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D.M. Williams, B. Peynircioglu Chapter 23 Physiopathology of Ischemic Complications of Aortic Dissections
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245
13. Suzuki T, Mehta RH et al (2003) Clinical profiles and outcomes of acute type B aortic dissection in the current era:
lessons from the International Registry of Aortic Dissection (IRAD). Circulation 108(Suppl 1):II312±317.
14. Williams DM, Joshi A et al (1994) Aortic cobwebs: an
anatomic marker identifying the false lumen in aortic dis-
section-imaging and pathologic correlation. Radiology
190:167±174.
15. Williams DM, Lee DY et al (1997) The dissected aorta. III.
Anatomy and radiologic diagnosis of branch-vessel compromise. Radiology 203:37±44.
Endovascular Treatment
https://t.me/med1917
of the Complications
of Aortic Dissection:
Fenestration and Stenting
Jean-Paul Beregi, Philippe Asseman, Alain Prat,
Frdric Thony, Virginia Gaxotte,
Christophe Lions, Ziad Negaiwi, Serge Willoteaux
Chapter
24
Contents
24.1 Introduction ......................
24.2 Malperfusion Symptomatology ............ 247
24.3 Mechanisms ....................... 248
24.4 Para-clinical Examinations .............. 249
24.5 Endovascular Treatments ............... 249
24.6 Conclusion ± Therapeutic Guidelines ........ 251
247
24.1 Introduction
Acute aortic dissection is a medical, radiological and
surgical emergency that rapidly compromises the patient's chances of survival [1, 2]. Dissection of the ascending aorta almost invariably requires emergency
surgical replacement; when the ascending aorta is not
involved, dissection is primarily treated medically, except in the event of complications [3]. The traditional
management, based on Stanford classification, is discussed because of emergent endovascular treatment for
aorta and malperfusion syndrome.
Malperfusion is defined in this context by the ischemia of an organ during aortic dissection. Malperfusions can concern the heart, brain and spinal cord, and
in the case of extension of the dissection to the abdominal aorta and the iliac axes, the digestive tract, kidneys
and lower limbs. This type of complication aggravates
the already high morbidity and mortality linked to the
thoracic complications of dissection [4, 5]. Several
mechanisms may be responsible for this malperfusion,
and the necessity for endovascular treatment is dependent on these mechanisms.
The purpose of this chapter is to describe the mechanisms behind the malperfusions and to propose the in-
dications and endovascular treatment techniques. In
this publication, we only cover renal, digestive and lower-limb malperfusions.
24.2 Malperfusion Symptomatology
In accordance with the Stanford classification, type A
dissection concerns the ascending aorta, regardless of
the entry site; type B dissection concerns the descending aorta, the entry site being generally situated on the
descending aorta, sometimes on the aortic branch. Malperfusion of the visceral branches of the abdominal
aorta or the iliac axes can occur in cases of extension
of the dissection to the abdominal aorta, whether or
not the ascending aorta is concerned with the dissection.
In the case of an aortic dissection with acute symptoms of malperfusion (Table 24.1), diagnosis must be
done quickly in order for emergency treatment to be
administered.
An aneurysm and/or renal insufficiency should make
the practitioner suspect renal ischemia. It is particularly
important to check the condition of the renal vascular
system rapidly, as soon as dissection is diagnosed. In-
Table 24.1. Symptoms due to malperfusion syndrome in the
case of aortic dissection with involvement of the abdominal
aorta
Organs Acute symptoms Chronic
Kidneys Renal failure,
anuria
Digestive Abdominal pain,
biological signs
(hepatic enzymes)
Lower limb Acute ischemia with
white and painful leg
symptoms
Refractory
hypertension
Digestive
angina
Claudication
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IV. Dissection
deed, secondarily, the onset of renal insufficiency in the
recovery period or postoperatively (replacement of the
ascending aorta) can depend on multiple factors. Early
diagnosis of renal malperfusion allows the appropriate
endovascular treatment to be initiated without delay.
In the context of aortic dissection extending to the
abdominal aorta, spontaneous pain or palpation-induced pain must lead to the rapid diagnosis of intestinal ischemia. This ischemia is difficult to confirm with
para-clinical examinations but, if untreated in the hours
following the onset of the symptoms, will prove fatal.
Lastly, ischemia of the lower limbs is easily detected
using the usual symptomatology (coldness and pain in
the limbs and lack of pulse).
The symptoms observed in the acute phase of an
aortic dissection must lead to the rapid administration
of treatment. Such treatment must sometimes be carried out before the ascending thoracic aorta can be repaired, as in the case of a type A aortic dissection [6,
7].
At the chronic stage, whether a medically treated
type B dissection or a type A surgical dissection is involved, the symptoms of malperfusion can appear during follow-up. This can consist of refractory arterial hypertension, digestive angina or intermittent claudication
of a lower limb. A morphological analysis of the dissection must be conducted in order to plan the appropriate
treatment according to the mechanism of the malperfusion.
Fig. 24.1. Type 1A, 1 B, 1 C and 1 D lesions. FL false lumen,
TL true lumen
24.3 Mechanisms
Malperfusions can currently be treated by endovascular
means: implantation of arterial stents in the visceral
branches of the abdominal aorta, in the iliac axes, in
the abdominal aorta, fenestration of the intimal flap,
implantation of a thoracic aortic stent-graft and a combination of these different techniques. These forms of
treatment seem to yield better results than surgery in
cases of malperfusion-related complications. In order to
choose the appropriate treatment, it is essential to know
the morphology of the aortic dissection and the extension into vascular branches to understand the mechanisms responsible for the malperfusion(s).
These mechanisms of visceral malperfusion were
studied in 1997 by Williams et al. [8]. These authors
proposed a system of classification that separates the
so-called static mechanisms from those considered dynamic. The static character is described by analogy to
classic athermatous lesions that narrow the diameter of
the artery like ostial or proximal stenosis. Dynamic lesions are described as resulting from compression of
the true arterial lumen by a false lumen secondary to
extremely high pressure in the latter. However, this classification system does not describe all possible cases
Fig. 24.2. Type 2A, 2 B, 2 C and 2 D lesions. FL false lumen,
TL true lumen
and it is often difficult to link the symptoms with the
mechanisms, thus resulting in treatment problems. In
fact, all lesions are dynamic. The lesion defined as static is an extension of the dissection into a dead-end visceral artery. This extension leads to a reduction in the
true channel by compression of the false channel where
the blood enters but cannot exit. Given the blind aspect
of the lesion, it tends to thrombose, giving rise to the
erroneous diagnosis of a static lesion.
We propose an analysis of lesions in relation to the
position of the dissection flap in the aorta followed by
examination of the visceral arteries to investigate a possible dissection or an ostial tear (Fig. 24.1). This
approach, in a study of 61 patients [9], demonstrated
that type 1c and 1d lesions with malperfusion lead to
fenestration (Fig. 24.2), whereas type 2 a, 2 b, 2 c and 3 c
lesions lead to the implantation of a stent in the artery
affected by the dissection with downstream ischemia
(Fig. 24.3).
J.-P. Beregi et al. Chapter 24 Endovascular Treatment of the Complications of Aortic Dissection: Fenestration and Stenting
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Table 24.2. Objectives of imaging techniques when aortic dis-
section is suspected
To perform the diagnosis of aortic dissection or hematoma
To determine the level of the extension into the aorta
(ascending, cross, descending)
To analyse the trajectory of the true and false lumens
throughout the total aorta and to evaluate the position of the
intimal flap (compression or not of the true lumen)
To detect entry tears: numbers and location
To diagnose thoracic complications of the aortic dissection
To analyse possible extension into branches of the aorta and
disconnection of the origin; to look for ischemic signs in the
organs:
Supra-aortic vessels (brain ischemia)
Visceral arteries (kidneys and bowel ischemia)
Iliac arteries (lower limb ischemia)
Fig. 24.3. Type 3 A, 3 B and 3 C lesions. FL false lumen, TL true
lumen
To evaluate tortuosity, calcification and the diameter of the
iliac and common femoral arteries for a possible endovascular treatment such as a thoracic stent-graft
249
24.4 Para-clinical Examinations
The objectives of imaging techniques in cases where
aortic dissection is clinically suspected are given in Table 24.2. The diagnostic imaging techniques at our disposal are transthoracic echocardiography, transoesophageal echocardiography (TOE), computed tomography
(CT) angiography, MRI and arteriography. TOE, CT angiography and MRI display high, identical levels of sensitivity (greater than 90%) in the diagnosis of aortic
dissection [2, 10±12]. TEE responds partially to the objectives mentioned; it does not facilitate complete diagnosis of the dissection, as it is limited to the study of
the thoracic aorta. However, this technique can be used
in the intensive care unit with no displacement of the
patient.
There is less access to MRI in France and we have
few machines dedicated to emergencies and to the treatment of haemodynamically unstable patients.
A CT angiogram acquires a large volume of data
(thoracic±abdominal±pelvic), allowing thorough investigation of the dissected aorta. Its performance in the exploration of the aorta has been well established [13±15].
The technological contribution of helicoidal data acquisition in the diagnosis of aortic dissection has improved
its sensitivity, which now varies between 88 and 100%.
The essential objectives mentioned can be achieved
using this technique. Exploration is conducted without
and then with the injection of a contrast medium. The
data acquisition techniques for axial sections are variable and depend on the performance of the equipment
used. This technology has allowed more extensive investigation and thorough comprehension of malperfusions.
It is also the preferred technique for detecting and analysing malperfusions on a practical level.
Although the technique has been in use for a long
time, arteriography is no longer used to diagnose dis-
section but is employed only as a complementary technique (e.g. before implantation of a thoracic stent-graft)
or for an endovascular procedure.
24.5 Endovascular Treatments
Besides surgical treatments such as bypasses, surgical
fenestration [16] or closure of the entry points, endovascular techniques have developed as they are better
tolerated in the context of aortic dissection with malperfusion [11].
Endovascular fenestration is specific to the treatment
of aortic dissections. This technique is carried out whenever malperfusion is suspected in association with a dynamic mechanism or with types 1c and 1d. The principle
consists in creating a wide orifice of communication between the true and false channels or in increasing the
passage of blood between these two channels [17]. The
former technique involves creating an exit site by perforating the intimal flap, from the true channel towards the
false channel, using a trans-septal needle. This technique
is currently made safer by the use of an endovascular ultrasound probe; this enables surgeons to better locate the
position of the intimal flap and to guide movements on
perforation [18]. Once the aperture has been made in
the flap, it is enlarged by angioplasty with a balloon measuring over 12 mm in diameter. The second possibility
for carrying out fenestration, termed the scissor technique [19], involves the introduction of a rigid guide wire
into the true channel and another into the false channel,
both using the same sheathed introducers (8-F minimum,
45 cm long) installed by the femoral route. A fixed point
on the guide wires and graduated, clear-cut advance of
the introducer allow a tear to be made in the flap. A tear
is observed either in the centre of the flap or at the ex-
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IV. Dissection
Fig. 24.4. Schematic proposition
for new clinical practices in aortic
dissection
tremities of the flap, or else the dissection is continued
around the remainder of the circumference, extending
the height of the fenestrated aorta. This latter mechanism
is the most frequent. It can then be useful to unfold the
flap by inflating a large-diameter balloon (over 12 mm)
inside the thoracic aorta and retracting it as far as the
iliac junction, with the balloon inflated. The risk of a torn
flap folding back on itself must be taken into account as
this can turn and trigger ischemia in the lower limbs [20].
The insertion of a complementary stent will then become
necessary. It is also important to carry out stenting of the
flap beneath the fenestration site if the false channel is
perfused without an exit; there is a risk of aortic rupture
linked to the very high pressure in the false channel.
Lastly, the scissor fenestration technique does not need
to be extensively long; fenestration of 3±5 cm seems sufficient. This generally lowers the pressure in the false
channel, relieves compression of the true channel, relieves the ischemia linked to the dynamic mechanism, inhibits complications and gives the surgeon the option of
returning at the end of the acute episode with a view to
closing all the entry sites. However, in certain cases, fenestration of the intimal flap at the subrenal level is not
sufficient to relieve dynamic compression on the renal
and digestive arteries; this can be explained by blood
flowing predominantly in the true channel, to the low-resistance organs, provoking an attraction of the intimal
flap, which remains pressed against the ostium. It then
becomes necessary also to install an aortic stent in the
true lumen, above the visceral branches. The technique
of fenestration is reserved for emergency cases with severe intestinal ischemia (Fig. 24.2). This technique, which
is carried out in less than 1 h in the angiography room,
provides immediate relief from the symptoms. In the
event of renal lesion and delayed treatment, an acute tubular necrosis can also arise with recovery of renal functions in 3 weeks. In patients presenting with chronic
symptoms, it is rare to have to carry out a fenestration.
Implantation of bare stents in the abdominal aorta
or in the arteries of the organs affected by the malperfusion is carried out using classic endoprostheses. The
use of a strong radial action stent is preferable in cases
where the true channel is compressed by the false channel. This is why we currently prefer to use balloonmounted stents. The positioning of a stent at the root of
a visceral branch can sometimes prove tricky; this stent
must, in effect, push back the false channel that is compressing the true channel in the artery but also at the
root. The stent must therefore overlap into the aorta
and apply pressure on the false channel (Fig. 24.3), but
the latter does not provide stable support; a sufficiently
long stent is required in the artery to maintain the
whole system. Negotiation of the bend between the aorta and the malperfused artery can be difficult if the balloon-mounted stent, with strong radial action, exceeds
3 cm in length. Account should also be taken of the lack
of atheroma, which normally maintains the stent after
expansion, and therefore of the risk, after retraction of
the balloon, of the stent falling into the aorta, carried
away by the balloon. The implantation diameter of the
stent must be equal to or greater than that of the
treated artery to prevent any secondary movement. The
ostial tears, with malperfusion (type 3c) (Fig. 24.1), also
necessitate implantation of a stent (Fig. 24.3).
The mechanisms of malperfusion of the visceral
branches of the abdominal aorta and the iliac axes can
J.-P. Beregi et al. Chapter 24 Endovascular Treatment of the Complications of Aortic Dissection: Fenestration and Stenting
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251
be related. When fenestration is necessary, it is this
treatment that is carried out first; it is often necessary
to complement fenestration with the implantation of a
stent on one or several branches. However, the full extent of the remaining lesions is not always easy to ascertain by postfenestration angiography. This highlights
the importance of preoperative contrast angiography
for a better understanding of the mechanisms of malperfusion, before carrying out arteriography. It is sometimes useful to carry out the procedure in two phases
with a new clinical evaluation and diagnostic imaging
(echo-Doppler or contrast angiography).
In cases of type B dissection, the implantation of a
stent-graft to close the entry site at thoracic level is a
therapeutic possibility [21]; it is rarely carried out in
the emergency treatment of malperfusion. The availability of stent-grafts, the necessity for a full examination
beforehand and the slow regression of the symptoms
after implantation are the principal reasons. Emergency
implantation of a thoracic stent-graft is indicated in
cases of rupture of the false channel. In cases of subacute or chronic symptoms, treatment with a stent-graft
can be proposed after anatomical evaluation. The symptoms can take several weeks to disappear owing to
thrombosis in the false channel and the slow regression
of the latter.
We systematically combine endovascular treatment
with medical treatment and observation in recovery or
in the cardiac intensive care unit [2]. Blood pressure
must be controlled, even if this requires the intravenous
administration of several antihypertensive drugs. We
start an anticoagulant treatment with intravenous heparin in cases of malperfusion in order to combat organ
ischemia. Aortic dissection is no longer a contraindication to the use of heparin in cases of associated malperfusion. The dose administered must ensure efficient anticoagulation. After fenestration, regardless of whether a
stent was installed in the visceral branches or a stent graft
was used, anticoagulant treatment is continued until malperfusion is relieved and the symptoms disappear. No
antiaggregation treatment is used.
24.6 Conclusion ± Therapeutic Guidelines
To conclude, visceral malperfusions must be systematically investigated (preferably by thoracic, abdominal
and pelvic CT angiography) during the course of aortic
dissections as their presence leads to high mortality. Yet
visceral malperfusions can be treated using effective endovascular therapies. Their presence leads to a change
in the treatment guidelines and lends too much credence to the overly classic dogma: a type A dissection
must be surgically corrected and a type B dissection
must be treated medically. Modern treatment guidelines
are based on the presence or absence of complications.
The dissection complications must be treated immediately before considering prophylactic treatment. Type B
dissections, just like type A ones, can become complicated owing to malperfusion. It is therefore important
to hospitalise the patients, in order to carry out essential diagnostics and design an appropriate course of
treatment. Relying on a multidisciplinary treatment
protocol, we propose that the organisation chart in
Fig. 24.4 should reduce the mortality and morbidity of
patients with this condition.
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11. Rousseau H, Otal P, Soula P, Colombier D, Joffre F. Diagnostic et traitement endovasculaire de la pathologie aortique thoracique. J Radiol 1999; 80:1064±1079.
12. Sommer T, Fehske W, Holzknecht N, Smekal AV, Keller E,
Lutterbey G, Kreft B, Kuhl C, Gieseke J, Abu-Ramadan D,
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13. Ledbetter S, Stuk JL, Kaufman JA. Helical (spiral) CT in
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Traumatic aortic rupture, aortic aneurysm, aortic dissection, intramural hematoma, and penetrating atherosclerotic ulcer. Radiol Clin North Am 1999; 37:575±589.
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14. Sebastia C, Pallisa E, Quiroga S, Alvarez-Castells A, Dominguez R, Evangelista A. Aortic dissection: diagnosis and
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Thoracic Infectious Aortitis
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Matthieu Revest, Patrick Jgo
Chapter
25
Contents
25.1 Introduction ......................
25.2 General Case ...................... 255
25.2.1 Epidemiology ................. 255
25.2.2 Physiopathology ............... 256
25.2.3 Risk Factors .................. 257
25.2.4 Microbiology ................. 257
25.2.5 Clinical Presentation ............. 257
25.2.6 Diagnosis ................... 258
25.2.7 Histological Findings ............ 258
25.2.8 Outcome and Treatment ........... 259
25.3 Syphilitic Aortitis ................... 259
25.3.1 Epidemiology ................. 259
25.3.2 Physiopathology ............... 259
25.3.3 Clinical Presentation ............. 260
25.3.4 Diagnosis ................... 260
25.3.5 Complications and Prognosis ........ 260
25.3.6 Treatment ................... 260
25.4 Aortitis due to Salmonella .............. 261
25.4.1 Epidemiology ................. 261
25.4.2 Physiopathology and Risk Factors .....261
25.4.3 Clinical Features ............... 261
25.4.4 Diagnosis ................... 261
25.4.5 Prognosis and Treatment .......... 262
25.5 Tuberculous Aortitis ..................262
25.5.1 Epidemiology ................. 262
25.5.2 Physiopathology ............... 262
25.5.3 Presentation .................. 262
25.5.4 Prognosis and Treatment .......... 263
255
25.1 Introduction
The infectious attacks of the thoracic aorta remain a
rare disease. They are characterized by an endarteritis
of infectious origin generally followed by the formation
of an aneurysm commonly called mycotic aneurysm.
The adjective ªmycoticº can be a source of confusion. It
could suggest a fungal nature of the aneurysm, whereas
bacteria represent the majority of the causes of these
infections. This term was introduced by Osler [1] in
1885 to describe an infectious vascular aneurysm taking
the aspect of a ªfresh mushroomº in a patient suffering
from an infectious endocarditis. It should be understood as indicating any vascular aneurysmal formation
of infectious origin.
Before the era of antibiotics, the diagnosis was generally made by autopsy and 86% of the cases were secondary to an infectious endocarditis [2], syphilis excluded. Currently the causes are varied. Each aetiology
has particular characteristics with physiopathological,
clinical and therapeutic aspects. It is thus currently difficult to regard the infectious attack of the thoracic aorta as a single pathology. It should rather be seen like a
collection of different diseases having the same anatomical tropism. Certain causes have a very particular importance, like syphilis, salmonellosis or tuberculosis in
addition to the traditional pathogenic bacteria like Sta-
phylococcus aureus or Streptococcus, and will thus be
studied separately.
25.2 General Case
25.2.1 Epidemiology
These infections are currently rare. In an autopsic series
reporting 22,000 cases realized in Boston between 1902
and 1951, mycotic aneurysms (thoracic and abdominal)
accounted for 2.6% of all thoracic aneurysms, themselves being rare (1.5% of the patients) [3]. In another
study (20,000 autopsies) of the Mayo Clinic conducted
between 1925 and 1954 [4], only six of 178 aortic aneurysms found were of infectious origin. The analysis of
four more recent series (between 1946 and 1975) [5±8]
found 78 cases of mycotic aortic aneurysms. Lastly, a
retrospective study of the Mayo Clinic found between
1976 and 1999 [9] 29 cases of aortic infectious aneurysms, nine of them involving the thoracic aorta and 20
the abdominal aorta. There is a male prevalence in
these affections with a sex ratio of 3 : 1. This must undoubtedly be linked to the significant role that atherosclerosis plays in the genesis of these infections. Athero-
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V. Infections
sclerosis is indeed more frequent in men than in women [10]. The average age of occurrence is 65 years old
[11±13]. In the particular context of infectious endocarditis, the average age is lower (40 years old) and there
is no prevalence of gender [14].
25.2.2 Physiopathology
Four principal mechanisms are found [15]:
1. Secondary aneurysm with the embolism of the vasa
vasorum by the germ in question
2. Arterial infection of the intima injured at the time of
a bacteremia
3. Traumatism of the arterial wall with direct contamination
4. Infection of the vascular wall by extension of a contiguous infectious site.
The infectious attack of the arterial wall leads to an
endarteritis, generally followed by the formation of an
aneurysm or a false aneurysm. These aneurysms will
generally have a saccular aspect but can also appear fusiform or cupular. The first mechanism of contamination of the arterial wall occurs in particular in the case
of infectious endocarditis. The contaminant source is
then the valvular vegetation. The germ disseminates
in a haematogenous way, embolizes the vasa vasorum
and is fixed in the arterial media [14]. An infection
appears right inside the arterial wall, which extends in
a centrifugal way. The result is major vascular brittleness and the development of an aneurysm with a considerable risk of rupture. It is the same physiopathological mechanism in tuberculosis and especially in syphilis.
The second mechanism involves directly the pre-
viously injured arterial wall. The normal intima of the
aorta is very resistant to infection, but when it is damaged, infection is likely to develop there. The risk factors of this type of attack are primarily represented by
the atherosclerosis with or without an aneurysm, and
the intraluminal thrombi. Secondary infections of a preexisting aneurysm are most commonly found in the abdominal aorta (70%), but 30% of them concern aneurysms of the thoracic aorta (15% for the ascending aorta and 15% for the thoracic descending aorta) [14].
Thus, the intima is the first arterial zone involved in
the development of the infection of the interior towards
the depth of the vascular wall leading to a thinning of
this wall and thus to weakness. The germs in question
are classically represented by the germs responsible for
infectious endocarditis, the physiopathology of these
two infections being very similar. Moreover, salmonellas
too are very often found in this type of attack.
In infectious endocarditis, one can see these two
mechanisms of aortic attack. More than 70% of mycotic
aneurysms found within this pathology concern the
proximal part of the thoracic aorta [14]. They are
caused by the embolism of the vasa vasorum but can
also develop while profiting from an injured zone of the
aortic intimae and in particular on the supravalvular
level where the arterial wall can be deteriorated by the
infective flow of blood [16]. These aneurysms are then
of small volume and cupular. In parallel, the physiopathology of infectious endocarditis, with an increased
susceptibility in the event of preexisting valvular lesions, is very close to the superinfection of atherosclerotic aneurysms and it is easily understood that a germ
which was fixed at the level of an injured cardiac valve
can also be fixed at an atherosclerotic aneurysm. Lastly,
another mechanism of the aortic attack within the
framework of this pathology is the attack of the proximal aorta by the extension of the valvular infection.
The acquired lesions of the aorta are thus a factor of
risk of superinfection. Certain congenital lesions can
also be to blame. Coarctation of the aorta can indeed
be the seat of an endarteritis with a mycotic aneurysm
developing just above the stenosis [17]. This aneurysm
is then of small volume, of saccular aspect and generally develops on the left edge of the aorta [14].
Traumatisms of the thoracic aortic wall leading to
an infection are rare. They generally occur in an iatrogenic context (arterial catheterization, surgery) and can
in this case involve nosocomial germs. Injuries caused
by knives and firearms can also be involved but they remain an exceptional cause of aortitis.
Attacks of the aortic wall by a neighbouring infectious site are more frequent. The causes are mainly thoracic osteomyelitis, pulmonary infections and mediastinitis. The aortic wall is then eroded with an infection
developing from outside the artery towards the luminal
canal and a major risk of arterial rupture.
Apart from these four large physiopathological
mechanisms, two other contexts are to be mentioned.
Firstly, cases of prosthetic superinfection of material
of the thoracic aorta. These cases are outside the field
of infectious aortitis and will not be treated here.
Secondly, real immunological attacks of arteries following an infectious episode are possible, in particular
on the level of small arteries. In the thoracic aorta,
these postinfectious arteritis remain controversial. However, this type of attack can be found in poststreptococcic acute rheumatoid arthritis. In this pathology, one
can indeed in rare cases see an endarteritis of the thoracic aorta resulting in an arterial attack of the media,
with oedema and leucocytic infiltrate, also able to affect
the adventitia and the vasa vasorum. Aneurysm is, in
this context, exceptional. The arterial attack is here of
immunological origin with a certain antigenic proximity between the Streptococcus and the arterial media. It
is followed by an immune reaction directed against the
components of the arterial wall leading to endarteritis
[16].
M. Revest, P. Jgo Chapter 25 Thoracic Infectious Aortitis
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25.2.3 Risk Factors
The risk factors are mainly marked by those of atherosclerosis: male sex, age, tobacco smokers, hypertension,
diabetes mellitus, dyslipidemia [9, 11, 12]. Congenital
anomalies of the aorta (coarctation of the aorta, ductus
arteriosus) also represent risky situations [14]. The immune statute of the patient also seems to play a role
with probably an increased risk in the event of immune
system depression mainly caused by diabetes mellitus,
treatments (corticosteroids, immunosuppressive treatments) or haematological malignancies. Infection by
the human immunodeficiency virus (HIV) does not
seem to represent a risk of infectious aortitis. In fact,
the major risk factor is atherosclerosis and therefore
concerns patients over 45 years old. Patients suffering
from HIV are frequently younger, without any atherosclerotic arteries. However, the HIV infection and the
therapeutic treatment necessary for its control are
probably responsible for vascular attacks of atherosclerotic origin [18]. This coupled with the lengthening of
lifespan in the event of HIV seropositivity could, in the
future, favour the emergence of infectious aortitis in
this context.
25.2.4 Microbiology
Before the era of antibiotics, the most common germs
were Streptococcus and syphilis [19]. Since the introduction of antibiotics and their significant use, the nature
of responsive germs has changed. Currently, the commonest bacteria in the thoracic aortitis are the grampositive cocci which occur in 60% of cases (Table 25.1).
Among them, Staphylococcus aureus represents, accord-
ing to studies, between 30 and 50% of all aortitis cases.
Streptococcus is the second commonest bacterium
found. It is frequently associated with infective endocarditis. In such a situation, the proximal aorta is frequently involved. Then come Enterococcus and Strepto-
coccus pneumoniae [20±22]. Gram-negative bacilli are
also frequent (between 20 and 40% of the cases according to the studies) [9, 11±14, 23±26]. Among the gramnegative bacilli, salmonellas are the commonest kind in
the aorta in general. They often affect the abdominal
aorta and less frequently the thoracic aorta (12%) [9].
In the same way, some cases (nine) of infection by
Campylobacter fetus have been reported but they concern mainly the abdominal aorta [27±31]. With this
germ we notice a fast increase in the size of the aneurysm. These infections generally occur on immunodepressed grounds, and associations with neoplasia and
especially with digestive neoplasia are often noted [32,
33]. Infection by mycobacteria can also occur and will
be detailed in Sect. 25.5.
Table 25.1. Clinical and microbiological characteristics of tho-
racic aortitis
Data Results
Sex ratio men/women
General case 3 :1
Infectious endocarditis 1: 1
Mean age
General case 65 years old
Infective endocarditis 40 years old
Risk factor Atherosclerosis
Smoking
Diabetes mellitus
Hypertension
Hyperlipidemia
Immunodepression
Diabetes mellitus
Corticoids
Malignancy
Symptoms Fever (70%)
Pains
Dorsal and thoracic (60%)
Abdominal (20%)
Chills
Compressive signs: dyspnea,
dysphagia, changing voice,
vena cava superior syndrome
Microorganisms Gram-positive (60%)
Staphylococcus aureus
(30±50%)
Streptococcus
Streptococcus pneumoniae
Enterococcus
Gram-negative (20±40%)
Many other germs were occasionally described in
isolated case reports (Listeria monocytogenes [34], Clos-
tridium septicum [35], Pasteurella multicoda [36], Haemophilus influenzae [37], Brucella melitensis [38], Nocardia asterodes [39], Burkholderia pseudomallei [40]).
Finally, fungal aortic attack is seldom due to Candi-
da, Aspergillus, Cryptococcus and paracoccidioidomyco-
sis. It occurs in a context of disseminated fungal infection associated, in the cases of aspergillosis or paracoccidioidomycosis, with a preexisting pulmonary fungal
infection [11, 14, 41].
25.2.5 Clinical Presentation
The clinical signs are not very specific. Diagnoses are
therefore often delayed. Fever is the most constant sign
(70%). Shoulder, dorsal or thoracic pains are often
present (60%). Abdominal pains may also be noticed
(20%). Shivering can be the sign of a persistent bacteraemia and secondary infectious locations are possible
by septical embolisms [9, 11, 12]. Compressive signs are
present in the event of large aneurysms and their character depends on the location of this aneurysm: dyspha-
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