Dissection, Aortic, Thoracic

Disorders of Neuronal Migration

Gyration Disorders, Cerebral

Disorders of Neurulation
Congenital Malformations, Cerebral (neuro view)

Dissection, Aortic, Thoracic

M ARIA S CHODER
Medizinische Universitat Wien, Vienna, Austria
maria.schoder@meduniwien.ac.at

Definition
Etiology of Aortic Wall Dissection
Aortic dissection is defined as a separation of aortic
wall layers. In the majority of cases, an intimal tear
through which blood surges into the media is the initial
event. Less common is a dissection caused by intramural
hemorrhage and an intramural hematoma (IMH) without a detectable intimal tear. Chronic systemic hypertension is the most common factor predisposing the aorta to
dissection. Further causes such as inherited connective
tissue disorders (i.e., Marfans syndrome, EhlersDanlos
syndrome, and annuloaortic ectasia and familial aortic
dissection), degenerative, atherosclerotic, inflammatory, or
toxic processes, as well as traumatic events, may precede the
aortic dissection (Table 1).

Characteristics
Diagnostic Imaging
Aortic dissection may occur anywhere within the aorta.
If there are clinical suspicions for aortic dissection,
identification of the aortic segments involved is mandatory for further management. It is mandatory to visualize
the entire aorta including arch vessels and iliac arteries.
The imaging modalities that are highly accurate in
diagnosis include multislice computed tomography

641

Dissection, Aortic, Thoracic. Table 1 Aortic disease

etiologies with risk for aortic dissection
Inherited diseases
Marfans syndrome
EhlersDanlos syndrome
Annuloaortic ectasia and familial aortic dissection
Atherosclerosis
Inflammatory diseases
Takayasus arteritis
Giant cell arteritis
Behcets disease
Aortitis associated with rheumatoid disease
Ormonds disease
Syphilis
Toxic etiologies
Cocaine
Amphetamine
Traumatic/iatrogenic dissection

(MSCT), magnetic resonance imaging (MRI), and transesophageal echocardiography (TEE). Due to technical
limitations, such as narrow intercostal spaces, obesity,
pulmonary emphysema, and patients on mechanical
ventilation, the value of transthoracic echocardiography
(TTE) remains limited. Intra-arterial angiography is
invasive, and is not the current standard method for initial
diagnosis.
MSCT: Multislice scanners allow rapid diagnosis and
their accuracy has been improved by the availability of
two- and three-dimensional reconstructions. An optimized vascular enhancement is essential for the diagnosis
of dissection. Therefore, the use of an automated bolus
tracking system for contrast injection in combination
with the saline chaser bolus technique is recommended
(1). Acquisition parameters depend on the performance
of the scanner used.
Diagnostic difficulties might be caused by artifacts
such as streak artifacts and aortic motion artifacts. Streak
artifacts are caused by sharp contrast interfaces or cardiac
motion. These straight lines of low attenuation are usually
restricted to a few transverse images. Aortic motion
artifacts, which may mimic aortic dissection, are predominantly seen in the ascending aorta (2). They appear as
a localized duplication or pseudo-thickening of the aortic
wall. These artifacts are caused by pendular movements of
the aortic wall between the systolic and diastolic phase. To
overcome this diagnostic uncertainty caused by cardiac
motion, retrospective or prospective electrocardiographyassisted MSCT has been shown to be relevant in imaging of
the ascending aorta. With a 16-slice CT scanner, cardiac
gating is limited by a reduced volume coverage; however,
64-slice scanners do not have this limitation.

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Dissection, Aortic, Thoracic

MRI: A combination of three-dimensional contrastenhanced MR angiography with cross-sectional MR

images provides an overview of the aortic anatomy and
details of the dissecting membrane and the aortic wall.
Furthermore, flow in the false and true lumen can be
quantified with phase contrast cine MRI or tagging techniques. A further advantage is the accurate assessment of
aortic regurgitation. Moreover, MRI permits detection of
acute and subacute intramural hemorrhage on the basis
of methemoglobin which occurs after several days and
persists for several months. However, MRI is contraindicated in patients with pacemakers and certain metallic
implants, and is inappropriate in hemodynamically
unstable patients.
TEE: Besides the ability to identify the entry site of
dissection, the presence of an intimal flap, abnormal flow
characteristics within the false and true lumen, involvement of coronary and arch vessels, TEE is highly accurate
in the diagnosis of aortic valve regurgitation. A disadvantage of TEE is the limited field of view, with inability to
visualize the distal extension below the celiac trunk.

Dissection, Aortic, Thoracic. Table 2

variants of aortic dissection

Classification of

Class
1
2

Classic aortic dissection

Separation of intima/media; dual lumen
Intramural hematoma/hemorrhage
Separation of intima/media; no intraluminal tear or
flap imaged
Subtlediscrete aortic dissection
Intimal tear without hematoma (limited dissection)
and eccentric bulge
Atherosclerotic penetrating
Ulcer penetrating to adventitia with localized
hematoma
Traumatic/iatrogenic dissection

Dissection, Aortic, Thoracic. Table 3

requirements in aortic dissection

Diagnostic

Localization of intimal tears

Communicating versus noncommunicating dissection

Classification and Diagnostic

Requirements in Aortic Dissection
Regarding the radiological and pathological variants of
aortic dissection, a differentiation of subtypes (Table 2)
has been proposed (3, 4). Diagnostic considerations must
include extension of the dissection, involvement of aortic
side branches, and concomitant complications (Table 3).
All dissection subtypes can be seen in their acute and
chronic stages. A dissection is classified as acute if it is
2 weeks old or less.
Class 1: Classic aortic dissection. Due to the anatomical
location of the dissection, the Stanford classification
distinguishes between type A and type B. A type A
dissection includes the ascending aorta regardless of the
entry site location, whereas a type B dissection presents with
the primary intimal tear in the descending thoracic aorta,
mostly located just beyond the insertion of the ligamentum
arteriosum. The DeBakey classification subdivides the aortic
involvement in a type I dissection, involving the entire aorta,
a type II dissection that involves the ascending aorta, and a
type III dissection that involves the descending aorta.
It is important to differentiate between the true and
the false lumen and to visualize the extension of the
dissection. The true lumen is usually compressed and is
close to the inner curvature of the aortic arch. Intimal
calcification indicates the true lumen in acute dissection.
The false channel often enhances later than the true
lumen. However, the contrast gradient between the aortic
channels may reverse during the acquisition.
Malperfusion of abdominal branches and iliac arteries
may be caused by the so-called static and dynamic

Differentiation between true and false lumen

Extension of dissection
Involvement of aortic branches
Coronary arteries
Arch vessels
Visceral and renal arteries
Iliac arteries
Complications
Rupture/contained rupture
Pericardial effusion
Pleural effusion
Perfusion deficit/infarction in organs

mechanism, as proposed by Williams et al (5). The

dynamic narrowing of a branch vessel occurs when the
dissection flap is positioned across the vessel origin
provoked by the hyper-pressure of the false lumen. In the
static mechanism, the intimal flap intersects the vessel
origin and in the absence of a peripheral intimal tear, the
false lumen constricts the vessel origin.
Class 2: Intramural hematoma/hemorrhage. Intramural hematoma (IMH) and hemorrhage may be the result of
ruptured vasa vasorum. There are two types of IMH/
hemorrhage. Type I shows a smooth inner aortic lumen
and the aortic diameter is usually less than 3.5 cm with a
wall thickness greater than 0.5 cm. Type II occurs with
atherosclerosis. It demonstrates a rough inner aortic
surface and is found more often in the descending than in
the ascending thoracic aorta. The aortic diameter is
dilated and the wall thickness has a range of 0.64 cm. On

Distant Recurrence

unenhanced CT scans, IMH appears as a crescent-shaped

area of attenuation in the aortic wall and remains
unenhanced after injection of contrast material. IMH
tends to maintain a constant circumferential relationship
with the aortic wall, differentiating it from a thrombosed
false lumen in a classic aortic dissection which usually
spirals longitudinally around the aorta.
Class 3: Subtlediscrete aortic dissection. A subtle
dissection has been described as a partial intimal tear
covered by thrombus. When the tear forms a scar, this
constellation is called a discrete dissection.
Class 4: Penetrating atherosclerotic ulcer. A penetrating
ulcer occurs from an atherosclerotic plaque that has
penetrated the internal elastic lamina into the media.
A penetrating atherosclerotic ulcer (PAU) can lead to an
IMH and aortic dissection, to a pseudoaneurysm, and
to rupture. Diagnosis is made by demonstrating a focal
contrast material-filled outpouching that might be
associated with an IMH or an aneurysmal formation.
Class 5: Traumatic/iatrogenic aortic dissection. Blunt
chest trauma may cause aortic dissection frequently at the
region of the ligamentum botalli at the aortic isthmus.
Untreated dissections often lead to pseudoaneurysms and
may rupture.
Iatrogenic dissections are mostly catheter-induced
and retrograde, and usually they decrease in size as the
false lumen thromboses.

Therapy
Alternatively to conventional open repair, less invasive
endovascular techniques for the treatment of dissections
have gained widespread application, and encouraging
results have been reported (610).
Acute uncomplicated type B dissections are preferably
managed by conservative medical treatment. Complicated
type B dissections with signs of rupture or imminent
rupture, compromised branch vessels, rapidly expanding
aortic diameter, refractory pain, or malignant hypertension require surgical or endovascular therapy. Stent grafts
have a self-expanding stent structure covered by polyester
or expanded polytetrafluoroethylene (ePTFE). Closure
of the entry tear by stent-graft placement may lead to
thrombosis of the false lumen with remodeling of the true
lumen. Primary closure of the entry tear is reported in
89100% of cases, with consecutive thrombosis of the
false lumen in the descending aorta in 70100%.
Furthermore, lowering the pressure in the false lumen
restored the perfusion in branch vessels that were compromised by a dynamic mechanism, as reported by Dake
et al (6). However, in vessels with a narrowed origin caused
by an intimal flap (dynamic mechanism) additional
stenting of the vessel lumen may be required in up to
60% of cases (6). In cases were the branch vessel perfusion

643

is compromised by a hypertensive false lumen, fenestration of the dissection membrane may be necessary (10).
The puncture is performed from the true lumen of
the infrarenal aorta into the false lumen, which generally
tends to have a larger diameter. After placement of a stiff
guide wire, the dissection membrane is fenestrated with a
balloon until equalization of pressure is achieved.
In traumatic transection, the reported numbers of
patients who were treated with stent-graft therapy are still
limited. However, perioperative mortality rates in endovascular repair were between 0 and 13%, and were
related to comorbid injuries and not associated with the
stent-graft procedure (8, 9). Furthermore, paraplegia was
not reported after endovascular repair, which compares
favorably with surgical results.

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Distant Recurrence
Also called systemic recurrence or metastatic disease. In
this situation, malignant cells can be demonstrated in a
distant organ, such as bone, lungs, liver, brain, or other
places. The survival rate is considerably lower than for
local or regional recurrences.
Recurrent Neoplasms, Breast