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VII. Aortic Injury
Table 32.4. Comparison of mortality and paraplegia rates ac-
cording to the method of spinal cord protection. (From Von
Oppell [2])
1,492
patients
Clamp and sew 443 16 19.2
Total distal perfusion 985 15 6.1
Passive 424 12.3 11.1
Active 561 17.1 2.3
Mortality
(%)
Paraplegia
(%)
Von Oppell et al. [2]. In 1984, Mattox et al. [14] recommended the technique of simple aortic cross-clamping
without any adjunct for intraoperative management of
the traumatic injury of the descending aorta. In their
series, the rate of paraplegia was not significantly different whether CPB was used or not (4.5 vs 8.3%, respectively). This led many surgeons to believe that they
could avoid using CPB and to consider that the clampand-sew technique was as safe as the distal perfusion
technique. However, Katz et al. [15] have demonstrated
that beyond 30 min of cross-clamping without distal
perfusion, the risk of spinal cord injury dramatically increases. Therefore, considering the very significant differences in the rate of paraplegia highlighted by many
authors, there is presently an obvious trend within the
surgical community to clearly advocate the use of active
distal perfusion systems during the time of aortic repair
for acute traumatic isthmic rupture [18, 19].
To reduce the conflict between the necessary use of
distal perfusion and the increased risk linked to heparinization, it has been recommended to use heparinless
bypass systems with a centrifugal pump [2]. Heparincoated circuits could also represent a tempting alternative as they make theoretically possible the reduction or
the suppression of total heparinization. But those systems are still being evaluated and the possible risk of
thrombosis entailed by the circuits limits their indications and makes their use still controversial.
32.4.4 Endovascular Therapy
means that patients have to fulfill certain anatomic prerequisites.
In view of literature data, emergency endovascular
treatment of acute lesions appears safe and efficient,
showing encouraging early and midterm results. It is
particularity indicated in complex multitrauma patients
avoiding CPB and allowing for prompt treatment of associated lesions. But questions regarding long-term
complications and durability of stent grafts remain unanswered and long-term follow-up will therefore be necessary and allow for a definitive conclusion. So today
conventional surgical treatment remains our first choice
and endovascular treatment is proposed only for highrisk patients.
32.4.5 Medical Treatment
The concept of pharmacological treatment and medical
support of acute aortic dissection introduced by Wheat
et al. [27] in 1984 was first proposed by Aronstam et al.
[28] for the treatment of traumatic rupture of the aorta.
This attitude was confirmed by several groups in the
ensuing years [29, 30]. Walker et al. [31] in an extensive
review of the literature found 64 patients medically
treated waiting for aortic surgery. Stulz et al. [35] in
1991 did not observe any death among patients treated
in a conservative manner. Those good results associated
with the higher mortality due to the coexisting lesions
have led many surgeons to question the dogma of ªnodelayº emergency aortic repair in any case and to redefine the therapeutic priorities. Therefore, new strategies
have recently been reported for the medical and surgical management of traumatic rupture of the aorta [3, 4,
19, 32±35]. Even if most of these authors have reported
no death while waiting for the aortic repair, one cannot
consider that there is no risk as Maggisano et al. [35]
reported two deaths as a result of aortic rupture within
72 h of admission to an intensive care unit [35]. Fortunately, this seems to be very rare because except in
cases of complete rupture the adventitia and surrounding mediastinal structures may form a solid fibrous
wall, reducing the risk of delayed rupture [31, 33, 34].
The endovascular implantation of a prosthesis has been
proposed, for around 10 years now, for the elective but
also emergent treatment of thoracic aortic rupture. It is
a less invasive technique which necessitates only a surgical or percutaneous femoral artery access, with only
light systemic heparinization (or even not in case of
contraindication). Hospital mortality appears low, from
0 to 6% [20±26]. In addition, procedure-related morbidity is lower than under conventional surgery. No paraplegia and no renal insufficiency have been reported.
But this new technique is not free of problems, i.e., access failure because of small and calcified iliac arteries,
iliac dissection and primary endovascular leaks. This
32.5 Current Therapeutic Strategy
The prevalence and the gravity of the lesions associated
with the aortic rupture (Table 32.1) in our series are in
accordance with data recently published. It is to be
noted that no patient died from hemorrhage. Six deaths
out of ten (60%) were directly related to an associated
lesion, five being possibly worsened by full heparinization during CPB: two cases of intracerebral hematoma
following a major head injury and three cases of respi-
T. Langanay et al. Chapter 32 Surgical Treatment of an Acute Isthmus Traumatic Rupture
https://t.me/med1917
Fig. 32.10. The two periods of our therapeutic
strategy
Fig. 32.11. Hospital mortality according to our
new strategy
327
ratory distress syndrome after lung contusion. The
fourth case of respiratory disease complicated the outcome of an endoprosthesis.
Considering our experience and literature data, we
decided in 1995 to modify our therapeutic strategy. Between 1976 and 1994, 43 patients (group A) were
treated according to the golden rule of ªimmediate aortic repairº and since 1995, 19 patients (group B) have
been managed taking into account associated lesions
(Fig. 32.10). Though it is always very difficult to compare different patients operated at different periods, operative mortality appears much lower, 10 vs 18.6% in
group B (Fig. 32.11). It is also to be noted that no patient died from aortic rupture in the case of delayed
aortic repair.
32.6 Proposal for a Timing Reappraisal
of Aortic Repair
In view of literature and our recent results, we are now
convinced that the best chance for patients is based on
first treating surgically the most life-threatening lesion.
This policy is summarized in Fig. 32.12. The aortic repair should be undertaken immediately if the aortic
rupture is isolated or associated with a non-life-threatening lesion. In the case of a severe life-threatening associated lesion with a stable aortic lesion, the aortic repair should be performed in a second stage after treatment or healing of the coexisting lesion. In this case,
the patient should be maintained in a surgical intensive
care unit, the aortic evolution being closely monitored
by CT scan or TEE under strict control of blood pressure and aortic wall stress through the use of betablocking therapy. In the case of unstable aortic lesion
(e.g., recurring left hemothorax or pseudocoarctation
syndrome), requiring an emergency repair despite the
presence of severe associated lesions, endovascular repair represents the technique of choice today. If it does
not meet the required conditions the aortic repair
should be carried out with the use of heparinless systems such as centrifugal pumps and not by using the
clamp-and-sew technique.
328
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VII. Aortic Injury
Fig. 32.12. Algorithm representing our proposition for a modern therapeutic strategy. CPB cardiopulmonary bypass
4. Pate JW. Is traumatic rupture of the aorta misunderstood?
32.7 Conclusion
Acute traumatic rupture of the thoracic aorta is, indeed,
a life-threatening lesion which deserves surgical repair.
It is, however, generally associated with other severe
life-threatening lesions and may be hidden among
those. It, therefore, justifies early, active, exhaustive diagnostic procedures in the case of polytraumatism.
Should the patient show evidence of impending rupture
or major distal malperfusion, emergency surgical repair
is mandatory. But in some instances, surgical treatment
of the aortic rupture must be delayed under strict monitoring. This attitude allows management of other severe life-threatening lesions which, otherwise, would
deeply increase the risk of the aortic repair, and which
are responsible for the major contributor to hospital
mortality in those patients. Whatever the circumstances
of surgery, distal perfusion downstream from the aortic
cross-clamping must be maintained, using either CPB
or a heparinless centrifugal pump.
References
1. Fabian TC, Richardson JD, Croce MA, Smith JS, Rodman
G Jr, Kearney PA. Prospective study of blunt aortic injury:
multicenter trial of the American Association for the surgery of trauma. J Trauma 1996; 42:374±383.
2. Von Oppell VD, Dunne TT, De Groot MK, Zilla P. Traumatic aortic rupture: twenty year metanalysis of mortality
and risk of paraplegia. Ann Thorac Surg 1994; 58:585±
593.
3. Kipfer B, Leupi F, Schuepach P, Friedli D, Althaus U.
Acute traumatic rupture of the thoracic aorta immediate
or delayed surgical repair? Eur J Cardiothorac Surg 1994;
8:30±33.
Ann Thorac Surg 1994; 57:530±531.
5. Langanay T, Verhoye JP, Corbineau H, et al. Surgica treatment of acute traumatic rupture of the thoracic aorta, a
timing reappraisal? Eur J Cardiothoracic Surg 2002;
21:282±287.
6. Kirklin JW, Barrat-Boyes BG. Acute traumatic transection.
In: Cardiac surgery. Kirklin JW, Barrat-Boyes BG, editors.
New York: Churchill Livingstone; 1993; p. 1701±1709.
7. Gandjbakhch I, Jault F, Lima L, Pavie A. Rupture traumatique de l'aorte. In: Carli P, Gandjbackch I, Jancovici R,
Ollivier JP, editors. Plaies et traumatismes du thorax.
Paris: Arnette; 1997; p. 313±323.
8. Parmley LF, Mattingly TW, Manion WC, Jahnke EJ. Nonpenetrating traumatic injury of the aorta. Circulation
1958; 17:1085±1101.
9. Merill WA, Lee RB, Hammon JW, Frist WH, Stewart JR,
Bender HW. Surgical treatment of acute traumatic tear of
the thoracic aorta. Ann Surg 1988; 207:699±706.
10. Pate JW. Traumatic rupture of the thoracic aorta: emergency operation. Ann Thorac Surg 1985; 39:531±537.
11. Williams JS, Graff JA, Uku JM, Steinig JP. Aortic injury in
vehicular trauma. Ann Thorac Surg 1994; 57:726±730.
12. Cernaianu AC, Cilley JH Jr, Baldino WA, Spence RK,
Delkassi Ad. Determinants of outcome in lesions of the
thoracic aorta in patients with multi-organ system trauma. Chest 1992; 101:331±335.
13. Kodali S, Jamieson WRE, Leia-Stephens M, Miyagishima
RT, Janusz MT, Tyers GFO. Traumatic rupture of the thoracic aorta. A 20 year review: 1969±1989. Circulation 1991;
84(Suppl III):III40±46.
14. Mattox KL, Holzman M, Pickard LR, Beall AC Jr, De Bakey ME. Clamp/repair: a safe technique for treatment of
blunt injury to the descending thoracic aorta. Ann Thorac
Surg 1985; 40:456±463.
15. Katz NM, Blackstone EH, Kirklin JW, Karp RB. Incremental risk factors for spinal cord injury following operation
for acute traumatic aortic transection. J Thorac Cardiovasc Surg 1981; 81:669±674.
16. Nicolosi AC, Almassi HG, Bousamra M II, Haasler GB,
Olinger GN. Mortality and neurologic morbidity after repair of traumatic aortic disruption. Ann Thorac Surg
1996; 61:875±878.
T. Langanay et al. Chapter 32 Surgical Treatment of an Acute Isthmus Traumatic Rupture
https://t.me/med1917
329
17. Zeiger MA, Clark DE, Morton JR. Reappraisal of surgical
treatment of traumatic transection of the thoracic aorta. J
Cardiovasc Surg 1990; 31:607±610.
18. Read RA, Moore EE, Moore FA, Haenel JB. Partial left
heart bypass for thoracic aorta repair. Survival without
paraplegia. Arch Surg 1993; 128:746.
19. Pate JW, Fabian TC, Walker WA. Acute traumatic rupture
of the aortic isthmus: repair with cardiopulmonary bypass. Ann Thorac Surg 1995; 59:90±99.
20. Rousseau H, Soula P, Perreault P, et al. Delayed treatment
of traumatic rupture of the thoracic aorta with endoluminal covered stent. Circulation 1999; 99:498±504.
21. Meites G, Conil C, Rousseau H, et al. Place des endoprothses dans le traitement des ruptures traumatiques de
l'aorte thoracique. Ann Fr Anesth Reanim. In press 2005.
22. Duham MB, Zygun D, Petrasek P, et al. Endovascular stent
grafts for acute blunt aortic injury. J Trauma 2004;
56:1173±1178.
23. Doss M, Balzer J, Martens S, et al. Surgical vs endovascular treatment of acute thoracic aortic rupture: a singlecenter experience. Ann Thorac Surg 2003; 76:1465±1470
24. Iannelli G, Piscione F, Di Tommaso L, Monaco M, Chiariello M, Spampinato N. Thoracic aortic emergencies: impact of endovascular surgery. Ann Thorac Surg 2004; 77:
591±596.
25. Richeux L, Dambrin C, Marcheix B, et al. Vers une nouvelle prise en charge des ruptures traumatiques aigus de
l'isthme aortique. J Radiol 2004; 85:101±106.
26. Rousseau H, Dambrin C, Marcheix B, et al. Acute traumatic aortic rupture: a comparison of surgical and stentgraft repair. J Thorac Cardiovasc Surg 2005; 129:1050±
1055.
27. Wheat MW, Palmer RF, Bartley TD, Seelman RC. Treatment of dissecting aneurysms of the aorta without surgery. J Thorac Cardiovasc Surg 1965; 50:364±373.
28. Aronstam EM, Gomez AC, O'Connell TJ, Geiger JP. Recent
surgical and pharmacological experience with acute dissecting and traumatic aneurysms. J Thorac Cardiovasc
Surg 1970; 59:231±238.
29. Akins CW, Buckley MJ, Daggett W, Mellduff JB, Austen
WG. Acute traumatic disruption of the thoracic aorta: a
ten year experience. Ann Thorac Surg 1981; 31:305±309.
30. Svensson LG, Antunes MJ, Kinsley RH. Traumatic rupture
of the thoracic aorta. A report of 14 cases and a review of
the literature. S Afr Med J 1985; 67:853±857.
31. Walker WA, Pate JW. Medical management of acute traumatic rupture of the aorta. Ann Thorac Surg 1990;
50:965±967.
32. Stulz P, Reymond MA, Bertschmann W, Graedel E. Decision making aspects in the timing of surgical intervention
in aortic rupture. Eur J Cardiothorac Surg 1991; 5:623±
627.
33. Galli R, Pacini D, Di Bartolomeo R, Fattori R, Turinetto
B, Grillone G, Pierangeli A. Surgical indications and timing of repair of traumatic ruptures of the thoracic aorta.
Ann Thorac Surg 1998; 65:461±464.
34. Lee RB, Stahlman GC, Sharp KW. Treatment priorities in
patients with traumatic rupture of the thoracic aorta. Am
Surg 1992; 58:37±43.
35. Maggisano R, Nathens A, Alexandrova NA, Cina C, Boulanger B, McKenzie R, Harrison AW. Traumatic rupture of
the thoracic aorta: should one always operate immediately? Ann Vasc Surg 1995; 9:44±52.
Acute Traumatic Aortic Rupture:
https://t.me/med1917
Stent-Graft Repair
Herv Rousseau, Jean Phillipe Bolduc,
Camille Dambrin, Bertrand Marcheix,
Guillaume Canevet, B. Leobon, C. Cron,
Philippe Otal, Jean-Michel Bartoli, Gerard Fournial
Chapter
33
Contents
33.1 Introduction .......................
33.2 Pathophysiology ..................... 331
33.3 Conventional Treatment ................. 331
33.4 Concept of Delaying Repair ............... 332
33.5 Stent-Graft ......................... 332
33.6 Our Therapeutic Strategy ................332
33.7 Results ........................... 334
33.8 Potential Limitations ................... 336
33.9 Discussion ......................... 338
331
33.1 Introduction
For many decades, standard surgical practice has dictated that traumatic rupture of the thoracic aorta must
be diagnosed quickly and managed aggressively by immediate surgical repair. More recently, with the introduction of endoluminal aortic stent-graft therapy, a new
approach was introduced for treatment of traumatic
aortic ruptures (TAR). The goal of endovascular stenting is to provide a durable exclusion of the lesion while
minimizing the morbidity and mortality of the open
procedure. The advantages include the avoidance of
thoracotomy, possible heparinization and the likely lower risk of paraplegia.
33.2 Pathophysiology
Blunt aortic injury is relatively frequent and accounts
for up to 20% of fatal motor vehicle accidents, with extremely high prehospital mortality rates between 80 and
90% [1, 2]. Without appropriate treatment, 30% of sur-
vivors who reach the hospital die within the first 6 h
[3]. Trauma to the thoracic aorta occurs mostly as a
consequence of rapid deceleration forces. In order of
frequency, rupture occurs at the aortic isthmus, the ascending aorta, the aortic arch, the distal descending
aorta, and the abdominal aorta. Feczko et al. [4] and
Williams et al. [5] reviewed autopsies of blunt trauma
victims and found that 55±65% of injuries occurred at
the aortic isthmus and 10±14% occurred in the ascending aorta or the aortic arch.
The rapid deceleration forces that tear the aorta often lead to other organ injuries. Pate et al. [6] found
that associated injuries were present in more than 90%
of patients with aortic transection and 24% of those patients required a major operation before aortic repair.
The aortic tear may be limited to the intima or may
extend to both the intima and media or to all aortic
layers [2, 7]. In the vast majority of patients who survive the initial traumatic impact, the tear involves both
the intima and the media [2].
33.3 Conventional Treatment
Since the classic study of Parmley et al. [2] in 1958, the
extremely high death rate of patients with acute blunt
rupture of the thoracic aorta has led surgeons to repair
the aortic tear as quickly as possible. But despite advances in surgical and reanimation techniques, surgery
is still associated with significant morbidity and mortality rates [1, 8]. The overall death rate reported by
Von Oppell et al. [8] in a meta-analysis of articles including 1,492 hemodynamically stable patients who
reached the operating room was 21.3%, ranging from 0
to 54.2% depending on the study. The majority of these
deaths occurred in the postoperative period. In a more
recent review of the literature, the surgical mortality
rate ranged between 8 and 15%, depending on whether
circulatory assistance was used or not to maintain satisfactory perfusion of the distal aorta [9]. Risk factors as-
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VII. Aortic Injury
sociated with a high rate of postoperative mortality include the presence and severity of associated traumatic
lesions, preoperative shock (of which only 25% was related to aortic rupture), and coronaropathy or other
cardiac anomaly. Paraplegia is a main complication of
surgical treatment. When aortic repair is achieved without circulatory assistance, the postoperative paraplegia
rate can be as high as 19%, and this risk increases significantly when the aorta is clamped for more than
30 min [8]. With circulatory assistance, the rate is about
2% [9]. On the other hand, the systemic anticoagulation
required for the extracorporeal circulation, even at a reduced dose as with heparin-coated systems, is undesirable
in traumatic patients with multiple fractures and/or parenchymatous or cerebral lesions. Postoperative complications, including renal, pulmonary, cardiac and neurological, have been reported with rates as high as 50%.
33.4 Concept of Delaying Repair
During the early 1970s, Akins et al. [10] began to delay
the repair of blunt aortic tears in selected patients with
associated major injuries. Before the aortic repair, they
were treated with antihypertensive drugs and no rupture
of the traumatic false aneurysm was reported. Similarly,
in 1995, Pate et al. [6] reported no rupture of pseudoaneurysm of the thoracic aorta in 41 patients whose arterial pressure was maintained below 140 mmHg and who
underwent delayed repair of the aortic tear between
12 h and 24 weeks after the event. Since that time, several
studies showed, for stable and nonbleeding lesions, that
surgical mortality after aortic injury can be significantly
reduced when surgical repair is deliberately delayed [6,
10±14]. These studies support the fact that free rupture
of a contained acute traumatic tear of the thoracic aorta
is unlikely to occur under proper control of blood pressure. Therefore, it appears safe to allow patients who suffered a major trauma to be stabilized, undergo other
emergent operations if needed, and then have elective repair of the aortic tear. The satisfactory results obtained
with this management have led some authors to systematically propose delayed surgery. Although this attitude
is justified by objective data [15, 16], it is not entirely
risk-free because as many as 4% of patients awaiting surgery die of a ruptured aorta usually within 1 week of the
traumatic injury [1, 13, 17]. Current indications to delay
the aortic repair include the following: trauma to the central nervous system, contaminated wounds, respiratory
insufficiency from lung contusion or other causes, surface
burns, blunt cardiac injury (myocardial contusion), tears
of solid organs that will not undergo surgical management, retroperitoneal hematoma, age of 50 years or older,
and medical comorbidities. However, in the case of active
bleeding or obstruction of the aortic lumen, immediate
treatment has to be provided.
33.5 Stent-Graft
The advent of endovascular stent-graft technology provided a less invasive alternative to thoracic aortic injury
treatment. This substitute to open thoracic aortic replacement is attractive for several reasons: much of the
surgical morbidity is reduced, sparing thoracotomy,
aortic cross-clamping, and cardiopulmonary bypass.
Moreover, spinal cord ischemic complications are infrequent probably because the duration of medullary hypotension is significantly reduced.
Until now, the largest series of thoracic aortic stentgraft installations reported mortality and paraplegia
rates of 8.7 and 3.6%, respectively [18], knowing that
these results improved for second- and third-generation
devices [19]. Advancements in device and delivery system design, such as thinner profile and greater flexibility, have markedly improved our ability to repair aortic
abnormalities with endovascular grafts.
However, a few elements of TAR treatment with an
endovascular stent should be borne in mind. Adequate
computed tomography (CT) scan measurements of
proximal and distal diameters are needed, as well as the
length of the proximal neck. Also, sufficient femoral diameter is needed because of the relatively large introducer sheath used.
33.6 Our Therapeutic Strategy
On arrival in the intensive care unit, patients are immediately submitted to intensive resuscitation with continuous monitoring of ECG, arterial and central venous
pressures, renal function, as well as all other hemodynamic and clinical measurements. In the case of hypertension, a drug regimen of beta-blocking agents and arterial vasodilators (nitroprusside and calcium-blocking
drugs) is given in order to maintain systolic blood pressure below 120 mmHg. Once the patient is hemodynamically stable, the antihypertensive therapy is given orally. The delay and the choice of treatment are dictated
by the general conditions of the patient, the surgical
risk factors, and the type of aortic trauma.
Diagnosis and feasibility of stent-graft therapy are
evaluated by contrast-enhanced CT, and so far the endovascular option is considered for patients with a contained rupture having a proximal neck longer than
10 mm (Fig. 33.1). The stent-graft diameter is oversized
by 15% to achieve a tight seal and the length is, at least,
4 cm longer than the lesion to be treated. Usually one
straight stent-graft of 24±36-mm diameter and 80±
100 mm in length is used. The introducer caliber ranges
between 18 and 24 F (i.e., 6±7.2 mm in diameter), depending on the device available.
The endovascular procedure is performed under general anesthesia with tracheal intubation and mechanical
H. Rousseau et al. Chapter 33 Acute Traumatic Aortic Rupture: Stent-Graft Repair
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is surgically exposed and a transverse arteriotomy is
performed after giving an intravenous heparin bolus of
5,000 IU. Per procedural transesophageal echocardiography (TEE) is done to guide the stent-graft procedure
before and after deployment of the device. An initial
aortogram with a 5-F pigtail catheter introduced
through the left brachial access helps visualization of
the arterial anatomy. A 260-cm-long, 0.035 stiff guide
wire (Back up Meier, Boston) is advanced up to the aortic arch under fluoroscopic guidance. If an Excluder
(Gore) stent-graft is used, a 24-F Cook introducer
sheath is inserted. For the Talent device, the stent-graft
is contained inside the sheath which helped to insert it.
The delivery system is positioned at the preestablished
level of the aortic tear. A mean arterial pressure below
70 mmHg is maintained during implantation. The outer
sheath is slowly withdrawn to fully deploy the implant.
Thereafter, a compliant balloon is inflated to fully anchor
the stent into the proximal and distal neck of the aorta.
In our practice, the uncovered portion of the stent-
Fig. 33.1. The success of the endovascular procedure greatly de-
pends on the rigorous respect of anatomic criteria, mainly the
diameter and the length of the proximal neck, which must be
10 mm or more beneath the origin of the left subclavian artery.
Diagnosis and feasibility of stent-graft therapy are evaluated by
contrast-enhanced computed tomography (CT), with 3D recon-
structions. The stent-graft diameters are oversized by 15% to
achieve a tight seal and the length is, at least, 4 cm longer than
the lesion to be treated. The reference diameter is the diameter
of the normal aorta at the level of the left carotid artery
graft was intentionally deployed over the ostium of the
left subclavian artery because of the close proximity of
the pseudoaneurysmal sac in 17 of the 29 patients
treated without occlusion of this artery in all cases. The
origin of the left subclavian artery was intentionally
overstented in six of the 29 patients without significant
clinical consequences and therefore a carotid to subclavian artery bypass was not needed [20].
Finally, the introducer delivery system is removed
and the arteriotomy is repaired with interrupted 5-0
ventilation. Patients are put in the dorsal decubitus position. Drapes are placed to include the abdomen and
both groins in the operative field, thus permitting access to the common femoral arteries and, if needed, the
iliac arteries or the abdominal aorta. The femoral artery
polypropylene sutures after arteriographic and TEE
controls (Figs. 33.2, 33.3). Anticoagulation is maintained
for 48 h and is then followed by aspirin (250 mg/day).
Patient surveillance must be strict to ensure that the
false aneurysm is properly excluded. Further imaging
333
Fig. 33.2. Left: Spiral CT shows a typical aortic injury of the
isthmus before stent-graft treatment. Right: Angiographic con-
trol immediately after the intervention shows the proximal extremity of device soon after the left subclavian artery ostium,
with a complete exclusion of the pseudoaneurysm. There is a
slight indentation of the expanded poly(tetrafluoroethylene)
graft at the site of the rupture (Gore device)
334
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VII. Aortic Injury
Fig. 33.3. Angiography before and just after the implantation of the uncovered part of the Talent device over the left subclavian ar-
tery ostium, with complete exclusion of the pseudoaneurysm
follow-up consists of TEE and spiral CT or MRI (before
discharge and at 3, 6, and 12 months, then annually)
after the intervention. If there is a complete shrinking
of the aorta over the stent-graft on follow-up CT scans
at 1 year, only plain X-ray study follow-up from several
angles could be done to avoid expensive studies and irradiation of young patients.
33.7 Results
In our experience of 29 patients, digital subtraction angiography and per operative TEE revealed complete exclusion of the pseudoaneurysm in all but one patient
who showed an immediate minor proximal endoleak
that spontaneously resolved on CT follow-up after
1 month. Only one stent-graft was needed in each patient. The mean procedure time was 96 Ô 24 min (median, 83 min; range, 75±180 min) [20]. No significant
kinking, twisting, stenosis, intragraft thrombosis, migration, perigraft leak, pseudoaneurysmal expansion, or
rupture was observed. In one case, an iliac bypass was
performed during the same procedure to repair an iliac
rupture.
No death, neurological complication, or infection
was observed. However, early after intervention, fever,
neutrophilic hyperleukocytosis, and biological inflammatory syndrome were observed in six patients for 1±
5 days (mean, 2.7 days); no causal infectious agent
could be identified. Blind broad-spectrum antibiotics
Fig. 33.4. This simple plain film control at 5-years follow-up
demonstrated the fractures of the nitinol filaments of the uncovered part of this Talent device
were given to the first two patients to cover an eventual
stent-graft infection.
Acute compression of the left main bronchus and
homolateral pulmonary atelectasis occurred soon after
one procedure; it was believed to be related to a sudden
rise in pressure inside the freshly thrombosed pseudoaneurysmal sac. An endobronchial silicone stent was
placed with good clinical and bronchoscopic results; it
was retrieved 3 months later. After a 7-year follow-up,
this patient still presents no sequelae.
We had one case of deteriorated prosthetic material
without clinical consequence on late follow-up. None
H. Rousseau et al. Chapter 33 Acute Traumatic Aortic Rupture: Stent-Graft Repair
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Table 33.1. Endovascular treatment: results of literature review
n Mortality Paraplegia Complications (n)
335
Thompson et al. [33] 5 0 0 0
Fujikowa et al. [29] 6
Orend et al. [34] 11 1
Lachat et al. [35] 12
Daenen et al. [37] 7 1
Czermak et al. [28] 6 0 0 1 endoleak secondary stent graft
Melnitchouk et al. [32] 15 1 0 Type I endoleak (1)
Scheinert et al. [39] 10 0 0 Renal failure (1)
Marty-An et al. [38] 9 0 0 0
Orford et al. [36] 9 1 0 Arm ischemia (1)
Amabile et al. [41] 9 0 0 0
Personal experience 29 0 0 1 atelectasia
Total 128 6 (5%) 0
a
Emergency cases,bNot procedure related
a
a
b
1
b
b
1
b
00
0 2 secondary vascular surgery
0 1 endoleak secondarystent-graft
00
Fig. 33.5. Spiral CT with 3D surface-shaded display reconstruc-
tions, before (left) and 48 months after (right) treatment, showing complete regression of the pseudoaneurysm and the initial
were reported in other series exclusively based on aortic
trauma including only midterm results [21]. This could
be explained by the fact that we observed the fracture
on late follow-up 5-years after the procedure (Figs. 33.4).
We must keep in mind that if the stent deteriorates during
follow-up, it is always possible to treat the complication
either by elective endovascular or surgical conversion.
The presence of a stent-graft does not seem to have significant effect on secondary surgery [22]. It must be remembered that surgical treatment itself is not entirely devoid of late complications, mainly false aneurysms, anastomotic stenosis, or, rarely, infected prosthetic materials
for which the prognosis is catastrophic.
noncovered portion of stent-graft over left subclavian artery
ostium, which stays patent
As expected from other studies in the literature (Table 33.1), our patients showed complete healing of the
aortic wall without any residual pseudoaneurysm and
complete shrinking of the aorta over the stent-graft on
follow-up CT scans (mean follow-up of 46 months)
(Figs. 33.5, 33.6) [14, 20, 23±41]. This good result is
probably explained by the fact that the aorta is usually
healthy proximally and distally from the rupture, which
means that a satisfactory seal can easily be accomplished without type I endoleak. As the rupture is always limited to the aortic isthmus no or just a few intercostal arteries arise from the pathologic aortic segment, limiting the risk of type II endoleak. Further-
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VII. Aortic Injury
Fig. 33.6. The CT control at 1 year demonstrates the complete
healing of the aortic wall, without any endoleak. Note the intentional exclusion of the left subclavian artery, with a reverse
more, as a single stent-graft is used, the risk of type III
endoleak is avoided.
Finally, our comparative study (with similar lesions
and severity scores, ISS) confirms that stent-graft therapy is an advantageous alternative to conventional open
surgery to treat aortic rupture. The mortality and the
paraplegia rates were 21 and 7%, respectively, for the
35 patients treated surgically compared with 0% for the
29 patients treated with a stent-graft with a mean follow-up of 46 months (range, 13±90) [20].
33.8 Potential Limitations
The potential limitations to endovascular treatment are
the site of the rupture in regard to other anatomic land-
flow from the left vertebral artery. The patient did not complain of any symptoms
marks, the difficulty of vascular access, and the availability of the device in an emergency situation.
The success of the endovascular procedure greatly
depends on rigorous respect of anatomic criteria,
mainly the length of the proximal neck, which must be
10 mm or more beneath the origin of the left subclavian
artery. If needed, covering the left subclavian artery to
lengthen the proximal neck could be a good alternative
as we did in six out of our 29 patients (Fig. 33.7) [20].
The safety of overstenting the subclavian artery was
demonstrated in different series [20, 42, 43]; thus,
transposition of the subclavian artery onto the carotid
artery before thoracic stent-graft implantation is not
mandatory [44] but could be done in a second step in
the event of vertebrobasilar insufficiency or upper limb
ischemia. But before excluding the left subclavian artery, a strict check of the patency of collaterals between
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