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L. Labrousse et al. Chapter 26 Is There a Place for Endovascular Treatment in Thoracic or Thoraco-abdominal Mycotic Aneurysms?
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269
not confirmed by the last series from Hsu et al. [18],
with no death among 14 consecutive patients.
26.3 Endovascular Strategy
Long-term biological monitoring usually involves
measurement of the white cell count, erythrocyte sedimentation rate and C-reactive protein level as these are
regarded as sensitive indicators for the presence of infection. Our own method as well as that of others [20]
is to stop the antibiotherapy after at least three consecutive months with strictly normal biological monitoring.
To conclude, clinical, biological and imaging followup lifelong seems reasonable and should include at least
quarterly biological examinations, and an imaging examination yearly. MRI or a computed tomography (CT)
scan is usually advocated [16, 19], but one can also use
a labeled white blood cell scan with gallium-67 isotope,
which seems to distinguish reliably between seroma/hematoma and adjacent infection, and so excludes recurrence of the infection [25].
The development of the endovascular treatment of thoracic aneurysm, which has shown, since the middle of
the 1990s, good results even in challenging situations
[26], explains that the endoluminal technique appears
to be very attractive in this clinical setting. Moreover,
results of open-chest surgical series (Table 26.1) are not
yet satisfactory in term of morbidity and mortality.
Lastly, these series are from teams known to be ªleadersº in the thoracic surgery field. In other places, these
patients are basically either contraindicated for surgery,
or results are not good enough to be published.
The main problem facing the endovascular approach
is that extensive excision and debridement of the infected field, which are part of the surgical strategy, are
impossible to perform. So, the potential benefit due to
this minimally invasive approach has to be compared
with the obvious higher risk of recurrence of the infection. However, there are an increasing number of cases
Table 26.2. Results of endovascular stent-graft placement for thoracic mycotic aneurysms
Number
of patients
Organism Follow-up
Semba et al. [27] 3 Proteus mirabilis
Clostridium septicum
Unknown
Madhavan et al. [28] 1 Staphylococcus 12 months alive
Kinney et al. [29] 1 Escherichia coli 10 months died (NR*)
Kråmer et al. [30] 4 Escherichia coli
Staphylococcus epidermitis
Staphylococcus aureus
Staphylococcus aureus
Lepore et al. [31] 3 Staphylococcus aureus Alive. Follow-up < 3years
Ishida et al. [32] 1 Staphylococcus aureus 2 days died (R**)
Stanley et al. [33] 4 Streptococcus
Staphylococcus aureus
Enterococcus
Streptococcus pneumoniae
Bell et al. [34] 1 Staphylococcus aureus 15 months alive
Lamme et al. [35] 2 Clostridium/Salmonella 27 months alive
Stoica et al. [36] 1 Salmonella 24 months alive
Krohg-Sorensen et al. [37] 3 Staphylococcus aureus
Streptococcus empyema
Streptococcus
Ting et al. [38] 1 Salmonella 12 months alive
Nishimoto et al. [39] 1 Salmonella 12 months alive
Kotzampassakis et al. [40] 1 Salmonella 6 months alive
Jones et al. [2] 9 Salmonella (n=2)
Strptococcus pneumoniae
Unknown (n=6)
Total 36 4 deaths (R)
25 months died (NR*)
24 months alive
4 months alive
34 months alive
3 months alive
12 months alive
7 months alive
12 months alive
15 months alive
10 months alive
1 month died (R**)
15 months alive
18 months alive
11 days died (NR)
2 deaths (R) at 5 and 62 months
2 deaths (NR)
Follow-up: 11 months (1±62)
NR death not related to the aneurysm or to the endoprosthesis, R death related to failed endovascular treatment
270
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V. Infections
Fig. 26.1. Preoperative angiogram of a tuberculosis mycotic an-
eurysm of the descending aorta (68-year-old patient hospitalized for hemoptysis)
and small series reported in the literature [2, 27±39]
with encouraging results (Table 26.2). All of the patients
involved were usually contraindicated for classic openchest surgery; with a very short life expectancy.
The first issue to be raised here is that of imaging.
Because secondary infection of the arterial wall can
arise anywhere it is recommended to perform a thoraco-abdomino-pelvic angio CT scan. This technique is
now possible with recent multidetector row CT in a single contrast bolus and in single breath hold. Triphasic
CT should be used because late enhancement of the arterial wall will help to diagnose inflammatory or in-
fected aortic wall, as well as end-organ damage in the
case of infective embolism. Jones et al. [2] reported on
one early death related to a misdiagnosed remote false
aneurysm. Magnetic resonance angiography can be
used, but caution should be applied when interpreting
images because calcifications are not visualized and
spatial resolution is less optimal; thus, the relation to
side branches can be misinterpreted.
Care should also be taken to carefully assess the access site at preoperative or perioperative angiography
because these patients can have narrow and calcified
native arteries, and complications during endograft delivery can be of concern.
The bacteria involved are similar to those found in
surgical series. Even tuberculosis aneurysms have been
reported to be successfully treated by an endovascular
approach [41]. Figures 26.1 and 26.2 show a similar example of a tuberculosis thoracic mycotic aneurysm
treated with a Talent (Medtronic, Minneapolis, USA)
endoprosthesis.
The mortality rate of the patients in the reported
cases is inferior to surgical rates. Note that the two ªunrelated to the endovascular treatmentº deaths were due
to cardiac disease. And even if there is bias in the fact
that usually only successful procedures are reported, the
same bias exists in surgical results. In terms of morbidity, and as for the other endovascular indications, stentgrafts avoid full heparinization, aortic cross clamping,
distal ischemia and the use of a shunt. All these aspects
lead to a theoretically less aggressive surgery with earlier extubation, better perioperative hemodynamic state
with less organ(s) failure and neurological complications [31]. However renal failure [28, 33], ischemic colitis [28, 33] and paraplegia [28] have been reported. The
deployment of the device is without any specific aspect,
although a perioperative rupture [2], a migration [33]
and a malpositioning with a type I endoleak [2] have
been described.
Fig. 26.2. Postoperative computed tomography scan with perfect exclusion of the tuberculosis aneurysm
L. Labrousse et al. Chapter 26 Is There a Place for Endovascular Treatment in Thoracic or Thoraco-abdominal Mycotic Aneurysms?
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271
Owing to the usually limited or sacciform aspect of
mycotic aneurysms, the endovascular approach can be
useful in paravisceral localization; and to deal with visceral perfusion, fenestrated stents [28, 29, 33, 41] are
advocated.
Lastly, as for surgery, different types of devices are
recommended. Some authors use homemade devices
with Z Gianturco stents covered by an autologous arterial wall [28], but the simplest and theoretically most
efficient method seems to use a commercial device with
a Rifampicin- or vancomycin-soaked graft [33] (the
antibiotherapy is injected perioperatively into the delivery system). Different devices have been used successfully, including the Talent and the Aneurx (Medtronic),
the Cook thoracic and the TAG excluder (Gore). The
fabric is either polyester or polytetrafluoroethylene
(PTFE) and the metal is nitinol or surgical stainless
steel. The possible higher resistance of PTFE to infection has been suggested but the available literature reported here is not sufficient to advocate one device over
the other [42].
The stent-graft should be selected for availability,
size and conformability to the lesion to be covered.
Covering at least 2 cm above and below the arterial wall
disruption should be advocated. In fact, enough security margins should be reserved because the likelihood
of a more extended arterial lesion is always high in this
setting.
The main limitation of this literature review is the
limited follow-up with a mean delay around 1 year. At
that time, it is obviously too early to say that patients
are cured; even if in some cases imaging controls have
shown reduction of the aneurysm sac size [34, 39]. The
issue of the duration of systemic antibiotherapy is unclear. On one hand, it is recognized that even if mycotic
aneurysms are an infectious disease, when debridement
tissues are cultured 25% of them do not show any bacterial growth [2]. Moreover, negative blood cultures are
frequent at the time of treatment. In the literature the
largest series comprising nine patients is of interest regarding this issue. Antibiotherapy was not used at all in
two cases and relatively short treatment was administered for the rest (up to 6 weeks) with no evidence of
reinfection. In most series treatment for 6-months was
performed [33, 36, 38, 40, 41]. In our opinion prolonged
antibiotherapy seems reasonable but could be tailored
to the general condition of the patient and to the results
of blood cultures.
It is also very important to follow these patients lifelong. We suggest a protocol combining an annual angio
CT scan and a lateral and postero-anterior chest radiograph to verify the position and integrity of the stentgraft. Strict long-term biological monitoring is also
needed as a function of the patient condition.
26.4 Conclusion
Owing mainly to the rarity of the condition, this literature review is unable to conclude from a scientific point
of view on the exact place of endovascular treatment
for thoracic mycotic aneurysms.
However, endovascular treatment appears to be associated with morbidity and mortality rates similar to or
below those of open surgery [43]. Associated with an
Fig. 26.3. Proposed medical strategy
for treatment of thoracic mycotic
aneurysms
272
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V. Infections
aggressive and long-term antibiotherapy, it seems reasonable to conclude that in the case of good anatomical
conditions, midterm control of the disease is possible.
So, a theoretical strategy can be proposed (Fig. 26.3)
with three situations for the endovascular treatment:
destination therapy, final therapy or bridge for surgery.
If patients are not eligible for open-chest surgery
(usually because of comorbidities), the endovascular
approach is the only way to palliate rupture and death.
For other patients, the endovascular option might be
proposed either as a bridge in the case of temporary
surgical contraindication or as a first ªlow-riskº surgical step with following strict monitoring. In this last
case, the efficiency and the availability of long-term oral
antibiotherapy and anatomical criteria (especially the
landing zone) might be two of the main criteria of selection.
As surgical and radiologist teams are waiting for
more data to optimize the strategy for treatment of thoracic mycotic aneurysms, an international registry
seems necessary to confirm the long-term results of the
endovascular treatment [42]. Because this review has
shown at least equivalence if not superiority of the endovascular approach, we propose treating all anatomically suitable patients using stent-grafts and performing
close and prolonged follow-up while in the meantime
all consecutive patients could be entered in this registry.
It is thus likely that enough data could be obtained to
support or contraindicate this strategy.
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570.
Intramural Aortic Hematoma
https://t.me/med1917
and Aortic Ulcers, Physiopathology
and Natural History
Isidre Vilacosta, JoaquÌn FerreirÕs, Ana Bustos,
Jos Alberto San Romn, Paloma Aragoncillo
Contents
Chapter
27
27.1 Introduction ......................
27.2 Intramural Aortic Hematoma ............. 277
27.2.1 Physiopathology ............... 277
27.2.2 Vasa vasorum .................278
27.2.3 PAU Versus Rupture of Vasa Vasorum . . 278
27.2.4 Absence of Entrance Tear .......... 279
27.2.5 Intraparietal Hemorrhage .......... 279
27.2.6 Classification ................. 281
27.3 Natural History ..................... 281
27.4 Penetrating Aortic Ulcers ...............284
27.4.1 Physiopathology ............... 284
27.4.2 Natural History ................ 284
277
27.1 Introduction
Intramural aortic hematoma (IAH) and penetrating aortic ulcers (PAU) are part of the so-called acute aortic
syndrome (AAS). This new cardiovascular syndrome
embraces a heterogeneous group of patients with a similar clinical profile that includes classic aortic dissection, IAH and PAU (Fig. 27.1) [1]. The physiopathological mechanism that precipitates the appearance of each
of these entities is different and the natural history of
the last two aortic lesions is not well known. Currently,
we know that IAH in some patients may evolve into an
aortic dissection, that many cases with PAU are accompanied by some degree of intramural hemorrhage, and
that occasionally PAU may act as the entrance tear of an
aortic dissection (Fig. 27.1) [1±3]. In addition, some patients may exhibit several or all of these lesions. Is,
therefore evident, the existence of a link between them.
In this chapter the physiopathology and natural history
(evolutive patterns) of IAH and PAU are discussed.
Fig. 27.1. The three elements that constitute the acute aortic
syndrome (AAS) are depicted. Ar rows indicate the possible
progression of each of these aortic lesions
27.2 Intramural Aortic Hematoma
27.2.1 Physiopathology
IAH was described by Krukenberg [4] in 1920 as a ªdissection without intimal tear.º IAH has been defined as a
novel variant of classic aortic dissection characterized
by the absence of an entrance tear. It is, therefore, a
noncommunicating type of dissection (Fig. 27.2) [5].
Here, the false lumen is created by a hemorrhage into
the aortic media, most likely after rhexis of the vasa vasorum that penetrate the outer half of the aortic media
from the adventitia and arborize at this level.
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VI. Aortic Hematoma and Ulcers
ab
Fig. 27.2. Autopsy specimen of type A intramural aortic hematoma (IAH)(asterisk). Transversal (a) and longitudinal (b) sections.
Notice the absence of an entrance tear
27.2.2 Vasa vasorum
In normal circumstances, the intima and the inner part
of the aortic media are avascular. It is important to
point out that the vasa vasorum are present in the medial layer only when this layer has more than 29 lamellar units and, in such cases, they will only be found in
the region of the medial layer that is beyond these 29
units [6]. The region of the medial layer corresponding
to the 29 subintimal units is an avascular area and one
may presume that the nutrients flow via transintimal
diffusion from the aortic lumen. Therefore, we may say
that the thoracic aorta has a double, yet precarious,
means of nutrient delivery: the adventitia and the outer
third of the medial layer depend on the vasa vasorum,
while the intima and the inner third of the medial layer
are nourished via diffusion [6]. Accordingly, the middle
third of the medial layer, where degenerative changes
are most frequently seen [7], will nutritionally depend
on both sources [7]. Clarke [8] described the aortic wall
vasa vasorum being distributed so as to form a deep
and superficial plexus. The vessels of the superficial
plexus are arterioles 80±100 lm in diameter and they
lie at the junction of the media and the adventitia; this
superficial plexus leads to a deep plexus of vessels
where small tortuous arterioles 10±20 lm in diameter
penetrate into the medial layer and arborize in its two
outer thirds [8]. Medial vasa vasorum have a larger role
in nourishment of the aorta in aortic atherosclerosis, as
blood flow through the vasa vasorum in the outer layers
of the aortic wall is increased [9]. It appears that increased blood flow in the atherosclerotic aorta cannot
be accounted for by dilatation of the existing vasa vasorum and must be produced by proliferation of new
vessels in the aortic wall [9]. The morphology and
structure of these new vessels differs from that of normal vasa vasorum [10]. Thus, the effectiveness and contribution of these new vasa vasorum to nourishment of
the aorta is not well known. Proliferation of these vasa
in the atherosclerotic aorta could have unfavorable effects and, in fact, some authors think that these vessel
abnormalities may be involved in the pathogenesis of
IAH [11].
The development of an IAH may not only be attrib-
uted to the spontaneous rupture of ªsickº vasa vasorum, it can also be the result of a traumatic rupture of
ªhealthyº vasa vasorum during a traumatism of the aortic wall [12, 13, 14]. A medial hemorrhage secondary to
a fracture of an atherosclerotic plaque may also lead to
an IAH [3, 5, 15].
27.2.3 PAU Versus Rupture of Vasa Vasorum
Although these aortic lesions (IAH and PAU) are physiopathologically different, in some cases it may be difficult to differentiate between them. Mohr-Kahaly et al.
[5] identified 15 patients with IAH by transesophageal
echocardiography (TEE) and analyzed the amount of
aortic atherosclerosis of these patients. Atherosclerotic
lesions were detected in 11 patients (mild in eight,
moderate in two, and severe in one); there were no atherosclerotic plaques in the remaining four patients. Accordingly, these authors divided IAH in two physiopathologically different groups: patients with mild aortic atherosclerosis or without aortic atherosclerosis
would have had a rupture of the vasa vasorum, whereas
in those with severe atherosclerosis a complication of
an atherosclerotic plaque was the most likely cause of
IAH. This concept is shared by Sheldon et al. [15], who
studied 20 patients with IAH identified by TEE; they
also had two groups, one with moderate or severe
atherosclerosis and another with mild atherosclerosis or
without atherosclerosis. Patients from the first group
were older and had coronary and peripheral vascular
disease more frequently than the others. Sheldon et al.
I. Vilacosta et al. Chapter 27 Intramural Aortic Hematoma and Aortic Ulcers, Physiopathology and Natural History
https://t.me/med1917
attributed the origin of IAH associated with severe
atherosclerosis to intimal atherosclerotic complications
(atherosclerotic plaque rupture or PAU). The work of
Sueyoshi et al. [16] supports the existence of a link between PAU and IAH. These investigators studied retrospectively 32 patients with IAH and they could identify
the existence of PAU at hospital admission or at followup in 21 cases. When IAH originates from a complicated atherosclerotic plaque, the ulcerated aortic plaque
behaves like an intimal tear.
279
27.2.4 Absence of Entrance Tear
In the literature [17, 18] and in our own experience,
some patients with AAS have been initially diagnosed
of IAH, and later, at surgery, a tiny intimomedial entrance tear with a clotted false lumen has been identified (Figs. 27.3, 27.4). In these cases, the false channel
not been decompressed by a reentrance tear and an immediate thrombosis of the false lumen occurred; consequently there would be no possibility of detecting flow
within the aortic wall. These observations raise the
question of the diagnostic accuracy of noninvasive
imaging techniques to detect the intimomedial tear,
which is considered a critical criterion to differentiate
classic ªdouble channel aortaº from IAH. The fact is
that some small entrance tears will not be visualized by
current imaging modalities. One may also speculate
that because of the rapid morphologic evolution of
IAH, the tear found at surgery may have occurred as a
decompression mechanism after admission of patients
and the diagnostic imaging.
Fig. 27.4. Histological section (Mason's technique) of the as-
cending aorta of the patient from Fig. 27.3. Notice the existence of a small entrance tear (arrow)
If we take all these considerations into account, one
may say that the distinctive event in IAH is the existence of a noncommunicating dissection. In our opinion, for an IAH to develop, it is important that a reentrance tear is absent. The entrance tear can be absent
or, if present, it must be very small [19].
27.2.5 Intraparietal Hemorrhage
IAH has also been documented at autopsy. Necropsy series have demonstrated that in some patients (5±13%)
with dissection the entrance tear is not evident [20±22].
On histologic analysis, a hematoma disrupting the aortic media is well documented (Fig. 27.5). In our experience, this hematoma is most often intramedial, but occasionally it is subadventitial (between the media and
the adventitia). A subadventitial hematoma might have
a greater risk of aortic rupture.
This intramedial or subadventitial hemorrhage results in a circumferentially oriented blood-containing
Fig. 27.3. Computed tomography of a patient with an AAS who
was first diagnosed of having an IAH, axial section. Notice a
clear thickening of the wall of the ascending aorta. No entrance
tear nor flow within the aortic wall could be detected
Fig. 27.5. Histological section (Mason's technique) of a patient
with IAH. Splitting of the aortic media by a hematoma (asterisk) is clearly seen. Notice also a dysplastic arteriole with a
hemorrhage inside
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VI. Aortic Hematoma and Ulcers
Fig. 27.6. Computed tomography (CT) of a patient with an IAH
located in the ascending aorta without and with contrast medium. There is a circular high-attenuation area along the aortic
wall without contrast, and notice that there is no enhancement
of the aortic wall after contrast medium administration
space seen in echotomographic imaging studies (Fig.
27.6). Because there is no entrance tear, the intramedial
hematoma does not communicate directly with the aortic lumen and, unlike the false lumen of classic aortic
dissection, the presence of flow (color Doppler imaging
on TEE) within the hematoma is not seen. For the same
reason, this thickened aortic wall does not generally
show enhancement with contrast administration on
computed tomographic scanning (CT), MRI and angiography.
TEE may identify in many patients with IAH small
echolucent zones within the aortic wall thickening.
Sixty-seven percent of patients of our series [2], two
thirds of patients from the series of Mohr-Kahaly et al.
[5] and 19 out of 23 out aortic segments from the series
of Harris et al. [23] presented with echo-free spaces
within the aortic thickening; when these areas are located immediately below the intimomedial flap, the dissection flap can be seen [2]. These spaces were initially
thought to represent areas of liquefaction within the intraparietal hematoma. Now, this aspect may be better
studied by MRI and CT; we have observed that these
areas correspond to pools of low blood flow that come
from the aortic lumen through tiny flap ruptures or the
ostia of the intercostal or lumbar arteries that have been
severed by the dissecting hematoma (Fig. 27.7) [24].
Song et al. [25] studied the clinical significance of this
finding in patients with type B IAH. Patients were classified according to the extent of the echo-free spaces;
no differences with respect to in-hospital mortality, surgical intervention, development of an aortic dissection
or complete resolution of the IAH between those with
or without echo-free spaces were found. They concluded that the presence or development of echo-free
spaces is not a poor prognostic sign.
F
F
F
Fig. 27.7. 3D magnetic resonance angiography of a patient with
a distal IAH (left). Notice the existence of small areas of contrast medium (arrows) within the hematoma. In a 3D intravascular reconstruction of the same case (right) one may see an
intraluminal view of the descending aorta and the ostium (ar-
row) of an intercostal artery permitting flow to pass from the
aortic lumen to the IAH
I. Vilacosta et al. Chapter 27 Intramural Aortic Hematoma and Aortic Ulcers, Physiopathology and Natural History
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27.2.6 Classification
As in classic aortic dissection, patients with IAH are divided in two groups according to Stanford classification: type A, when the involved segment is the ascending aorta and type B when it is confined to the descending aorta. In the meta-analysis done by Maraj et
al., type A IAH was commoner than type B (57% type A
vs 43% type B), but in our experience type B is commoner than type A. From a surgical and prognostic
standpoint we use the following classification: if the affected segment is the ascending aorta and/or the aortic
arch ± proximal IAH; if the involved segment is the
descending aorta ± distal IAH [1].
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27.3 Natural History
One of the key features of IAH is its evolving behavior
over time; therefore, the appearance of this lesion can
be interpreted differently depending on when a diagnostic examination is performed. The clinical course of
these patients is unpredictable, and in many cases, unfavorable. Thus, it is difficult to predict a precise evolution in a particular patient. We will describe in broad
outline the evolutive patterns of patients with IAH
(Fig. 27.8). It is worth emphasizing that documentation
of progression or regression of IAH is closely related to
the timing of the evaluation.
The most worrying of all the evolutive possibilities is
the adventitial rupture and bleeding out to adjacent
structures. Increased permeability of the aortic wall
leading to a pericardial, pleural and mediastinal hemorrhage, and progression to an aortic rupture, has been
Fig. 27.8. Dynamic behavior of IAH. Arrows indicate the possi-
ble evolution of this type of acute aortic pathology
reported [2, 26]. In contrast to evolution to overt aortic
rupture, some authors have found that contained rupture from disintegration of outer layers of the aortic
media is relatively frequent (28 out of 66 patients in the
series of von Kodolitsch et al.) [26]. In some cases this
segmental noncommunicating aortic dissection can progress to a localized communicating dissection owing to
intimal disruption (Fig. 27.9) [2, 26±29].
Besides progression from IAH to communicating
dissection, some patients may exhibit both lesions in
different aortic segments at the same time, demonstrating a link between these acute aortic pathologies. The
physiopathologic mechanism that fully explains these
ªhybridº cases is unknown. Three hypothesis are plausible: (1) early and segmentary false lumen thrombosis
Fig. 27.9. MRI of a patient with a distal IAH. In the left panel
an IAH localized immediately after the ostium of the left subclavian artery is seen as a hyperintense lesion. A magnetic res-
onance angiogram of the same patient 4 months later shows a
localized small dissection (right panel)
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