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17 • Blunt Thoracic Aortic Injury 205
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Adult
B
a
b
Pediatric
C
A
Fig. 17.8 Surgical treatment options for blunt thoracic aortic injury. (A) Partial left heart bypass to distal aorta or femoral artery. (B) “Clamp-and-sew”
technique with interposition graft in adult patients. (C) “Clamp-and-sew” with primary repair in selected pediatric patients.
Although open surgical repair is far less common in
today’s practice secondary to the advent of endovascular
stent grafts, there are instances in which EVAR is prohibitive, such as in aortic arch injuries, in young patients with
small aorta, hemodynamic instability, active extravasation
from the aorta seen on CTA (see Fig. 17.7), and patients
with occlusive disease at vascular access routes. Distal perfusion is strongly associated with better outcomes when
open repair is required.
Endovascular Aortic Repair
EVAR (Figs. 17.9 and 17.10) for traumatic thoracic aortic
injuries was rst utilized in 1997 by Kato and colleagues.4
Initially, endovascular repair was recommended only for
high-risk patients sustaining BTAI with severe associated
injuries or with comorbid conditions.46 The next decade
saw a steady increase in the use of endovascular stents in
the management of BTAI. In the AAST1 study in 1997, no
patient was treated with the EVAR technique.5 A systematic
review of the published literature up to 2006 found a total
of only 284 patients with traumatic aortic injury treated
with endovascular repair.47 However, the more recent
AAST2 study in 2007 reported that almost 65% of the
193 patients with BTAI were managed denitively with
EVAR. Furthermore, 60% of patients with no major extrathoracic injuries, and 57% of patients under 55 years of age
with no major associated trauma were treated with endovascular techniques.
Endovascular repair is associated with signicantly
better early outcomes than open repair. In the AAST2 study,
multivariate analysis (adjusting for age over 55, GCS 8 or
less, hypotension on admission, and critical extrathoracic
injuries) showed a signicantly lower adjusted mortality
and fewer blood transfusions in the endovascular group
as compared to the open repair group. In the subgroup of
patients with no critical extrathoracic injuries, endovascular repair was associated with a signicantly lower case
fatality and fewer blood transfusions than open repair. A
signicant survival benet was likewise identied in the
subgroup of victims with associated critical extrathoracic

206 SECTION 4 • The Management of Vascular Trauma
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Fig. 17.9 Illustration of deployed endovascular stent graft for blunt
thoracic aortic injury.
injuries.6 In a more recent meta-analysis of 699 procedures in which 370 patients were treated with endovascular repair and 329 patients were managed with open
repair, the observed mortality rates were 7.6% and 15.2%
(P = .008), respectively, in favor of EVAR. The incidence of
procedure-related paraplegia was 5.6% in the open repair
group and 0% in the endovascular group. The incidence of
stroke was likewise signicantly lower in the EVAR group
(0.8% vs. 5.3%, P = .003).
48
Despite the improved early outcomes with the endovascular repair, there is a signicant concern because of the high
incidence of device-related complications. In the AAST2
study, 20% of patients subjected to EVAR developed devicerelated complications, including endoleaks, access-site
vessel complications, occlusion of the left subclavian or left
common carotid arteries, device collapse, and stroke (Table
17.3). The most common complication was the presence
of an endoleak, observed in 14% of patients. The proper
sizing of the stent is essential in avoiding complications such
as endoleaks (Fig. 17.11A) or stent collapse (Fig. 17.11B).
Optimal deployment of the stent requires oversizing the
device by 10% to 20%.
47,49,50
However, in earlier years,
this was not always possible (especially in young patients)
because commercially available devices were only available
in a limited range of sizes. Another factor that increased the
risk of endoleak was the anatomy of the aorta, especially
the angle between the left subclavian artery and the distal aorta (which can be up to 90 degrees). This resulted in
poor apposition between stent graft and aortic wall, especially in the inner corner (Fig. 17.12).51 Excessive oversizing
of the stent (in order to reduce the risk of endoleak) may
A
B
B
Fig. 17.10 (A and B) CT scan shows a successfully deployed endovascular
stent graft on sagittal and axial images.
cause collapse of the device with potentially catastrophic
consequences. These problems have been addressed with
the improvement of stent-graft design, which are now
available in smaller sizes and in curved shapes more suited
to the younger aorta.
The other major concern with endovascular treatment of
BTAI is the lack of long-term follow-up, especially in young
individuals undergoing EVAR. Because of this paucity
of data, it is unclear how these devices will behave when
the aorta becomes tortuous, atherosclerotic, and dilated
with advancing age. Furthermore, the durability of endografts over time is unknown. Medium-term results are now
available and show signicant device-related complications. Fernandez et al.52 in a follow-up study (range 5.5 to
108 months) of 20 patients with BTAI treated with EVAR
reported signicant problems: two patients with left subclavian artery occlusion needed late revascularization for steal

17 • Blunt Thoracic Aortic Injury 207
AB
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Table 17.3 Device-Related Complications in Patients Treated with Endovascular Repair in AAST2 Study.
Complications n 125 (%)
Endoleak 18 (14)
Access vessel injury 4 (3)
Subclavian artery occlusion 4 (3)
Stroke 2 (1.6)
Paraplegia 1 (0.8)
Carotid artery occlusion 1 (0.8)
Partial collapse of the device 1 (0.8)
Insertion site infection 1 (0.8)
From Demetriades D, et al. Operative treatment or endovascular stent graft in blunt thoracic aortic injuries: results of American
Associations for the Surgery of Trauma multicenter study. J Trauma. 2008;64;561–571.
Fig. 17.11 CT scan showing stent-graft–related complications. Poor apposition between the graft and the aortic wall may cause (A) endoleak (arrows)
and (B) partially collapsed stent graft.
syndrome; one case developed stent collapse at 6 months
and needed re-intervention; in one case the stent fractured
at 4 years; and in one case the stent thrombosed at one year.
Forbes et al.,53 in a series of 17 patients treated with EVAR
and with a minimum of one-year follow up, reported that
the proximal thoracic aorta, just distal to the left subclavian
artery, expanded at a greater rate than the aorta distal to the
graft. The clinical signicance of this nding is unknown.
Currently, the most common complication of endovascular stenting of BTAI is occlusion of the left subclavian
artery (Fig. 17.13). Khoynezhad et al.,54 in a prospective
trial of 50 patients treated with EVAR, reported a complete
or partial occlusion of the left subclavian artery in 58%.
DuBose et al.,55 in a database study of 190 patients treated
with EVAR, reported occlusion of the left subclavian artery
in 41% of cases. Although most patients tolerate subclavian artery occlusion well, a signicant number develop
subclavian steal syndrome or arm claudication and require
revascularization with carotid-subclavian bypass graft.
52,56
A carotid-subclavian artery bypass procedure in a young
person should be considered as a serious adverse event that
is associated with signicant complications, such as iatrogenic injury to the phrenic nerve, the recurrent laryngeal
nerve, and axillary nerve. Despite these very real concerns,
the low early mortality rates observed in patients with BTAI
treated with endovascular repair (Table 17.4) has proven
very attractive to surgeons, and it has become the new standard of care. For optimal results, it is essential that these
procedures are performed in centers of excellence staffed
with well-trained multidisciplinary teams with experience
in the management of the multitrauma patient. It has
been shown that high-volume centers have signicantly
fewer systemic and local complications and shorter hospital
lengths of stay than low-volume centers.6 Results, especially
device-related complications, should be monitored closely
and reported through the quality improvement process.
Advances in Endograft Design
Since the introduction of stenting as a denitive treatment for BTAI in the mid-1990s, endograft technology

208 SECTION 4 • The Management of Vascular Trauma
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Fig. 17.12 Poor apposition between the stent graft and the aortic wall
may occur in the inner corner of the graft (arrow).
has evolved with several improvements specic to trauma
patients. One of the most clinically relevant differences
between the injured aorta and the chronically diseased
aorta is anatomic size differential. The often-young, previously healthy injured thoracic aorta is much smaller in
diameter with a well-dened, distal taper. This size discrepancy continues down into the ilio-femoral region as well,
impacting the capacity of this segment to accept a deployment device, which may result in major iatrogenic injury to
the femoral or the iliac artery. Implantation of an oversized
graft can lead to endoleak, in-folding, and even collapse. In
response to this, grafts that can be utilized in patients with
aortic diameters even as small as 16 to 24 mm have been
developed. Smaller-sized deployment sheaths have reduced
the incidence of complications at the insertion site. In
addition to the size considerations, the aorta in the young
trauma patient may not be fully unfolded and as such, the
acute angle prevents close apposition of the graft, especially
Fig. 17.13 Occlusion of the left subclavian artery by a deployed stent
graft (arrow).
on the inner corner. This may over time result in a “bird’s
beak deformity” with the propensity to develop into a type I
endoleak or, if sufciently severe, may result in migration or
graft collapse. New generation devices incorporate this curvature into the design and can better conform to the natural
contours of the injured aorta.
As discussed previously, aortic stenting may result in
occlusion of a major aortic arch branch. Whereas preservation of antegrade ow to the left subclavian can be
maintained through the use of follow-on left common
carotid to subclavian by-pass graft, where injuries involve
sealing across the more proximal arch, the at-risk branch
vessels will need to be accessed by median sternotomy and
reimplanted upstream of the proximal sealing zone prior
to stenting (Fig. 17.14); chimney grafts can also be used
to preserve perfusion.57 Recent advances with the use of
advanced branched grafts may eliminate the need for reimplantation (Fig. 17.15). These engineering advances have
the potential to improve stent delivery and seating, thereby
reducing the complications associated with endovascular
treatment.
58.
Table 17.4 Open Versus Ensovascular Aortic Repair (EVAR) of Thoracic Aortic Injuries in AAST2 Study.
n 193 58 125
Mean ISS 39.5 38.9 39.4 .83
Severe associated injuries 39.2% 31.3% 43.4% .10
Mortality 13.0% 23.5% 7.2% .001
Paraplegia 1.6% 2.9% 0.8% .28
Systemic complications 45.1% 50.0% 42.4% .31
From Demetriades D, et al. Operative treatment or endovascular stent graft in blunt thoracic aortic injuries: results of American Associations for the Surgery of
Trauma multicenter study. J Trauma. 2008;64;561–571.
AAST, American Association for the Surgery of Trauma; ISS, injury severity score.
All Patients Open Repair EVAR P-value

17 • Blunt Thoracic Aortic Injury 209
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Minimal aortic injury (MAI) is defined as a small intimal flap with no periaortic hematoma, occurs in about
10% of BTAI, and is diagnosed with high-resolution
techniques.62 These injures may be managed with blood
pressure control and observation, without surgical or
endovascular interventions. Conservatively managed
patients need regular CT scan follow-up until resolution
of the aortic lesion. Traumatic aortic injury can also be
classified as grade I (intimal tear), grade II (intramural
hematoma), grade III (pseudoaneurysm), and grade
IV (rupture),63 where grade I injuries are equivalent
to MAI.
The available literature consists of mainly small case
series and the preliminary results are encouraging, with
no cases progressing to delayed rupture. In a study by
Malhotra et al.,64 six patients with MAI were observed. In
two, the flap completely resolved, and in one it remained
stable. The remaining three patients formed small pseudoaneurysms. The authors concluded that many intimal
injuries heal spontaneously and hence may be managed
nonoperatively. In another study, Akins et al. successfully managed nonoperatively five patients with MAI.59
Kepros et al.,65 in another small series of five traumatic
internal tears of the thoracic aorta, reported complete
resolution in all of them within 3 to 19 days. In a larger
series of 27 cases treated with blood pressure control and
Fig. 17.14 Debranching and reimplantation of arch-branches (arrow)
prior to stenting may be required ahead of stent-graft placement
where the blunt thoracic aortic injury zone is at or proximal to the origin of the left subclavian artery.
with a mean follow-up of 107 days, Caffarelli41 reported
stable lesions in 19, complete resolution in 5, progression requiring open repair in 1, with need of endovascular stenting in 2. It has been suggested that small false
aneurysms have the similar relatively low risk of rupture
as their true aneurysmal counterparts.60 However, the
long-term natural history of these injuries is not known,
and caution should be exercised when considering this
form of treatment.
Fig. 17.15 Arch branch grafts can address injuries to the aortic arch.
NONOPERATIVE MANAGEMENT
Experience with nonoperative treatment of BTAI is very limited and offered mostly to selected patients with advanced
age and minor aortic injuries.
59–61
Summary
The screening, definitive diagnosis, and treatment of
traumatic blunt thoracic aortic injuries have undergone
major evolution in the last two decades. Routine CT scan
of the chest in suspicious mechanisms of injury has
replaced plain chest x-rays as a screening tool. CT angiography has largely replaced invasive angiography for
definitive diagnosis. Delayed repair of the aortic injury
is now the preferred approach in most cases. Endovascular repair has largely replaced open repair. Finally, it
seems that there is a role for conservative management
of selected cases. These new approaches have resulted
in a significant reduction of mortality, paraplegia, and
other complications in patients with BTAI reaching hospital care. Improvement of the endovascular devices has
reduced some device-related complications. However,
there is still concern about remaining device-related
complications, such as the high incidence of subclavian
artery occlusion and limited long-term follow up. These
injuries should be managed in centers of excellence by
multidisciplinary teams with significant experience in
this field.

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References
1. Mattox KL, Wall Jr. MJ. Historical review of blunt injury to the tho-
racic aorta. Chest Surg Clin N Am. 2000;10(1):167–182. x.
2. Passaro Jr E, Pace WG. Traumatic rupture of the aorta. Surgery.
1959;46:787–791.
3. Demetriades D, Gomez H, Velmahos GC, etal. Routine helical com-
puted tomographic evaluation of the mediastinum in high-risk blunt
trauma patients. Arch Surg. 1998;133(10):1084–1088.
4. Kato N, Dake MD, Miller DC, et al. Traumatic thoracic aortic
aneurysm: treatment with endovascular stent-grafts. Radiology.
1997;205(3):657–662.
5. Fabian TC, Richardson JD, Croce MA, et al. Prospective study of
blunt aortic injury: multicenter trial of the American Association
for the Surgery of Trauma. J Trauma. 1997;42(3):374–380. discus-
sion 380–383.
6. Demetriades D, Velmahos GC, Scalea TM, et al. Operative repair or
endovascular stent graft in blunt traumatic thoracic aortic injuries:
results of an American Association for the Surgery of Trauma multicenter study. J Trauma. 2008;64(3):561–570. discussion 570–571.
7. Demetriades D, Murray J, Martin M, et al. Pedestrians injured by
automobiles: relationship of age to injury type and severity. J Am Coll
Surg. 2004;199(3):382–387. https://doi.org/10.1016/j.jamcoll-
surg.2004.03.027.
8. Demetriades D, Murray J, Brown C, etal. High-level falls: type and
severity of injuries and survival outcome according to age. J Trauma.
2005;58(2):342–345.
9. Demetriades D, Karaiskakis M, Toutouzas K, Alo K, Velmahos G, Chan
L. Pelvic fractures: epidemiology and predictors of associated abdominal injuries and outcomes. J Am Coll Surg. 2002;195(1):1–10.
10. Teixeira PG, Inaba K, Barmparas G, etal. Blunt thoracic aortic injuries: an autopsy study. J Trauma. 2011;70(1):197–202. https://doi.
org/10.1097/TA.0b013e3181df68b3.
11. Shackelford S, Nguyen L, Noguchi T, Sathyavagiswaran L, Inaba K,
Demetriades D. Fatalities of the 2008 Los Angeles train crash: autopsy
ndings. Am J Disaster Med. 2011;6(2):127–131.
12. Barmparas G, Inaba K, Talving P, et al. Pediatric vs adult vascular trauma: a national trauma databank review. J Pediatr Surg.
2010;45(7):1404–1412. https://doi.org/10.1016/j.jpedsurg.2009.
09.017.
13. Siegel JH, Smith JA, Siddiqi SQ. Change in velocity and energy dis-
sipation on impact in motor vehicle crashes as a function of the
direction of crash: key factors in the production of thoracic aortic
injuries, their pattern of associated injuries and patient survival. A
crash injury research engineering network (CIREN) study. J Trauma.
2004;57(4):760–777. discussion 777–778.
14. Siegel JH, Belwadi A, Smith JA, Shah C, Yang K. Analysis of the mechanism of lateral impact aortic isthmus disruption in real-life motor
vehicle crashes using a computer-based nite element numeric model:
With simulation of prevention strategies. J Trauma. 2010;68(6):
1375–1395. https://doi.org/10.1097/TA.0b013e3181dcd42d.
15. Burkhart HM, Gomez GA, Jacobson LE, Pless JE, Broadie TA. Fatal
blunt aortic injuries: a review of 242 autopsy cases. J Trauma.
2001;50(1):113–115.
16. Burney RE, Gundry SR, Mackenzie JR, Whitehouse WM, Wu SC.
Chest roentgenograms in diagnosis of traumatic rupture of the aor ta.
Observer variation in interpretation. Chest. 1984;85(5):605–609.
17. Marnocha KE, Maglinte DD. Plain-lm criteria for excluding aortic rup-
ture in blunt chest trauma. AJR Am J Roentgenol. 1985;144(1):19–21.
18. Woodring JH. The normal mediastinum in blunt traumatic rupture
of the thoracic aorta and brachiocephalic arteries. J Emerg Med.
1990;8(4):467–476.
19. Mirvis SE, Bidwell JK, Buddemeyer EU, etal. Value of chest radiography in
excluding traumatic aortic rupture. Radiology. 1987;163(2):487–493.
20. Mirvis SE, Shanmuganathan K, Buell J, Rodriguez A. Use of spiral
computed tomography for the assessment of blunt trauma patients
with potential aortic injury. J Trauma. 1998;45(5):922–930.
21. Ekeh AP, Peterson W, Woods RJ, et al. Is chest x-ray an adequate
screening tool for the diagnosis of blunt thoracic aortic injury? J
Trauma. 2008;65(5):1088–1092.
22. Exadaktylos AK, Duwe J, Eckstein F, et al. The role of contrast-
enhanced spiral CT imaging versus chest X-rays in surgical therapeutic concepts and thoracic aortic injury: a 29-year
swiss retrospective analysis of aortic surgery. Cardiovasc J S Afr.
2005;16(3):162–165.
23. Parker MS, Matheson TL, Rao AV, etal. Making the transition: the role
of helical CT in the evaluation of potentially acute thoracic aortic
injuries. AJR Am J Roentgenol. 2001;176(5):1267–1272.
24. Mirvis SE, Shanmuganathan K. Diagnosis of blunt traumatic aortic
injury 2007: still a nemesis. Eur J Radiol. 2007;64(1):27–40.
25. Cohn SM, Burns GA, Jaffe C, Milner KA. Exclusion of aortic tear in the
unstable trauma patient: the utility of transesophageal echocardiography. J Trauma. 1995;39(6):1087–1090.
26. Smith MD, Cassidy JM, Souther S, etal. Transesophageal echocardiog-
raphy in the diagnosis of traumatic rupture of the aorta. N Engl J Med.
1995;332(6):356–362.
27. Wagner RB, Crawford Jr WO, Schimpf PP. Classication of parenchy-
mal injuries of the lung. Radiology. 1988;167(1):77–82.
28. Minard G, Schurr MJ, Croce MA, etal. A prospective analysis of trans-
esophageal echocardiography in the diagnosis of traumatic disruption of the aorta. J Trauma. 1996;40(2):225–230.
29. Hemmila MR, Arbabi S, Rowe SA, etal. Delayed repair for blunt tho-
racic aortic injury: Is it really equivalent to early repair? J Trauma.
2004;56(1):13–23.
30. Parmley LF, Mattingly TW, Manion WC, Jahnke Jr. EJ. Nonpenetrating
traumatic injury of the aorta. Circulation. 1958;17(6):1086–1101.
31. Fabian TC, Davis KA, Gavant ML, etal. Prospective study of blunt aortic
injury: helical CT is diagnostic and antihypertensive therapy reduces
rupture. Ann Surg. 1998;227(5):666–676. discussion 676–677.
32. Wheat Jr MW, Palmer RF, Bartley TD, Seelman RC. Treatment of dis-
secting aneurysms of the aorta without surgery. J Thorac Cardiovasc
Surg. 1965;50:364–373.
33. Pate JW, Gavant ML, Weiman DS, Fabian TC. Traumatic rupture of
the aortic isthmus: program of selective management. World J Surg.
1999;23(1):59–63.
34. Holmes 4th JH, Bloch RD, Hall RA, Carter YM, Karmy-Jones RC.
Natural history of traumatic rupture of the thoracic aorta managed nonoperatively: a longitudinal analysis. Ann Thorac Surg.
2002;73(4):1149–1154.
35. Wahl WL, Michaels AJ, Wang SC, Dries DJ, Taheri PA. Blunt thoracic
aortic injury: delayed or early repair? J Trauma. 1999;47(2):254–259.
discussion 259–260.
36. Maggisano R, Nathens A, Alexandrova NA, etal. Traumatic rupture
of the thoracic aorta: should one always operate immediately? Ann
Vasc Surg. 1995;9(1):44–52.
37. Estrera AL, Gochnour DC, Azizzadeh A, etal. Progress in the treatment
of blunt thoracic aortic injury: 12-year single-institution experience.
Ann Thorac Surg. 2010;90(1):64–71. https://doi.org/10.1016/j.
athoracsur.2010.03.053.
38. Marcaccio CL, Dumas RP, Huang Y, Yang W, Wang GJ, Holena DN.
Delayed endovascular aortic repair is associated with reduced inhospital mortality in patients with blunt thoracic aortic injury. J Vasc
Surg. 2018;68(1):64–73.
39. Fox N, Schwartz D, Salazar JH, etal. Evaluation and management of
blunt traumatic aortic injury: a practice management guideline from
the Eastern Association for the Surgery of Trauma. J Trauma Nurs.
2015;22(2):99–110.
40. DeBakey ME. Successful resection of aneurysm of distal aortic arch and
replacement by graft. J Am Med Assoc. 1954;155(16):1398–1403.
41. von Oppell UO, Dunne TT, De Groot KM, Zilla P. Spinal cord protection
in the absence of collateral circulation: meta-analysis of mortality
and paraplegia. J Card Surg. 1994;9(6):685–691.
42. von Oppell UO, Dunne TT, De Groot MK, Zilla P. Traumatic aortic rup-
ture: twenty-year metaanalysis of mortality and risk of paraplegia.
Ann Thorac Surg. 1994;58(2):585–593.
43. Steenburg SD, Ravenel JG, Ikonomidis JS, Schonholz C, Reeves S.
Acute traumatic aortic injury: imaging evaluation and management. Radiology. 2008;248(3):748–762. https://doi.org/10.1148/
radiol.2483071416.
44. Zeiger MA, Clark DE, Morton JR. Reappraisal of surgical treatment of
traumatic transection of the thoracic aorta. J Cardiovasc Surg (Torino).
1990;31(5):607–610.
45. Kodali S, Jamieson WR, Leia-Stephens M, Miyagishima RT, Janusz MT,
Tyers GF. Traumatic rupture of the thoracic aorta. A 20-year review:
1969-1989. Circulation. 84(5 Suppl):III40. 1991:6.
46. Semba CP, Kato N, Kee ST, etal. Acute rupture of the descending tho-
racic aorta: repair with use of endovascular stent-grafts. J Vasc Interv
Radiol. 1997;8(3):337–342.
47. Lettinga-van de Poll T, Schurink GW, De Haan MW, Verbruggen JP,
Jacobs MJ. Endovascular treatment of traumatic rupture of the thoracic aorta. Br J Surg. 2007;94(5):525–533.

17 • Blunt Thoracic Aortic Injury 211
https://t.me/medicina_free
48. Tang GL, Tehrani HY, Usman A, etal. Reduced mortality, paraplegia,
and stroke with stent graft repair of blunt aortic transections: a modern meta-analysis. J Vasc Surg. 2008;47(3):671–675.
49. Pratesi C, Dorigo W, Troisi N, etal. Acute traumatic rupture of the
descending thoracic aorta: endovascular treatment. Am J Surg.
2006;192(3):291–295.
50. Tehrani HY, Peterson BG, Katariya K, et al. Endovascular repair of
thoracic aortic tears. Ann Thorac Surg. 2006;82(3):873–877. discussion 877–878.
51. Borsa JJ, Hoffer EK, Karmy-Jones R, et al. Angiographic descrip-
tion of blunt traumatic injuries to the thoracic aorta with specic
relevance to endograft repair. J Endovasc Ther. 2002;9(Suppl 2):
II84–91.
52. Fernandez V, Mestres G, Maeso J, Dominguez JM, Aloy MC, Matas M.
Endovascular treatment of traumatic thoracic aortic injuries: shortand medium-term follow-up. Ann Vasc Surg. 2010;24(2):160–166.
https://doi.org/10.1016/j.avsg.2009.05.013.
53. Forbes TL, Harris JR, Lawlor DK, Derose G. Aortic dilatation after
endovascular repair of blunt traumatic thoracic aortic injuries. J Vasc
Surg. 2010;52(1):45–48.
54. Khoynezhad A, Azizzadeh A, Donayre CE, Matsumoto A, Velazquez O,
White R. RESCUE investigators. Results of a multicenter, prospective
trial of thoracic endovascular aortic repair for blunt thoracic aortic
injury (RESCUE trial). J Vasc Surg. 2013;57(4):899–905.
55. DuBose JJ, Leake SS, Brenner M, etal. Contemporary management
and outcomes of blunt thoracic aortic injury: a multicenter retrospective study. J Trauma Acute Care Surg. 2015;78(2):360–369.
56. García Reyes ME, Gonçalves Martins G, Fernández Valenzuela V,
Domínguez González JM, Maeso Lebrun J, Bellmunt Montoya S. Longterm outcomes of thoracic endovascular aortic repair focused on bird
beak and oversizing in blunt traumatic thoracic aortic injury. Ann
Vasc Surg. 2018;50:140–147.
57. Criado FJ, McKendrick C, Criado FR. Technical solutions for common
problems in TEVAR: managing access and aortic branches. J Endovasc
Ther. 2009;16(Suppl 1):I63–79.
58. Anthony Lee W. Status of branched grafts for thoracic aortic arch
endovascular repair. Semin Vasc Surg. 2016;29(1–2):84–89.
59. Akins CW, Buckley MJ, Daggett W, McIlduff JB, Austen WG. Acute
traumatic disruption of the thoracic aorta: a ten-year experience. Ann
Thorac Surg. 1981;31(4):305–309.
60. Camp Jr PC, Rogers FB, Shackford SR, Leavitt BJ, Cobean RA, Clark DE.
Blunt traumatic thoracic aortic lacerations in the elderly: an analysis
of outcome. J Trauma. 1994;37(3):418–423. discussion 423–425.
61. Camp PC, Shackford SR. Outcome after blunt traumatic thoracic
aortic laceration: identication of a high-risk cohort. Western
Trauma Association multicenter study group. J Trauma. 1997;43(3):
413–422.
62. Gavant ML. Helical CT grading of traumatic aor tic injuries: impact on
clinical guidelines for medical and surgical management. Radiol Clin
North Am. 1999;37(3):553–574.
63. Azizzadeh A, Keyhani K, Miller 3rd CC, Coogan SM, Sa HJ, Estrera
AL. Blunt traumatic aortic injury: initial experience with endovascular repair. J Vasc Surg. 2009;49:1403–1408.
64. Malhotra AK, Fabian TC, Croce MA, Weiman DS, Gavant ML, Pate JW.
Minimal aortic injury: a lesion associated with advancing diagnostic
techniques. J Trauma. 2001;51(6):1042–1048.
65. Kepros J, Angood P, Jaffe CC, Rabinovici R. Aortic intimal injuries
from blunt trauma: resolution prole in nonoperative management.
J Trauma. 2002;52(3):475–478.

18
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Abdominal Aortic Trauma, Iliac
and Visceral Vessel Injuries
CHRISTOPHER AYLWIN and MICHAEL JENKINS
Introduction
Major vascular injuries may be seen in up to 25% of abdominal trauma and are associated with a high mortality.
lowing penetrating abdominal trauma, vascular injuries
are the most common causes of death.3 Intra-abdominal
hemorrhage can be catastrophic due to the difculty of rapidly accessing the retroperitoneal vessels. It is for this reason that early recognition of a possible vascular injury is
essential and transfer to a center capable of early surgical
intervention is vital. The early diagnosis of these injuries
has been facilitated with the increasing use of computed
tomography (CT) angiography and with its availability close
to the resuscitation room.
Civilian vascular injury comprises approximately 1%
to 5% of all trauma
spective Observational Vascular Injury Treatment) registry
revealing the incidence of abdominal arterial injuries to be
7.8% of all of vascular trauma.6 The relative rarity therefore makes it difcult for a trauma center and its surgeons
to accumulate large caseloads of specic arterial injuries.
Although blunt trauma is the most common mechanism
of all vascular injury in the PROOVIT registry, there are
huge variations in the role of penetrating trauma causing
abdominal vascular injury. In urban US trauma centers this
is reported to be as high as 88%,7 whereas in Germany, over
a 16-year period, the incidence of penetrating trauma was
only 5% in 760 patients with abdominal vascular injury.2
The incidence of injuries differs between military and civilian trauma. During the Vietnam War and World War II,
the incidence of penetrating abdominal vascular injuries
was less than 3%,8 but in the recent conicts in Iraq and
Afghanistan, iliac injuries were found in 3.9% of injuries,
and aortic injuries in a further 2.9%.9 In civilian populations with a high incidence of knife crime, the incidence
approaches 10%; and this gure doubles to more than 20%
in populations with gun crime.10 For aortic penetrating
injuries, the incidence still remains low, and it is less than
3% for penetrating trauma.
4,5
with data from the PROOVIT (PRO-
11
1,2
Fol-
weapon. The type of injury that results from rearms is
variable depending on the nature of the rearm. Gunshot
wounds may be high velocity or low velocity. Low-velocity
gunshot wounds are dened as wounds caused by projectiles
such as bullets or missiles with speeds of less than 600 m/s.12
Low-velocity gunshot wounds such as those that occur with
handguns cause localized injury to the structures that lie in
the paths of the projectiles. They are associated with a lower
transfer of energy compared with high-velocity gunshot
wounds. Military wounds are more often a result of highvelocity (greater than 600 m/s) projectiles. A high-velocity
projectile carries with it a signicant amount of kinetic
energy that is transferred to the surrounding tissue and
results in extensive injury around the path of the projectile
as well as the immediate damage to any tissue in the path
of the projectile. The amount of energy transferred to the
patient will be decided by a combination of factors including
the energy carried by the missile, the cross-sectional area of
the missile that comes into contact with the tissue, and the
degree of retardation of the missile within the patient, that is,
whether the missile passes through the tissue (delivering less
energy) or comes to rest within the tissue (delivering all of its
kinetic energy). When military weapons are used in civilian
settings with no body armor, mortality from abdominal vascular injury may approach 100%.
The injury that results from shotgun wounds is dependent on the range at which the shotgun is red. If the range
is less than 5 m, the chance of survival is approximately
10%. At this range, although the shotgun cartridge contains multiple pellets (shot), the pellet mass has yet to disperse and thus acts as a more focused mass on impact with
tissue. When the shotgun is red from a greater distance
(e.g., 5 –15 m) the shot has spread, with each pellet carrying lower kinetic energy secondary to retardation from the
air – behaving as a low-energy missile, generally resulting
in less destruction to tissue. At close range, vascular injuries
tend to be multiple, complex, and frequently contaminated
either with bowel contents or external contaminants such
as the victims clothing.
14
13
Mechanism of Injury
PENETRATING INJURY
In the context of noniatrogenic injuries, penetrating injuries
usually occur either from stab wounds or rearms. Injuries
resulting from explosions (e.g., bomb blast) are complex,
resulting in mixed patterns of penetrating and blunt trauma.
Stab wounds (e.g., knife wounds) result in localized inju-
ries whereby the path of injury follows the track of the
212
BLUNT INJURY
Blunt abdominal vascular injury is rarely isolated, is often
associated with high injury severity scores (ISS) in competing injured body regions, and incurs signicant mortality.2
The mechanism by which blunt trauma results in vascular
injury is either by severe deceleration, by crush injuries, or
by direct laceration from a fractured bone fragment. Severe
deceleration can occur in the context of high-speed road
trafc accidents or falls from signicant heights. Crush injuries also occur in road trafc accidents and may result in an

18 • Abdominal Aortic Trauma, Iliac and Visceral Vessel Injuries 213
Zone
II
Zone
I
Zone II
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anteroposterior crush injury as seen in a seatbelt-restrained
passenger. This can also be associated with shearing injuries of the aortic branches. Fractures of the spine or pelvis
can result in direct laceration to the aorta and iliac vessels,
respectively. Renal vessels may be damaged with acceleration – deceleration-type injuries causing shearing forces to
be applied to the renal pedicle.
Whereas the adventitia is the most durable part of the
arterial wall, the intima remains the least elastic and therefore most likely to be torn during blunt injury. Hence the
artery is frequently injured from “inside to outside,” and the
adventitia may remain intact. This creates a thrombogenic
environment within the artery resulting in thrombosis and
occlusion. Alternatively, the intima may be sheared resulting in a dissection. If the adventitia remains intact, the
artery may still be weakened, contributing to delayed aneurysmal degeneration. Total transmural injury can lead to
perforation, hemorrhage, and false aneurysms.
Anatomy
Vascular injuries in the abdomen are classied according to
geographical location (Fig. 18.1). These are usually dened
within three zones, albeit a fourth zone is occasionally
included.
Zone I begins at the point of entry of the aorta through
the diaphragm (i.e., the aortic hiatus) and extends down
to the sacrum. The aorta enters the abdomen at the level
of the twelfth thoracic vertebra passing behind the median
arcuate ligament of the diaphragm. The aorta descends to
the level of the fourth lumbar vertebra where it bifurcates
into the left and right common iliac arteries. Zone I includes
the central retroperitoneal area and the base of the mesentery. The area is further divided into the supramesocolic and
inframesocolic areas. The supramesocolic and inframesocolic areas are dened by the levels of the renal arteries. The
suprarenal aorta, celiac axis, superior mesenteric artery
(SMA), renal arteries, inferior vena cava (IVC), and superior
mesenteric vein all lie within this supramesocolic area. The
inframesocolic area contains the infrarenal aorta, the inferior mesenteric artery, and the IVC.
Zone II exists either side of zone I and contains the paracolic gutters, kidneys, and renal vessels. It is also referred to
as the upper lateral retroperitoneum.
Zone III, containing the iliac vessels, is also known as the
pelvic retroperitoneum.
The hepatic artery, portal vein, retrohepatic IVC, and
hepatic veins all lie within an area occasionally referred to
as zone IV.
Clinical Presentation
The patient should be inspected for signs of penetrating
injury. Stab wounds in the abdomen should be obvious but
be aware that stab wounds in the chest, back, and gluteal
regions can result in injury to abdominal and pelvic vessels. With both penetrating and blunt trauma, examine for
bruising in the anks. This can be a sign of a retroperitoneal
bleeding. With gunshot wounds, examine the patient for
entry and exit wounds. An attempt to predict the trajectory
Fig. 18.1 The three anatomical zones of the retroperitoneum used to
describe the locations of vascular injuries presenting as retroperitoneal
hematomas. Zone I extends from the aortic hiatus to the sacrum and
includes the midline vessels and origins of the visceral branches. Zone II
exists on either side of Zone I and includes the kidneys, renal vessels,
and paracolic gutters. Zone III lies inferior to the level of the sacral
promontory and includes the iliac vessels and pelvic retroperitoneum.
Zone IV is not depicted in the diagram.
may provide some idea of the vessels and organs injured. Do
not assume that the injury is localized to the missile path.
The presentation of arterial injuries may be early or late
depending on the artery involved, as well as the type and
mechanism of injury.
Early presentation is usually in the form of hemorrhage
and hypovolemic shock. Urgent laparotomy will reveal either
blood in the peritoneal cavity or a retroperitoneal hematoma.
The zone should be dened according to Fig. 18.1. Some
patients may respond to resuscitation but presentation with
a distended abdomen should raise the suspicion of a vascular
injury. Patients who are stabilized and taken for trauma CT of
the abdomen revealing vascular injury may also be included
as early presenters. Thrombosis, dissections, and occlusions
may present with lower limb ischemia (absent or diminished
femoral pulses; cold, pale limbs). This should be considered
in the context of blunt injury resulting in pelvic fractures or
abdominal crush. Be aware that the presentation may not be
immediate with intimal tears, and repeated examinations are
mandatory. Injuries to the renal pedicles may present with
hematuria. Anuria as a result of bilateral renal artery thrombosis is rare.
Zone
III

214 SECTION 4 • The Management of Vascular Trauma
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Both penetrating and blunt trauma can result in vascular injuries that present late. With the increasing use of
CT angiography, arterial injuries are being detected early,
reducing the incidence of late presentation. Pseudoaneurysms frequently present late. They may each present as a
pulsatile mass compressing adjacent structures. Compression of the duodenum may present as bowel obstruction.
The false aneurysm may erode into the bowel resulting in
massive gastrointestinal hemorrhage. Similarly, internal
iliac pseudoaneurysms have presented with rectal bleed-
15,16
ing.
ent with hematuria. Arterial stulas have been seen with
hepatic artery injuries and penetrating liver injuries. These
stulas may present with hemobilia, right upper quadrant
pain, and upper gastrointestinal hemorrhage. Injuries
involving both arteries and veins can cause arteriovenous
stulas. The clinical manifestation may be obvious or
subtle. Aortocaval stulas are associated with lower limb
edema and an abdominal bruit. Other arteriovenous stulas may present later with high-output cardiac failure and
lower limb chronic venous skin changes.
Pseudoaneurysm of the renal artery can pres-
Investigations
The choice of investigation will depend on the patient's
physiologic status and the available local facilities. CT has
become the gold standard investigation. Availability close to
the resuscitation room is an important factor in the planning of a major trauma center. Catheter angiography still
maintains an important role in trauma and has the advantage of being coupled with therapeutic options such as stenting and embolotherapy. Early availability of experienced
interventional radiologists and the location of the radiology
suite often limit use to the hemodynamically stable patient.
The use of ultrasound in trauma has increased in the form
of focused assessment with sonography for trauma (FAST)
scans. Bedside ultrasonography is able to detect intraabdominal free uid, facilitating the decision for early exploratory laparotomy. The exploratory trauma laparotomy
remains an important diagnostic tool and is coupled with
the techniques of damage control surgery. Duplex scanning
is less useful in the acute trauma presentation. It has a role
in assessing neck trauma and can be used for surveillance to
detect late pseudoaneurysms and arteriovenous stulas. In
the context of abdominal vascular injuries, its use is limited.
Surgical Techniques
The operative approach will be dependent on the location
of the hematoma and the degree of urgency. The latter is
dictated by the degree of hemodynamic shock.
When a decision is made to proceed to surgery, the patient
should be prepared with sterile drape application allowing
exposure of the abdomen, chest, and groins. This allows
for incisions to be extended into the chest; and, if deemed
necessary, a left anterolateral thoracotomy can be utilized
to gain control of the descending aorta prior to entry to
the abdomen. To facilitate distal control, exposure of the
common femoral arteries may be required. The initial incision is a long midline laparotomy from the xiphisternum to
the pubis. If further access is required, the incision may be
extended in the midline to include a median sternotomy or
through the sixth or seventh intercostal spaces for a lateral
thoracotomy.
On initiating the laparotomy the surgeon may be presented with an abdominal cavity containing free blood. At
this stage it may be difcult to establish the source of bleeding and the principles of damage control surgery should
be applied. In order to identify the source of bleeding, the
surgeon should proceed with small bowel evisceration and
packing of the abdominal cavity, using large packs to either
stop or slow the bleeding. These packs are then removed
from each compartment until the source of bleeding is identied. The four-quadrant packing technique requires packs
to be placed in the right upper quadrant over the right lobe
of the liver, the left upper quadrant, the infracolic compartment (elevate the greater omentum and pack either side of
the small bowel mesentery), and the pelvis. Pelvic packing is
performed by lifting the small bowel out of the pelvis before
applying the packs into the pelvis.
Exposure of the aorta and its branches is best achieved
using the technique of a medial visceral rotation. This can
be performed from either the left or right side; the decision
will be dependent on which vessels need to be exposed. The
medial visceral rotation can be a time-consuming technique,
even in experienced hands, and temporary control may be
required, especially if active hemorrhage is occurring from
the supramesocolic aorta. Direct manual compression of
the aorta against the spine may control the bleeding but
frequently restricts exposure of the aorta and therefore subsequent repair. It can be a useful technique to control the
inow, but the ultimate aim should be to apply a clamp.
Division or creation of a window within the lesser omentum enables exposure of the supraceliac aorta. This technique is aided by retracting the stomach and the esophagus
to the left. The liver is retracted in a cephalad direction. Division of the diaphragmatic crura further aids exposure, and
then a supra celiac aortic clamp can be applied. This is the
quickest way to apply a supraceliac clamp and to gain control of the bleeding abdominal aorta. Although inow will
be controlled, back-bleeding from the visceral vessels and
lumbar arteries may be signicant. The presence of visceral
branches can make distal control challenging.
In order to perform a left-sided medial visceral rotation,
the peritoneal attachments of the sigmoid and the descending colon are divided. The incision is started in the lateral
avascular peritoneal reection of the sigmoid colon and is
continued proximally along the left paracolic gutter. The
plane is developed by mobilizing the sigmoid colon and the
descending colon to the midline. The retroperitoneal attachments of the left kidney, pancreatic tail, and spleen can be
divided, mobilizing these organs to the midline and hence
facilitating complete exposure of the abdominal aorta from
its origin at the diaphragm to its bifurcation at the level of
the fourth lumbar vertebra (Figs. 18.2 and 18.3). This technique carries a signicant risk of damage to the spleen, left
kidney, and left renal vessels. Developing a dissection plane
anterior to the left kidney can reduce the risk of intraoperative renal injury.
If rapid proximal control of the abdominal aorta is
required before the medial visceral rotation, a clamp can
be applied to the distal descending thoracic aorta. This is
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