentric one-sided Close imaging Poor Similar to that for
(Class III) bulge of aortic contour follow-up classic AD
Aneurysm fissured Crescent sign and CM in Fast indication Poor, Early surgery/early Missing calcium sign
intraluminal intraluminal thrombus for aggressive sign of endovascular Draped hung aorta
thrombus therapy imminent procedure Focal pointing
rupture Periaortic fat stranding
Saccular and A focal, contrast- Close imaging If small and asymp- If enlarging and Large aneurysmal size
mycotic aneurysm enhancing dilatation, follow-up con- tomatic medical symptomatic open enlarging on follow-up
usually saccular, sult previous therapy surgery/endovascular
narrow mouth, acute studies therapy
margins and ancillary
findings
Post- injury FAP If MAI abnormality Assess aortic Grade Grade I and II Grade III/IV Typically at ligamentum
and deformity of the branches, I/II/III injuries in open/endovascular repair arteriosum, others post-
internal contour of the close imaging good hemodynamic ally traumatic findings
aorta wall projecting follow-up Grade IV stable patients with
into the lumen poor anti-impulse
Post-surgical Anastomotic PSA or Fast indication Poor Therapy early re- Periprosthetic hematoma
infected, iv CM leak at graft for aggressive surgery >15 mm at the first
dehiscence and anastomosis therapy post-operative MDCT
traumatic PSA gas within or adjacent
to the graft after
6–12 weeks

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56 Radiol med (2015) 120:50–72

initial medical or surgical management of Stanford type

A IMH. As with type B AD, type B IMH are often man-
aged conservatively, with aggressive antihypertensive ther-
Poor prognostic

apy. These patients should be closely followed up during

the first 30 days. Surgical or endovascular treatment may
factors

be employed in case of complications such as progression,

luminal dilatation, penetrating ulcer, enlarging of the IMH,
or overt dissection.
therapeutic option
Alternative

Tiny IMH‑associated ulcers

In order to avoid confusion and misunderstanding, it is

possible to use the term ‘dissection variant IMH’ for a
therapeutic option

thrombosed AD that has no complete flow channel. Tiny

communications (opening neck <3 mm) between the true
Alternative

and false lumen in the descending thoracic aorta and tiny

or small ulcers associated with IMH in the acute phase at
initial imaging may commonly exist, and clearly show dif-
with a stent graft exten-

ferentiation from other aortic diseases with hemorrhagic

By angioplasty balloons,
Alternative therapeutic

By covering the defect

stents, or stent-graft

content within the aortic wall [15]. These small IMH-

associated ulcers may be defined as a focal, localized, and
subtle continuity disruption of the inner layer of the throm-
extensions

bosed false lumen (Fig. 4). The causes of these tiny ulcers

option

sion

remain uncertain. It has been postulated that they represent

the site of an intimal tear or erosion in a thrombosed open
aortic dissection [22, 23], the site of occlusion or detach-
High-pressure leaks

High-pressure leaks
Main therapeutic

ment of the orifice of aortic branches, a prior atheroma-

require urgent

require urgent
management

management

tous ulcer, or small areas of intimal rupture after intramu-

ral hematoma [21]. Their etiology remains uncertain since
option

pathologic specimens are not analyzed in most cases [15].

Those, like ulcer-like projections (ULPs), may represent an
epiphenomenon that is either a consequence or the cause of
Prognosis

the complex paradigm of IMH. Both require close imaging

follow-up (Fig. 5).
Imaging follow-

Imaging follow-
Management

New ulcer‑like projections (ULPs)

up

up

Deep ulceration of atherosclerotic aortic plaques can lead

to IMH, aortic dissection, or perforation. Non-invasive
graft into the aneurysm
alongside the proximal

graft while sparing the

or terminal ends stent-

MC non-tubular central
ing increased density
Focal region of enlarg-

manifests around the

imaging has further elucidated this disease process that

MDCT distinguishing

collection usually

often further complicates IMH and appears as an ulcer-like

sac periphery

projection (ULP) into the hematoma. ULPs include:

features

1. New ulcer-like projections (ULPs) as re-entry sites of

sac

the IMH or a (primary?) intimal defect/tear that exists

already at the onset of IMH [7];
Table 3  continued

Post TEVAR/EVAR

Post TEVAR/EVAR

2. Penetrating atheromatous ulcers (PAU).

Type III EL
Type I EL

Newly developed ULPs, also referred to as IMH re-

entry sites from the decompression of IMH, are new inti-
FAP

mal tears or disruptions, secondary to hematoma expansion

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Radiol med (2015) 120:50–72 57
or re-opening (primary or re-entry tears) intimal defects,
ulcers developing during the evolution of IMH and appear-
ing on IMH imaging follow-up. They usually occur at
points of greater mechanical stress [15–20], which are
not associated with atherosclerotic disease, but often with
recurrent back pain.
At MDCT, ULPs morphologically appear as localized,
well-defined, blood-filled pouches or localized CM-filled
projections protruding from the aortic lumen into the IMH
or from the true lumen into the closed and thrombosed false
lumen (Fig. 6). Therefore, these lesions (not observed at
the site of the IMH on cross-sectional images at the time of
initial diagnosis) are a possible indicator of the formation
of a flow channel between the true and thrombosed false
lumen. Hence they evolve into classic AD or aneurysmal
dilatation, with progression, occurring more commonly in
proximal rather than in distal IMH. On MDCT, they gener-
ally are defined as [9, 16–23]:
(a) A localized outpouching of CM, isodense with the aor-
tic lumen with a clear and evident communication with
aortic lumen with usually wide opening (>3 mm) or
wide-mouth communication; they do not communicate
with aortic branch arteries;
(b) The focal intima usually shows no atherosclerotic
plaque, which is frequently noted in a PAU;
(c) They are usually not noted at initial MDCT. They can
develop within the lesion in about one-third of patients
commonly within 1–4 months, but the complication
can be delayed;
(d) Location: descending aorta > ascending aorta > arch;
Fig. 4  FAP due to tiny ulcer. Type B IMH tiny ulcers with unfa-
vorable evolution in a 57-year-old man with hypertension peak who
presented with unstable thoracoabdominal pain. a Initial contrast-
enhanced MDCT axial MIP reconstruction shows a type B IMH
with 17 mm of maximal axial thickness and a subtle irregularity of
the intima, a slight intimal erosion or tiny ulcer (white arrow), in
proximal descending aorta. b Coronal oblique volume rendering
(e) Representing a site of new intimal disruption, portends
a poor prognosis and unfavorable outcome (a signifi-
cant risk factor for evolution to an overdissection, rup-
ture or, often saccular aneurysmal dilation).
Development of an ULP appears to be associated with a
higher incidence of disease progression under medical ther-
apy, whereas the absence of ULP may suggest a stable dis-
ease course in patients with AD with complete thrombosed
false lumen [7, 15, 16, 22]. The most frequent adverse
sequel of ULP is saccular or less often fusiform aneurysm
development, also at a later phase (4–8 months after the ini-
tial episode) [7, 21]. A newly developed ULP, during the
follow-up period has a much higher risk than a ULP seen
on the initial CT scan for the development of aortic aneu-
rysm [22]. In the literature, these ULPs appearing in the
evolution of IMH, are also termed localized dissection, aor-
tic outpouching or protrusion, pseudoaneurysm or saccular
aneurysm, therefore increasing confusion related to this
entity [15, 24].
Acute penetrating atheromatous ulcer (PAU)
In PAU of the aorta, an atherosclerotic plaque ulcerates and
disrupts the internal elastic lamina, and is therefore a mani-
festation of a diseased intima and not media, as in classic
AD or IMH. When this occurs, the media is exposed to pul-
satile blood flow. This causes bleeding into the wall lead-
ing to intra-medial hematoma. Its true incidence is difficult
to determine, but is estimated to vary between 2 and 8 %
(VR) reconstruction confirms tiny ulcer (white arrow). Although
this patient was managed with aggressive medical therapy, c 7-day
follow-up MDCT sagittal MIP reconstruction shows disease progres-
sion: a clear FAP due to intimal tear has replaced the intimal erosion
visible on the initial MDCT (arrow); the patient was treated by tho-
racic endovascular aortic repair (TEVAR)
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Fig. 5  FAP due to tiny ulcer. Type B IMH tiny ulcer with unfa-
vorable evolution during follow-up (ulcer-like projection, ULP, and
overt intimal tear). Initial (a) unenhanced and (b) contrast-enhanced
MDCT axial scans of type B IMH with intimal erosion (tiny ulcer) of
the descending aorta (white arrow). 4-day follow-up (c) unenhanced
Fig. 6  FAP due to new ULPs in the IMH follow-up in a 74-year-
old man with type B acute onset of intramural hematoma and chest/
back pain. a Initial unenhanced MDCT coronal MIP reconstruction,
b contrast-enhanced MDCT axial scan and c sagittal MIP reconstruc-
tion show a 16-mm diameter type B intramural hematoma (arrows).
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Radiol med (2015) 120:50–72
and (d) contrast-enhanced MDCT axial scans at the same level show
enlargement of the intimal defect and enhancing ulcer-like projection
with a wide neck (>3 mm) from the aortic lumen into the IMH (white
arrow), a finding suggestive of overt intimal tear
The patient received early aggressive medical therapy. d Contrast-
enhanced MDCT axial and e sagittal scans obtained 3 weeks after
acute initial event show a new ULP in the distal arch/proximal
descending aorta (arrows). This patient was finally treated by surgical
therapy
Radiol med (2015) 120:50–72 59
of all AAS [1–4, 25–28]. Clinically, the typical profile of a
patient with PAU is an elderly individual with multiple risk
factors for atherosclerosis and often already documented
manifestation of atherosclerotic disease, such as coronary
aortic disease, cardiovascular disease, and peripheral arte-
rial disease or abdominal aortic aneurysm [26–29].
The plaque may precipitate a localised intra-medial dis-
section associated with a variable amount of hematoma
within the aortic wall, which can spread into the adventitia,
forming a saccular aneurysm or pseudoaneurysm, or may
also cause transmural rupture. In rare cases, PAU may lead
to aortic dissection, but dissections arising from a PAU tend
to be less extensive and demonstrate a thick, calcified static
flap in a location atypical for entrance tears. A PAU begins
as an atherosclerotic intimal ulcer (stage I), subsequently
evolving into an intimal tear (stage II), followed by hemor-
rhage into the media (stage III), and finally resulting in a
full thickness penetration of the aortic wall (stage IV) [25].
Most often, MDCT of PAU reveals a small focal con-
trast-enhanced outpouching of the intima with an adjacent
sub-intimal hematoma due to intimal fracture of an athero-
sclerotic plaque or a deep ulcerated lesion that may be sin-
gle or multiple, usually (over 90 %) involving the middle to
distal third of the descending thoracic aorta or the abdomi-
nal aorta (Fig. 7) [13, 26–28]. On unenhanced scans, PAU
may be accompanied by localized IMH, a finding that helps
to distinguish an active PAU as the cause for AAS and to
differentiate it from chronic PAU or pseudoaneurysm
(Fig. 8).
In patients who have prominent atherosclerotic dis-
ease, tiny ulcerated lesions a few millimeters in size are
observed occasionally, also in the acute clinical setting.
Often, these lesions are asymptomatic and accompanied by
atheromatous plaques and intimal calcifications, typically
recognized as an irregularity along the luminal surface of
the aortic wall in contrast-enhanced CT images. They are
irrespective of IMH extent and represent intimal atheroma-
tous plaque ulcerations, confined within the intima, and
overlying the expected aortic contour and calcified intima
(chronic atheromatous aortic ulcers) (Fig. 9). They are eas-
ily distinguished from the typical appearance of a deeper
PAU extended outwardly and beyond the calcified intima.
However, when mural thrombus becomes calcified, differ-
entiation of PAU from the more superficial atheromatous
ulcer can be a diagnostic challenge. A PAU typically is [1,
9, 26–28]:
(a) An exuberant, irregular plaque (focal mushroom-like
or crater-like or collar button contrast-enhanced out-
pouching of the aortic lumen with overhanging jagged
edges) extended outwardly beyond the calcified intima
and communicating with the aortic lumen, usually
noted on the initial scan;
(b) IMH with the crescent sign and displaced intimal calci-
fications accompanies the penetrating ulcer 80 % of the
time in the absence of a dissection flap or a false lumen
(PAU-associated IMH);
(c) Patients who develop PAU are generally older and have
an extensive advanced vascular atherosclerotic lesions
(thick and diffusely fibro-calcified aortic wall). They
are often associated in other sites, apart from the ulcer-
ation, which may be absent in IMH.
Most authors have also considered these entities, irre-
spective of their location, to have a poorer prognosis than
classic aortic dissection with a higher incidence of aortic
rupture [26–29]. Patients with a PAU (and associated IMH)
that initially measured 20 mm or more in maximum diame-
ter or 10 mm or greater in maximum depth have a high risk
of disease progression and thus should be considered can-
didates for early surgical or endovascular repair [28–30].
It is apparent that not only PAUs in the ascending aorta or
arch but also those in the proximal descending aorta had
a more malignant course, compared with that observed for
PAUs in the middle and distal descending aorta [29].
PAU involving the ascending aorta is rare; however, the
ulcer usually ruptures and is commonly lethal. Thus early-
urgent or emergent operative intervention is clearly recom-
mended in these elderly patients with comorbidities, endo-
vascular stent grafting is an attractive therapeutic modality
[16, 29].
Intramural blood pool (IBP) or branch artery
pseudoaneurysm (BAP)
Another FAP that can also be seen in association with IMH
is an IBP or BAP or focal contrast enhancement within the
IMH. Secondary to damage caused by IMH propagation
across the origin of the aortic branch (bronchial, intercos-
tal, intercostobronchial, pericardial, lumbar) artery that is
partially or completely torn, IBPs become a natural re-entry
site of the IMH, characteristically occurring at the location
of a aortic branch vessel take-off [7, 24, 30–37]. They are
blood-filled spaces without their own wall confined within
an IMH/otherwise thrombosed false lumen that communi-
cate with both the aortic true lumen and an adjacent branch
vessel [37–39]. As a result, blood flow proceeds from the
aortic true lumen, across the interrupted origin of the aor-
tic branch within the intramural blood collection and,
lastly, within the aortic branch itself (Fig. 10); conversely
ULP has overt and wide intimal disruption and no con-
nection with branch artery. IMH with intramural blood
pools at multiple levels has been described as the “Chinese
ring sword sign” on MDCT coronal reconstruction of the
descending aorta [32].
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Fig. 7  FAP due to acute penetrating atheromatous ulcer (PAU). Case
1: PAU in the aortic arch in a 73-year-old man with back pain. a
Contrast-enhanced MDCT axial scan shows a penetrating ulcer in the
aortic arch (arrow) and localized IMH (star). The patient was treated
Fig. 8  FAP due to acute (PAU) in a 74-year-old man with sudden onset of chest pain. a Unenhanced and b contrast-enhanced MDCT axial
scans show a FAP image (small penetrating ulcer) in the aortic arch (arrow) with high-attenuation IMH (star)
On MDCT imaging IBP/BAP is described as:
(a) A localized island-like CM-filled pool or collection
isodense with the aortic lumen, lacking its own wall,
it is typically located along the non-pleural circumfer-
ence of the aorta at the origin of the aortic branch arter-
ies, inside the IMH on enhanced MDCT images;
(b) Usually, but not always, there is a communication
between the pool/collection and the affected aortic
branch artery;
(c) The communication at systemic arterial pressure
between the CM-filled pool and the true lumen exists,
but at imaging it is no obvious or is a tiny orifice (1–
2 mm in diameter) visible only using thin collimations
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Radiol med (2015) 120:50–72
conservatively. Case 2: PAUs in a 76-year-old man with back pain. b
Contrast-enhanced MDCT axial scan shows PAU (arrow) and exten-
sive, circumferential calcification of the distal descending aorta (“por-
celain aorta”)
(0.6–1.2 mm) and high temporal resolution of the latest
generation MDCT systems [39];
(d) They may propagate along the aortic circumference
and in a craniocaudal direction, from a few millimeters
up to several centimeters, with a possible confluence of
pseudoaneurysms arising from aortic branch arteries
adjacent to each other [38];
(e) IBP/BAP typically appears in IMH involving the
descending aorta with a thickness of greater than 10 mm;
(f) The clinical course of BAP is usually benign and self-
limited and not associated with a poor outcome; the
majority of BAPs spontaneously regress in size over
time and/or completely disappear on follow-up MDCT
[24, 37–39].
Radiol med (2015) 120:50–72 61
Fig. 9  FAP due to chronic atheromatous aortic ulcer and differential
findings with IMH. Case 1: advanced atherosclerosis with chronic
atheromatous aortic ulcer in an asymptomatic 65-year-old man. a
Contrast-enhanced MDCT axial scan in the upper abdomen shows
ulcerated atheromatous plaques of the abdominal aorta (arrowhead).
Case 2: a 55-year-old woman presented with chest pain at rest. b
Fig. 10  FAP due to IBP or branch artery pseudoaneurysm in IMH.
Case 1: follow-up MDCT of acute IMH progressed to overt aor-
tic type B dissection in a 64-year-old hypertensive patient admit-
ted because of chest pain radiating to the back. Contrast-enhanced
MDCT (a) axial and (b) sagittal MIP reconstructions show that a
lumbar artery originating from the true lumen is not affected by dis-
section and runs normally across the false lumen (arrows). Case 2:
In the absence of clinical symptoms or sustained growth,
IBP/BAP needs no specific treatment. However, in patients
with persistent symptoms and isolated enlarging aortic
BAP endovascular embolization can be an effective and
safe procedure [38]. If, in the evolution of the IMH, there is
the association with new intimal tear (ULP)/enlarging BAP,
the best treatment will be the open aortic reconstruction in
type A IMH or TEVAR/EVAR in type B IMH.
Limited intimal tear (class 3 of AD variants)
In 1999, Svensson et al. [40] suggested a five-class classi-
fication of AD, depending on the pathogenetic mechanisms
Contrast-enhanced MDCT axial scan in descending thoracic aorta
shows IMH with displaced intimal calcification (arrow). IMH is often
smoothly crescentic or concentric, whereas mural thrombus is usually
irregular. IMH shows attenuation greater than the unenhanced aortic
lumen, whereas mural thrombus is usually of equal or lower attenua-
tion than the unenhanced aortic lumen
FAP due to aortic branch artery pseudoaneurysms associated with
IMH in a 61-year-old hypertensive patient with acute chest pain. Con-
trast-enhanced MDCT (c) axial and (d) oblique sagittal MIP recon-
structions show the presence of a pseudoaneurysm of the left inter-
costal artery at T9 level in the context of the thoracoabdominal IMH
(arrows)
and consolidation of separate structural lesions inside the
aortic wall into one unit. According to this classification,
later adopted by the European Society of Cardiology [41]
and reiterated in the guideline of the American College of
Cardiology Foundation and the American Heart Associa-
tion in 2010 [1], there are classic type dissections (class
1) with association of intimal tear and the presence of dual
lumen; intramural hematoma (class 2); intimal tear without
hematoma (limited dissection) and eccentric aortic bulge
(class 3); atherosclerotic penetrating ulcers (class 4); iatro-
genic/traumatic dissection (class 5).
Limited intimal tear (class III), also known as ‘incom-
plete tear’, is a rare variant of AD qualified as subtle, dis-
crete dissection in which the limited stellate or linear
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intimal tear is associated with exposure of the aortic media
or adventitial layer and focal eccentric bulge at the tear site.
It has no extensive progression, significant separation of
medial layers, and an intima-medial flap and does not result
in a second flow channel, as seen in classic AD, or an evi-
dent intramural hematoma.
Patients often present with the classic symptoms of dis-
section and may also have associated aneurysms, aortic
regurgitation, or pericardial effusion. Although the inci-
dence of limited intimal tears is not well known and is
likely underestimated because of general unfamiliarity
with this dissection variant, imaging techniques such as
CT, magnetic resonance imaging (MRI), or transesopha-
geal echocardiography (TEE) may fail to detect this type
of dissection. In fact, each of these modalities depends on
the presence and identification of an intimal flap or true and
false lumen for the diagnosis, although Chirillo et al. [42]
have reported the benefit of TEE in detecting the intimal
abnormality. Aortography may show an eccentric bulge
in the aorta, which should raise the suspicion of this class
of dissection. Treatment is similar to that for classic AD.
On MDCT imaging, limited intimal tear is described as
(Fig. 11):
(a) Eccentric one-sided bulge as a minor contour abnor-
mality of the aortic wall that may be the only imaging
finding of this lesion;
(b) Eccentric one-sided bulges are sometimes accompa-
nied by hemorrhagic content within the aortic wall on
unenhanced MDCT imaging and linear filling defects
from subtle undermined edges on MDCT angiography.
Advanced post-processing techniques, particularly
3D-VR and virtual luminal views, can greatly increase the
conspicuity of these often extremely subtle limited intimal
tears [15].
The focal bulge associated with this lesion may be incor-
rectly diagnosed as either an atherosclerotic aneurysm
or pseudoaneurysm. As a limited intimal tear and classic
AD share the same pathophysiologic process (a weakened
medial layer), a class III lesion may evolve into a classic
AD, to form locally true and false lumens, suggesting the
need for close clinical/imaging surveillance.
Fissured intraluminal thrombus of unstable aortic
aneurysms
A true aortic aneurysm (AA) is defined as a dilatation of the
aorta that contains all layers of the aortic wall and usually
involves the entire circumference. An aneurysm is unsta-
ble if shows rapid enlargement and/or signs of impending
rupture.
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Radiol med (2015) 120:50–72
The intraluminal thrombus (ILT) adheres to the aneurysm
wall and it is often circumferential and most commonly
thicker on the ventral side of the aneurysm. The growth
rate of AA is related to thrombus growth and the growth of
the ILT is associated with an increased risk of rupture [43].
From the imaging point of view, there are three ILT char-
acteristics that may help to identify the risk of aneurysm
rupture: ILT size and growth rate, presence of fissures and
structural inhomogeneities in the ILT, and the presence of
calcifications in the ILT [43, 44]. In symptomatic patients,
ILTs may break or fissure, and their internal structure may
be inhomogeneous; thus, the pathophysiology is different
from that of an intramural hematoma in which the hemor-
rhage occurs from within the aortic wall. On MDCT imag-
ing, fissured thrombus (Fig. 12) is described as:
(a) The “hyper attenuating crescentic rim sign or crescent
sign” seen at unenhanced MDCT, as a localized usu-
ally curvilinear zone with higher attenuation in the
thrombus, caused by fresh blood that first insinuates
itself into the mural thrombus and later penetrates the
aortic wall;
(b) Penetration of CM (bleeding) through longitudinal,
transverse or oblique fissures, also of ulcer-like mor-
phology, that directly communicates with the lumen
and represents fissures or dissections between layers of
the intraluminal low-attenuating thrombus;
(c) Their presence is a sign of imminent rupture and there-
fore an indication for early surgery or, in the era of
endovascular repair of ruptured aneurysms, for stent-
graft technique.
Other findings of imminent rupture, often subject to
diagnostic error, include focal new discontinuity of the inti-
mal calcification (missing calcium sign) especially if they
point away from the aneurysm (“tangential calcium sign”),
eccentric shape of the aortic lumen and focal “pointing” of
aneurysm, “draped” aorta sign, unidentifiable posterior aor-
tic wall and the posterior aorta conforming to the contours
of the neighboring vertebral body (Fig. 13) [44].
Saccular and mycotic or infected aneurysm
Saccular aneurysms are eccentric dilatations involving
one side of the aorta, often atherosclerotic, occasionally
infected or mycotic. Pseudoaneurysms (PSA) have fewer
than three aortic layers and are contained by the adventi-
tia or periadventitial tissues, and are typically saccular with
a narrow neck [45]. Infected aneurysm (or mycotic aneu-
rysm) is defined as an infectious break in the wall of an
artery with formation of a blind, saccular outpouching that
is contiguous with the arterial lumen [46].
Radiol med (2015) 120:50–72 63

Staphylococcus and Streptococcus species are the most
common causes of infected aneurysms. The infectious
agents can either travel through the bloodstream and harbor
in the vasa vasorum of the arterial wall or implant on dam-
aged intima, ulcerated arteriosclerotic plaques, or mural
thrombus. Alternatively, the infectious agents can also
reach the artery either by contiguous spread of adjacent
infectious process or by traumatic and/or iatrogenic inocu-
lation [45]. Conversely, fusiform aneurysms are defined
as dilatations involving the entire aortic circumference.

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◂Fig. 11  FAP due to limited intimal tear with intramural hemor-
rhagic content in a 58-year-old male with sudden onset of chest and
back pain. a Transesophageal echocardiogram of the ascending aorta
shows a linear echogenic projection partially enclosing an echolucent
space (white arrow) and b an eccentric one-sided bulge of the aortic
wall (white arrow). Contrast-enhanced MDCT (c, d) axial scans dem-
onstrate a linear filling defect with subtle undermined edges (arrow)
and eccentric medial one-sided bulge of ascending aorta (solid arrow)
without clear intimal-medial flap or false lumen visualized; this was
initially diagnosed as a focal sinusal projection. e Slab-MIP coronal
MDCT reconstruction image demonstrates the ‘eccentric one-sided
bulge’ of the aortic wall along the ascending aorta (arrowhead). f
3D-VR coronal reconstruction confirms the aortic bulging and shows
a teardrop-shaped intimal tear with a localized intimal flap (white
arrow) at its inferior border. The patient was treated by Bentall pro-
cedure
Although the majority of atherosclerotic aneurysms are
fusiform, up to 20 % may be saccular. Infected aneurysms
commonly involve parts of the aorta that are not commonly
involved by atherosclerosis. Although the abdominal aorta
is the most frequently involved part of the aorta, the com-
bined involvement of the descending thoracic, thoracoab-
dominal, and suprarenal aorta, accounts for more cases
than the infrarenal aorta. MDCT features of saccular aneu-
rysms are (Fig. 14):
(a) A focal, contrast-enhancing dilatation that is usually
saccular with a narrow mouth, spherical-shaped bulge
with acute margins and a lobulated contour or an infec-
tious break in the wall of an artery with formation of a
blind, saccular outpouching that is contiguous with the
arterial lumen;
(b) The lumen can be central or eccentric and can be a sin-
gle compartment or multiloculated;
Fig. 12  FAP due to fissured thrombus in unstable aneurysm. a
Contrast-enhanced MDCT axial scan obtained in a symptomatic
78-year-old woman shows an ulcer-like extravasation of luminal con-
trast media through the mural thrombus in the descending thoracic
aorta aneurysm (arrow); note the high-attenuation fluid in both pleu-
ral spaces, a finding that represents acute hemothorax. b Contrast-
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Radiol med (2015) 120:50–72
(c) Having a more or less eccentric thrombus; calcifica-
tions within the aneurysm wall are uncommon;
(d) Adjacent helpful ancillary findings are subtle periaortic
inflammatory changes such as concentric or eccentric
periaortic soft-tissue mass (edema) or a hypoattenu-
ating concentric rim, stranding, and/or fluid and less
commonly gas bubbles and vertebral body abnormali-
ties.
Relatively rapid change in size or shape or progression,
compared with the natural history of atherosclerotic aneu-
rysm, is a feature that is present when sequential examina-
tions are obtained, and should arouse suspicion for super-
imposed infection. Earlier detection of infected aneurysms
is critical for timely treatment to optimize patient outcome,
because their no treatment or delayed treatment often
leads to fulminant sepsis, spontaneous arterial rupture, and
death [46]. The therapeutic options include open surgery,
endovascular stent placement, endovascular embolization,
medical therapy, or a combination of these. In general,
small, asymptomatic, and unruptured infected aneurysms
can be managed with a trial of intravenous antibiotics for
4–6 weeks along with surveillance imaging.
Acute traumatic aortic injury FAP
Approximately 90 % of blunt traumatic aortic injuries
occur at the anteromedial aspect of the aortic isthmus, 8 %
in the ascending aorta, 2 % in the descending aorta at the
level of the diaphragm, 5 % in the abdominal aorta, and
6 % multiple sites [47–50]. According to modified grad-
ing systems, blunt aortic injuries include intimal tear (Ia),
enhanced MDCT coronal MIP reconstruction shows the extent of the
aneurysm to the almost all the descending aorta and the fissuration
site (arrow). c Contrast-enhanced MDCT oblique coronal VR recon-
struction enhances the ulcer-like morphology of the fissuring throm-
bus (arrow)
Radiol med (2015) 120:50–72 65
Fig. 13  Findings of impending rupture in unstable aneurysms. Unen-
hanced MDCT (a) axial scan obtained in a symptomatic 70-year-old
man shows a hyperdense crescent sign due to an acute hemorrhage
within the thrombus. Contrast-enhanced MDCT (b) axial scan at
the same level shows opacified aortic lumen and a FAP from early
thrombus fissuration. Due to the high specificity and sensitivity of the
IMH (Ib), intimal injury with periaortic hematoma (II), par-
tial aortic transection with pseudoaneurysm (IIIa), multiple
aortic injuries (IIIb), free rupture (IV) [51–54]. Pseudoa-
neurysm and intramural hematoma are the most common
findings. Depending on location, careful attention should
be paid to intercostal arteries, internal mammary arteries,
lumbar arteries and arch branch vessels as they may be the
source of bleeding. Active extravasation of contrast mate-
rial, also ulcer-like, in practice is exceedingly rare as it
often portends impending exsanguination. Chronic pseu-
doaneurysms develop in 2.5 % of patients who survive the
initial trauma. These often calcify, may contain thrombus,
and have the potential to enlarge progressively, rupturing
even years after the initial trauma [50, 51].
Direct enhanced MDCT findings of acute aortic injury
(Fig. 15) include [48–57]:
(a) Minimal aortic injury (MAI): abnormality and deformity
of the internal contour of the aorta wall projecting into
the lumen without hematoma or pseudoaneurysm, inti-
mal flap (focal thin membrane-like filling defect), intra-
luminal debris and rounded or triangular filling defects,
intramural hematoma, no evidence of an abnormality to
the aortic external contour (i.e., no pseudoaneurysm);
(b) Pseudoaneurysm (from partial transection), and sudden
change in aortic caliber (aortic “pseudocoarctation”).
Some authors consider as a minor blunt aortic injury a
pseudoaneurysm <10 % of normal aortic diameter at the
same level. Rounded or triangular filling defects are likely
to be small endothelial or intimal injuries with adherent
mural thrombus [53–55]. Grade I and II injuries in hemo-
dynamically stable patients can be treated non-operatively
with anti-impulse therapy (β-blockers) and followed with
repeat MDCT angiography or alternative effective technique
hyperattenuating crescent sign, even without an evident fissuration,
its presence must be reported. Contrast-enhanced MDCT (c) axial
scan shows focal discontinuity of the intimal calcifications (arrow) or
“missing calcium sign”; this finding should also be reported in that it
is a sign of impending rupture, especially if the intimal calcification
points away from the aneurysm (“tangential calcium sign”)
(interval imaging should be done within 48–72 h), until they
have demonstrated resolution or stabilization of the injury.
Hypotension on admission is a strong predictor of death
from blunt aortic injury (BAI). All Grade III BAIs should
undergo repair, however, this may be done emergently or
with a reasonable delay depending on the overall clinical
picture. All Grade IV BAIs must be repaired immediately
[55]. In minimal aortic injury (approximately a quarter of
blunt thoracic aortic injuries) conservative management
with close imaging follow-up has been recommended and is
associated with an excellent outcome [57].
Mimics and pitfalls in interpretation
1. Occasionally, the take-off of bronchial and intercostal
arteries can have small infundibula that may give the
impression of a small pseudoaneurysm, tiny ulcer or
FAP. Infundibula are typically conical in shape and the
artery can be seen at the apex of the outpouching.
2. Ductus remnants or diverticulum may present as either
bumps or diverticula that may simulate FAP and can
be vexing due to their isthmus location. Clues to the
diagnosis include absence of mediastinal hemorrhage,
continuity with the aortic wall, with obtuse margins
and occasionally calcification [58].
3. The left superior intercostal vein runs adjacent to the
transverse aortic arch, and the hemizygous vein may be
seen posterolateral to the descending aorta. With both
the aorta and the vein opacified with contrast material,
the adjacent vessel walls can approximate the appear-
ance of an intimal flap. This is usually not a diagnos-
tic dilemma. It can be observed by scrolling images up
and down and tracing out the vein back to its insertion
into the left subclavian vein.
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Fig. 14  FAP due to infected aneurysm. Case 1: images obtained in
a 66-year-old woman with infected proximal descending aortic aneu-
rysm, steroid-dependent rheumatoid arthritis and β-hemolytic Strep-
tococcus sepsis. Contrast-enhanced MDCT a axial and b coronal MIP
reconstructions show a focal, contrast-enhancing saccular dilatation
with acute margins and lobulated contours (arrows), a saccular aneu-
rysm with prominent periaortic inflammation and fluid. c Contrast-
enhanced MDCT oblique coronal VR reconstruction confirms the
4-cm diameter saccular aneurysm arising from the lesser curvature
of the proximal descending aorta (arrow). Case 2: infected aneurysm
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Radiol med (2015) 120:50–72
of the aortic isthmus in a 58-year-old man with methicillin-resistant
Staphylococcus aureus sepsis due to an inflammatory complication
of urolithiasis. d Contrast-enhanced MDCT axial scan and e sagittal
MIP reconstruction show small pocket-like saccular aneurysms of the
arch with fat stranding and thick, heterogeneous, hypoechoic rind due
to inflammatory tissue. Contrast-enhanced MDCT f oblique axial and
g sagittal VR reconstructions better depict the relationships with the
aortic arch and the multilobulated nature of small infectious aneu-
rysms. This patient was managed with antibiotic therapy
Radiol med (2015) 120:50–72 67
Fig. 15  FAP due to acute traumatic aortic injury (four cases). a
Contrast-enhanced MDCT coronal multiplanar reconstruction (MPR)
shows a small tear, localized wall bulging and sudden change in aor-
tic caliber (pseudocoarctation) at the aortic isthmus with minimal per-
iaortic hematoma (arrow), classified as a grade II injury. b Contrast-
enhanced MDCT axial scan shows intimal tear or flap of descending
thoracic aorta with contour abnormality and filling defect projecting
4. The focal bulging of aortic contour arising distal to
the aortic annulus by Valsalva sinuses, the right atrial
appendage, superior pericardial recess, and left inferior
pulmonary vein, may play a role in interpretive errors.
Familiarity with these structures, the multiplanar imag-
ing, and a close attention to the true relationship of
these structures relative to the aortic wall, are usually
sufficient to eliminate these concerns.
Post‑surgical aorta
Mimics and pitfalls in post‑surgical aorta
Open repair of the thoracic aorta is performed using an
impermeable Dacron tube of variable length, which may
be grafted using either the interposition or the inclusion
technique [59]. The Dacron graft is not detectable on chest
radiographs but is visualized on non-enhanced MDCT
images as a high-density, thin-walled, curvilinear tubular
structure with a smooth and uniform appearance. On con-
trast-enhanced MDCT, the high-density graft is obscured
by intraluminal contrast, but the proximal and distal ends
of the graft may still be identified if high-density Teflon felt
rings are used to reinforce the anastomotic sites.
1. Polytetrafluoroethylene (PTFE) felt material (felt
pledgets) also can reinforce sites of arterial cannula
placement from cardiopulmonary bypass (CPB), punc-
ture sites used to evacuate air bubbles and coronary
artery reimplantation sites to reduce the tearing of
vessels [59, 60]. Pledgets are visualized on MDCT as
small, paired, extra luminal densities, which are spa-
tially well defined. Recognition of these appearances is
the key for differentiating them from areas of calcified
atherosclerotic plaque, contrast material extravasation
into the lumen (arrow), classified as a grade I (minimal aortic) injury;
collapsed lung mimics hematoma. c Contrast-enhanced MDCT axial
scan shows partial aortic transection with contained pseudoaneurysm
formation and periaortic hematoma (arrow), classified as a grade
IIIa injury. d Contrast-enhanced MDCT axial scan shows descend-
ing aorta transection (arrow) with periaortic, mediastinal and pleural
hematoma, classified as a grade IIIa injury
or contrast leak. The high-density felt material in these
locations, a normal postoperative imaging finding, can
mimic a pseudo aneurysm (PSA) on MDCT and unen-
hanced images must be used to confirm that these areas
are surgical materials (Fig. 16).
2. Sometimes a cannula may be placed through a graft
side branch and the branch oversewn after comple-
tion of the CBP procedure used during graft surgery.
An oversewn graft side branch may have a felt pledget
at the margin and/or may appear as an outpouching at
MDCT, thereby again mimicking a PSA or leak.
3. The interposition graft usually appears smooth and uni-
form in contour. Occasionally, there can be slight angu-
lation of the aortic graft itself or, where more than one
graft is used, at their junction. Graft margins can be
seen on sagittal oblique MPR/MIP images as an abrupt
change in caliber, contour or angulations at the junc-
tion of the graft and the native aorta, all of which are
normal except in the case of significant luminal nar-
rowing. Reformatted images are also helpful in identi-
fying kinks or focal outpouching at the junction of two
adjacent grafts or at the margin of a single graft. These
kinks/outpouching are regarded as a normal expected
postoperative finding but can simulate a dissection flap
or a PSA on axial CT images.
4. Another potential pitfall in the interpretation of post-
operative CT scans, after aortic root reconstruction
with a composite graft, lies in the variable appearance
of the coronary artery anastomosis. With composite
graft replacement, the coronary ostia are dissected
with a rim of surrounding aorta (button technique)
and reanastomosed individually to the composite
graft. The buttons along the proximal graft anastomo-
sis can occasionally be rather prominent and may pro-
duce a small bulge at the anastomotic site, simulating
a PSA [61, 62].
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Fig. 16  FAP mimics in native and post-surgical aorta. a In a 26-year-
old man involved in a motor vehicle collision, contrast-enhanced
MDCT axial scan shows evident linear flow and a mild contour irreg-
ularity in medial aspect of proximal descending thoracic aorta with-
out mediastinal hemorrhage (arrow), consistent with a partially patent
ductus. b In a 66-year-old man who had undergone replacement of
the ascending aorta and root with a mechanical valve prosthesis (Ben-
tall procedure) for a type A dissection 13 months earlier, contrast-
5. During open surgery of abdominal aortic aneurysms,
when the native proximal aorta is friable or severely
diseased, a PTFE belt may be used on the outside of
the aortic neck to reinforce a potentially friable proxi-
mal aortic anastomosis. This belt appears as a high-
attenuation ring at CT, and should not be confused with
an endoleak or PSA.
Post‑surgical infected, dehiscence and traumatic PSA
A periprosthetic hematoma larger than 15 mm at the first
post-operative imaging examination, indicates an elevated
risk for the development of a PSA. A chronic perigraft/
paravalvular collection can serve as a site of second-
ary infection, particularly in patients who are bacteremic,
and a correlation should be made with clinical indicators
of infection. Anastomotic prosthetic valve or graft dehis-
cence is often due to advanced perigraft/graft infection and
therefore abscess and hematoma may contribute to the CT
appearance simultaneously. MDCT findings suggestive
of an infected perigraft/paravalvular collection and PSA
include [59–63]:
(a) Contrast enhancement of the collection, bubble or
pockets of air within the collection, increasing size of
collection on serial scans and fistulous connections to
other adjacent structures or extension into other com-
partments;
13
Radiol med (2015) 120:50–72
enhanced MDCT MIP sagittal reconstruction image shows felt pledg-
ets (arrows) at the distal anastomosis site, a normal postoperative
imaging finding that can mimic a pseudoaneurysm without available
unenhanced images. c 3D oblique sagittal VR image shows expected
findings of composite graft with prosthetic valve (blue arrow), coro-
nary button anastomoses (white arrow), and distal anastomosis of
aortic graft to native aorta (yellow arrow) with Teflon felt rings used
to reinforce the anastomotic site
(b) Valve vegetations in the form of small, round, hypoat-
tenuating masses located on the sewing ring or leaflet
component, usually on the ventricular surface of the
prosthesis;
(c) Ulcer-like leaks, valve ring abscesses, and extension of
the infection into adjacent tissues;
(d) Valve dehiscence appears as a gap between the aortic
annulus and the opposing margin of the artificial valve
that allows visualization of an ulcer-like or continuous
column of CM from the left ventricular cavity into the
aortic root.
Dehiscence of the suture line can lead to a broad range
of complications (anastomotic PSA, perigraft perfusion,
confined perforation, suture line failure with hemorrhage).
The presence of CM external to an interposition graft is
consistent with dehiscence. Partial dehiscence of a suture
line can occur at any anastomotic site, but most commonly
either proximal or distal to the graft, at cannulation sites,
or ascending aorta needle puncture site (needle inserted for
pressure measurement, to purge the aorta of air, or to inject
cardioplegic solution). Less frequently dehiscence may
occur at the coronary anastomosis site (Fig. 17).
Post‑endovascular aortic repair procedures
An endoleak (EL) is defined as a persistent blood flow
within the sac outside the stent- graft. It may have a
Radiol med (2015) 120:50–72 69
Fig. 17  FAP due to post-surgical pseudoaneurysm in a 65-year-
old man with ascending composite aortic interposition graft and re-
implantation of coronary arteries (button Bentall procedure) for aortic
aneurysm. 8-day postoperative contrast-enhanced MDCT (a) axial
and (b) oblique sagittal MIP reformatted images obtained because
projecting morphology, of variable origin, flow rate, size,
and location and is classified into types I to V according
to the source of blood flow: type I, leak at the attachment
site; type II, leak from a branch artery; type III, graft
defect; type IV, graft porosity and type V, endotension
[61]. The type I and III endoleaks may show an ulcer-like
configuration and may be seen at MDCT as focal aortic
projections. Because endoleaks have variable flow rates,
they can be detected at variable times after CM injection
and delayed phase imaging, in particular, it is critical for
what ELs can demonstrate as they are not visualized dur-
ing the arterial phase. There are several MDCT findings
that may help distinguish between different types of ELs
[63–66]:
Type I, due to the inadequate seal between the stent-
graft and the host aorta, it is seen communicating with the
proximal (IA) or distal (IB) attachment site of the stent-
graft with reperfusion of aneurysm sac (Fig. 18); an EVAR
Type I endoleak may also refer to inadequate seal of an
iliac occluder (IC). MDCT angiography findings suggestive
of a Type I EL are [63–66]:
(a) MC collection that may be seen as a focal, generally
broad-based, region of enlarging increased density
alongside the proximal or terminal ends stent-graft
into the aneurysm sac, often non-tubular, rarely tubular
(when it appeared channel-like);
(b) Its location may be central, or combined (both central
and peripheral), depending on the position of its com-
of mild chest pain before hospital discharge show active contrast
extravasation arising from the right coronary anastomosis site (yellow
arrow) and extending in a large contained pseudoaneurysm (PSA)
(blue arrow) encompassing the ascending aortic graft
ponents relative to the endovascular grafts and the aor-
tic wall;
(c) EL size is graded as small (up to 25 % of the diam-
eter of the sac at the same level), medium (greater than
25 % but less than 50 %), or large (50 % or greater).
Type I endoleaks are always considered clinically signif-
icant and are generally treated as soon as they are detected,
as spontaneous resolution over time cannot be expected.
Type III, also called a connection leak or fabric leak,
occurs where the leakage is accompanied by an inadequate
joint between the modular or multi-modular devices or a
damage to the stent-graft itself. MDCT angiography find-
ings suggestive of a Type I EL are [63–66]:
(a) MC non-tubular central collection usually manifests
around the graft while sparing the sac periphery, while
large circumferential perigraft collections are indica-
tive of dislocation of the stent-graft or insufficient
length of a tube endoprosthesis.
These ELs are more likely when multiple prostheses
with short overlapping areas are used. In general, high-
pressure leaks (type I and type III) require urgent manage-
ment because of the relatively high short-term risk of sac
rupture. The former are managed by securing the attach-
ment sites with angioplasty balloons, stents, or stent-graft
extensions, and the latter by covering the defect with a stent
graft extension.
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70
Fig. 18  FAP due to type III endoleak in a 72-year-old man after
TEVAR for emergent, ruptured, descending thoracic aortic aneu-
rysm. Contrast-enhanced MDCT (a) axial and (b) oblique sagittal
MIP reformatted images of the thoracic aorta show contrast material
Mimics
Type II ELs are defined as retrograde flow through collateral
vessels into the perigraft space, preventing thrombosis of the
sac and creating a risk of continued aneurysm expansion and
possible rupture. They are the most common ELs after an
abdominal aortic repair, accounting for 80 % of cases. The
most common culprit vessels are lumbar arteries, inferior
mesenteric artery or internal iliac artery, whereas, in thoracic
endografts, type II endoleaks depend on the bronchial and
intercostal arteries. MDCT findings Type II EL are [63–66]:
(a) has a feeding vessel, such as a contrast material-
filled aortic branch directly contiguous to the aortic
aneurysm sac; when backflow enters the sac, it often
assumes a channel-like or tubular shape that insinuates
between the aortic wall and luminal thrombus at some
distance from the graft;
(b) it is located in the aneurysmal sac periphery (when at
least a portion of an endoleak is adjacent to the wall
without a gap or with a gap that do not exceed 2 mm)
without contact with the stent;
(c) the ventral collections without direct connection to the
endoprosthesis are supplied by the inferior mesenteric
artery, while dorsolateral endoleaks are supplied by the
intercostal, bronchial, lumbar arteries, or the median
sacral artery.
This type of leak has been reported in up to 25 % of
cases. It usually resolves spontaneously over time and
13
Radiol med (2015) 120:50–72
outside the double-stented aorta in the excluded aortic lumen (white
arrows) directly communicating with the native aorta, consistent with
a type III endoleak; note the large right mediastinal hematoma (blue
arrow) and bilateral pleural effusion (star)
requires no treatment. Embolization of the branch vessel is
only indicated if the aneurysm sac continues to expand in
size.
Conclusions
FAP may be present in a complex and dynamic group of
conditions affecting the aorta; although our understand-
ing of these entities continues to evolve, MDCT plays the
dominant role in their evaluation because various findings
help to distinguish among different types of aortic protru-
sions. The role of the radiologist begins with proper proto-
col design and the use of advanced display techniques for
image processing to optimize FAP; prompt and accurate
detection and characterization; radiologists should be aware
of the features, potential complications, and management
options of these patients, because some lesions require
treatment whereas others may be followed. Opportunities
for diagnostic error can be mitigated by familiarity with
the spectrum of imaging findings encountered at MDCT, as
well as common pitfalls in interpretation. Detailed evalu-
ation and knowledge of some related and distinguishing
high-risk MDCT features in FAP, may improve our under-
standing of aortic diseases, can be essential to provide the
surgeons with the necessary information for appropriate
patient triage and management decisions.
Conflict of interest  The authors declare that they have no conflict
of interest to the publication of this article.
Radiol med (2015) 120:50–72 71
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