Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3850_Библиотеки_им_академика_М_И_Перельмана
.pdf
R. Fattori, D. Pacini Chapter 31 Traumatic Aortic Rupture
https://t.me/med1917
Table 31.2. Operative mortality in patients operated on with delayed surgery for traumatic aortic rupture
Authors Year Patients (N) Overall mortality N (%) Mortality related
to aortic rupture (%)
Akins et al. [27] 1981 19 2 (10.5) ±
Kipfer et al. [44] 1994 10 0 (0) 0 (0%)
Maggisano et al. [28] 1995 44 2 (4.5) ±
Pate et al. [26] 1995 112 21 (18.8) 6 (5.4)
Fabian et al. [20] 1997 21 11 (52.4) 0 (0)
Holmes et al. [39] 2002 30 8 (26.7) 1 (3.3)
Kwon et al. [42] 2002 10 1 (10) 0 (0)
Langanay et al. [43] 2002 19 3 (15.8) 0 (0)
Pacini et al. [46] 2005 48 2 (4.2%) 1 (2.1)
315
quickly as possible. A prompt diagnosis of aortic wall
injury is mandatory and an aggressive intravenous therapy with vasodilators and beta-blocking drugs must be
started to reduce the aortic wall stress and the risk of
lethal aortic rupture. The risk of rupture of a periaortic
hematoma contained in the mediastinum can be
avoided if the systolic blood pressure is constantly
maintained below 140 mmHg. Pate et al. [26] analyzed
15 years of English-language literature, and their experience with 112 patients, in their search for evidence
of the risk of aortic free hemorrhage in patients affected
by acute TAR in the interval between diagnosis and delayed surgical repair. Of the 492 patients in reports
specifying the cause of death, 22 (4.5%) died of aortic
rupture, mostly presenting with hemodynamic instability and actively bleeding into the pleural space on arrival; in patients in whom the pseudoaneurysm or hematoma is contained within the mediastinum, and who do
not present with signs of hemodynamic instability or
exsanguination into the pleural space, free rupture appears to be uncommon.
On the subsequent days after the trauma, a process
of organization of the hematoma usually develops and
with time it will turn into a strong fibrous tissue, with
the formation of a pseudoaneurysm that has the same
risk of rupture as a true aneurysm of similar size. Patients must be admitted to an intensive care unit with
continuous monitoring of ECG, arterial and central venous pressure, renal function and peripheral metabolism. An arterial systolic pressure exceeding 90 mmHg
should be an indication to limit fluid replacement and
any hemodynamic support in hypotensive patients.
Monitoring of respiratory function and eventual intubation and mechanical ventilation is fundamental in polytraumatized patients with respiratory insufficiency due
to central nervous system injury, pulmonary contusion
and pleural effusion with measurement of chest tube
outputs [26, 41].
Considering this possible evolution, the strategy to
delay the surgical repair of posttraumatic aortic aneurysms in selected patients offers some clear advantages
[39±44]. The overall mortality and the incidence of major complications are lower when it is possible to delay
surgery than when unstable patients have to undergo
an emergency operation. All the necessary procedures
of distal aortic perfusion can be safely performed and
the mortality is also reduced by prior treatment of potentially lethal associated lesions, often encountered in
polytraumatizated patients. It is important to remember
that 90% of patients with aortic rupture have associated
other open and closed traumatic lesions of different
areas (orthopedic 81%, abdominal 42%, closed-head injury 40%) which may cause a rapid evolution into
shock and coma, thus influencing the patient's outcome
[20, 45] (Table 31.2). Therefore, the treatment of associated lesions is fundamental in these patients and it is
another incentive to delay surgical intervention in the
aorta.
In our experience [30, 46] delaying aortic surgery in
polytraumatized patients offers many advantages and is
aided by increasingly sophisticated diagnostic techniques. The spiral CT scan and MRI offer noninvasive assessment of the anatomical characteristics of the aortic
lesions and can be used to monitor their evolution [47].
However, delayed surgery cannot be applied in every
case. Even if the majority of TARs are stable lesions, in
approximately 5% of them the risk of rupture may be
high in the acute phase. Signs of impending rupture
such as periaortic hematoma, repeated hemothorax,
contrast medium extravasation, and uncontrolled blood
pressure are considered signs of instability. Sometimes
the aortic tear, acting with a valve mechanism, may
cause obstruction and reduction of flow in the descending aorta with lower extremity ischemia. Pseudocoarctation syndrome, which represents a surgical emergency,
is reported in a high number of cases.
The correct timing of aortic repair in a polytraumatized patient should be considered and balanced along
with other severe injuries, without a fixed priority.
Therefore, stent graft repair can be performed after
trauma earlier than surgical repair and also soon after
the management of other life-threatening lesions. In patients who do not have severe associated lesions, delaying the treatment of traumatic rupture of the thoracic
aorta does not provide any advantage and it should be
performed as soon as possible.

316
https://t.me/med1917
VII. Aortic Injury
31.7 Endovascular Treatment
For many years traumatic aortic injury has been considered a highly lethal lesion and a potential cause of
death in blunt chest trauma. Despite evidence in the literature of lower morbidity and mortality, initial medical
management of uncomplicated aortic injury and subsequent delayed surgery have not been easily accepted in
the clinical practice.
From 1996 the introduction of endovascular techniques for the thoracic aorta in the clinical practice
opened up a less invasive option for these patients for
whom emergency treatment is necessary and these
techniques represent a viable alternative with very low
risk and limited impact on trauma destabilization. After
initial limited series and case reports, endovascular
treatment is going to become the method of choice in
management of TAR [31±36, 48, 49]. Because of the
lower invasivity, avoiding thoracotomy and the use of
heparin, endovascular repair can be applied in acute
patients without the risk of threatening pulmonary,
head or abdominal traumatic lesions. The risk of paraplegia seems to be very low in endovascular techniques,
even in extensive atherosclerotic aneurysms in which
the coverage of the stent graft extends from the left subclavian artery to the celiac axis. Therefore, we may expect a very low rate of or absent paraplegia for the
short stent-graft coverage of a posttraumatic aneurysm.
At present, standard measurements of thoracic stent
grafts are available, allowing their use in an emergency.
Actually, in an unstable patient, endovascular techniques offer a suitable alternative to open repair.
For a chronic post-traumatic aneurysm endovascular
treatment represents a favorable alternative treatment of
asymptomatic disease that is frequently recognized several years after the trauma. Chronic posttraumatic aneurysms are potential evolving lesions. Death from rupture may occur many years after injury sometimes
without onset of any signs and symptoms. Because it is
impossible to predict which aneurysm still remains
quiescent, elective repair is always recommended for
both symptomatic and asymptomatic lesions.
References
1. Passaro E, Pace WG. Traumatic rupture of the aorta. Surgery 1959; 46:787±791.
2. Parmley LF, Mattingly TW, Manion WC, Jahnke EJ Jr.
Nonpenetrating traumatic injury of the aorta. Circulation
1958; 17:1086±1101.
3. Strassman G. Traumatic rupture of the aorta. Am Heart J
1947; 33:508±515.
4. Richens D, Kotidis K, Neale M, et al. Rupture of the aorta
following road traffic accidents in the United Kingdom
1992±1999. The results of the co-operative crash injury
study. Eur J Cardiothor Surg 2003; 23:143±148.
5. National Safety Council. Accident Facts. Preliminary condensed edition, March 1983.
6. Hunt JP, Baker CC, Lentz CW, Rutledge RR, Oller DW,
Flowe KM, Nayduch DA, Smith C, Clancy TV, Thomason
MH, Meredith JW. Thoracic aorta injuries: management
and outcome of 144 patients. J Trauma 1996; 40:547±556.
7. Ben-Menachem Y. Rupture of the thoracic aorta by broadside impacts in road traffic and other collisions: further
angiographic observations and preliminary autopsy findings. J Trauma 1993; 35:363±367.
8. Arajarvi E, Santarvirta S, Tolonen J. Aortic ruptures in
seat belt wearers. J Thorac Cardiovasc Surg 1989; 98:355±
361.
9. 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.
10. Lundevall J. The mechanism of traumatic rupture of the
aorta. Acta Pathol Microbiol Scand 1966; 62:34±36.
11. Sevitt S. The mechanisms of traumatic rupture of thoracic
aorta. Br J Surg 1977; 64:166±173.
12. Kouchoukos NT, Blackstone EH, Doty DB, Hanley FL,
Karp RB. Acute traumatic aortic transection. In: Kirklin
JW, Barrat B, editors. Cardiac surgery. Churchill Livingstone, New York, 1986. p. 1799±1819.
13. Eddy CA, Rush VW, Marchioro T, Ashbaugh D, Verrier
ED, Dillard D. Treatment of traumatic rupture of the thoracic aorta. Arch Surg 1990; 125:1351±1355.
14. Malm JR, Deterling RH. Traumatic aneurysm of the thoracic aorta simulating coarctation. J Thoracic Cardiovasc
Surg 1960; 40:271±278.
15. Cowley RA, Turney SZ, Hankins JR, Rodriguez A, Attar S,
Shankar BS. Rupture of thoracic aorta caused by blunt
trauma. A fifteeen-year experience. J Thorac Cardiovasc
Surg 1990; 100:652±661.
16. Cernaianu AC, CilleyJH, Baldino WA, Spence RK, Del
Rossi AJ. Determinants of outcome in lesions of the
thorcic aorta in patients with multiorgan system trauma.
Chest 1992; 101:331±335.
17. Von Oppell UO, Dunne TT, de Groot MK, Zilla P. Traumatic aortic rupture: twenty-year metaanalysis of mortality and risk of paraplegia. Ann Thorac Surg 1994; 58:585±
593.
18. Williams JS, Graff JA, Uku JM, Stening JP. Aortic injury
in vehicular trauma. Ann Thorac Surg 1994; 57:726±730.
19. Shorr RM, Crittenden M, Indeck M, Hartunian SL, Rodriguez A. Blunt thoracic trauma. Analysis of 515 patients.
Ann Surg 1987; 206:200±205.
20. 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; 42:374±383.
21. Jahromi AS, Kazemi K, Safar HA, Doobay B, Cin CS.
Traumatic rupture of the thoracic aorta: cohort study and
systematic review. J Vasc Surg 2001; 34:1029±1034.
22. Downing SW, Cardarelli MG, Sperling J, et al. Heparinless
partial cardiopulmonary bypass for the repair of aortic
trauma. J Thorac Cardiovasc Surg 2000; 120:1104±1111.
23. Jamieson WRE, Janusz MT, Gudas VM, Burr LH, Fradet
GJ, Henderson C. Traumatic rupture of the thoracic aorta:
third decade of experience. Am J Surg 2002; 183:571±575.
24. Razzouk AJ, Gundry SR, Wang N, del Rio MJ, Varnell D,
Bailey LL. Repair of traumatic aortic rupture: a 25-year
experience. Arch Surg 2000; 135:913±918.
25. Pate JW. Is traumatic rupture of the aorta misunderstood?
Ann Thorac Surg 1994; 57:530±531.
26. Pate JW, Fabian TC, Walker W. Traumatic rupture of the
aortic isthmus: an emergency? World J Surg 1995; 19:119±
126.

R. Fattori, D. Pacini Chapter 31 Traumatic Aortic Rupture
https://t.me/med1917
317
27. Akins CW, Buckley MJ, Dagget W, McIlduff JB, Austen
WG. Acute traumatic aortic disruption of the thoracic
aorta: a ten-year experience. Ann Thorac Cardiovasc Surg
1981; 31:305±309.
28. Maggisano R, Nathens A, Alexandrova NA, et al. Traumatic rupture of the thoracic aorta: should one always operate immediately? Ann Vasc Surg 1995; 9:44±52.
29. Hess PJ, Howe HR, Robicsek F, et al. Traumatic tears of
the thoracic aorta: improved results using the Bio-Medicus pump. Ann Thorac Surg 1989; 48:6±9.
30. Galli R, Pacini D, Di Bartolomeo R, et al. Surgical indication and timing of repair of traumatic aortic ruptures of
the thoracic aorta. Ann Thorac Surg 1998; 62:462±464.
31. Dake MD, Miller DC, Semba CP, et al. Transluminal placement of endovascular stent-grafts for the treatment of
descending thoracic aortic aneurysm. N Engl J Med 1994;
331:1729±1734.
32. Grabenwoeger M, Hutshala D, Ehrlich MP, et al. Thoracic
aortic aneurysms: treatment with endovascular self-expandable stent grafts. Ann Thorac Surg 2000; 69:441±445.
33. Mitchell RS, Miller DC, Dake MD, et al. Thoracic aortic
aneurysm repair with an endovascular stent graft: the
ªFirst Generationº. Ann Thorac Surg 1999; 67:1971±1974.
34. Fujikawa T, Yukioka T, Ishimaru S, et al. Endovascular
stent grafting for the treatment of blunt thoracic aortic
injury. J Trauma 2001; 50:223±229.
35. Fattori R, Napoli G, Lovato L et all. Indications for, timing
of and results after treatment of catheter based treatment
of the injury of aorta. AJR Am J Roentgenol 2002;
178:125±132.
36. Lachat M, Pfammatter T, Witzke H, at al. Acute traumatic
aortic rupture: early stent graft repair. Eur J Cardiothorac
Surg 2003; 21:959±963.
37. Kalmar P, Otto CB, Rodewald G. Selection of the proper
time for operation of traumatic thoracic aortic aneurysms. Thorac Cardiovasc Surg 1982; 30:36±37.
38. Hartford JM, Fayer RL, Shaver TE, et al. Transection of
the thoracic aorta: assessment of a trauma system. Am J
Surg 1986; 151:224±229.
39. Holmes 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; 73:1149±1154.
40. Stulz P, Reimond 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.
41. Fattori R, Celletti F, Bertaccini P, et al. Delayed surgery of
traumatic aortic rupture: role of magnetic resonance
imaging. Circulation 1996; 94:2865±2870.
42. Kwon CC, Gill IS, Fallon WF, et al. Delayed operative intervention in the management of traumatic descending
thoracic aortic rupture. Ann Thorac Surg 2002; 74:S1888±
1891.
43. Langanay T, Verhoye J, Corbineau H, et al. Surgical treatment of acute traumatic rupture of the thoracic aorta: a
timing reappraisal? Eur J Cardiothorac Surg 2002; 21:
282±287.
44. Kipfer B, Leupi F, Schuepbach 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.
45. Del Rossi AJ, Cernaianu AC, Madden LD, Cilley JH,
Spence RK, Alexander JB, Ross SE, Camishion RC. Traumatic disruptions of the thoracic aorta: treatment and
outcome. Surgery 1990; 108:864±870.
46. Pacini D, Angeli E, Fattori R, et al. Traumatic rupture of
the thoracic aorta: ten years of delayed management. J
Thorac Cardiovasc Surg 2005; 129:880±884.
47. Fattori R, Celletti F, Descovich B, et al. Evolution of posttraumatic aneurysm in the subacute phase: magnetic resonance imaging follow-up as a support of the surgical timing. Eur J Cardiothorac Surg 1998; 13:582±587.
48. Rousseau H, Soula P, Perreault P, Bui B, Janne d'Othee B,
Massabuau P, Meites G, Concina P, Mazerolles M, Joffre F,
Otal P. Delayed treatment of traumatic rupture of the
thoracic aorta with endoluminal covered stent. Circulation
1999; 99:498±504.
49. Fattori R, Napoli G, Lovato L, et al. Descending thoracic
aortic diseases: stent-graft repair. Radiology 2003;
229:176±183.

Surgical Treatment of an
https://t.me/med1917
Acute Isthmus Traumatic Rupture
Thierry Langanay, Bertrand De Latour,
Alain Leguerrier
Chapter
32
Contents
32.1 Introduction ......................
32.2 Clinical Features .................... 319
32.2.1 Patients .................... 319
32.2.2 Diagnosis ................... 320
32.2.3 Surgical Treatment .............. 321
32.2.4 Results ..................... 322
32.3 Technique of Surgical Repair .............322
32.4 Special Situations and Controversies ........ 325
32.4.1 Update in Natural History ......... 325
32.4.2 Associated Lesions .............. 325
32.4.3 Postoperative Paraplegia .......... 325
32.4.4 Endovascular Therapy ............ 326
32.4.5 Medical Treatment .............. 326
32.5 Current Therapeutic Strategy ............. 326
32.6 Proposal for a Timing Reappraisal of Aortic Repair 327
32.7 Conclusion ....................... 328
319
32.1 Introduction
Acute ruptures of the aortic isthmus account for about
85% of aortic injuries due to blunt trauma. They are
generally related to a violent crash involving a sudden
deceleration. Polytraumatisms and other life-threatening
injuries are often associated with cardiovascular lesions.
It is generally admitted that about 80% of casualties die
at the accident scene and that among the survivors only
20% would survive without emergent surgical repair of
the aortic injury.
After surgery, however, the hospital mortality rate remains high, and stands around 20% in most reports in
the literature [1, 2]. This high mortality rate seems to
be mostly linked to lesions associated with aortic rupture. On the other hand, paraplegia is the most feared
complication after surgery requiring aortic cross-clamping. The use of cardiopulmonary bypass (CPB), which
provides distal perfusion during the duration of aortic
cross-clamping, appears to dramatically reduce the risk
and the actual rate of postoperative spinal cord injury
[2]. But the necessity of full systemic heparinization
during CPB entails the risk of inducing or severely worsening bleeding in a coexisting internal wound and particularly brain or pulmonary contusion, leading to fatal
hemorrhage in many cases. This raises the difficult
question of surgical priority and/or of delaying the aortic repair until the associated life-threatening lesions
are sufficiently healed or under control [3±5].
32.2 Clinical Features
32.2.1 Patients
From October 1976 to October 2004, 62 patients (52 men
and ten women) were operated on for an acute rupture of
the thoracic aorta in our institution. The age ranged between 14 and 72 years with a mean of 28 Ô 10.5 years. Forty
patients (63%) were less than 30 years old (Fig. 32.1).
The patients' files were analyzed retrospectively from
the data collected at the time of hospitalization. Those
data together with the data collected during the followup were entered into the database of our center, and
were treated statistically with a Hewlett-Packard 9000
computer using Statview statistical software.
All patients had been victims of a violent accident
involving a mechanism of sudden deceleration. Fifty-six
patients (90%) experienced a traffic accident: car crash
in 41 cases (66%), motorcycle crash in 13 cases (21%),
and pedestrian knock over in two cases (3%). Six patients (10%) had been the victim of fall (8±10 m).
On admission, 26 patients (42%) showed evidence of
hypovolemic shock with unstable hemodynamics. Ten
patients (16%) presented with acute respiratory distress,
in connectionwith a flail chest in six patients (10%).
Five patients (8%) suffered from a pseudocoarctation
syndrome with complete abolition of the femoral
pulses. In two of those (3%) there was evidence of ischemia of the lower limbs in relation to a complete
thrombosis of the distal aorta.

320
https://t.me/med1917
VII. Aortic Injury
Fig. 32.1. Repartition of patients according to age
One patient (1.5%) had paraplegia due to a coexisting spine fracture and spinal cord lesion, one patient
(1.5%) had paraparesis and one patient (1.5%) suffered
from neurological deficit of the right upper limb.
32.2.2 Diagnosis
The possibility of an aortic rupture was suggested by
several signs associated in various manners. Widening
of the upper mediastinum was present on plain chest
film in 51 patients (82%) (Fig. 32.2). In 23 patients
(37%) the aortic rupture was suspected because of the
loss of parallelism of the aortic walls or the widening
of the aortic isthmus on routine computed tomography
(CT) scans performed to check the thoracic lesions of
the polytraumatism (Fig. 32.3).
Fig. 32.3. Aortic rupture on the computed tomography scan
Fig. 32.4. Aortogram showing the loss of parallelism of the aor-
tic walls
Table 32.1. Lesions associated with aortic rupture
Patients N Percentage
Fig. 32.2. Widening of the upper mediastinum on the standard
chest X-ray
Thoracic lesions
Rib fracture
Flail chest
Sternal fracture
Head injury
Skull fracture
Brain contusion and coma
Orthopedic injury
Lower limb fracture
Upper limb fracture
Pelvic fracture
Rachis fracture
Maxillo-facial fracture
Clavicule fracture
Abdominal lesions
Ruptured spleen
Kidney contusion
Liver wound or contusion
Ruptured diaphragm
Other
37
25
47
21
60
46
74
12
19
7
11
40
2
13
27
15
19
10
3
21
76
43
24
30
4
6
8
13
3
5
34
16
7
11
7
11
2
3
2
3

T. Langanay et al. Chapter 32 Surgical Treatment of an Acute Isthmus Traumatic Rupture
https://t.me/med1917
Fig. 32.5. Delay between the accident and the
aortic repair
321
Fig. 32.6. Techniques of aortic repair and spinal cord protection
In one patient (1.6%) the occurrence of a systolic
murmur 11 days after the accident led to the diagnosis,
which was confirmed by a transesophageal echocardiogram (TEE) and a subsequent aortogram.
Forty-four patients (71%) underwent an aortogram
(Fig. 32.4). For the remaining 18 patients (29%), an aortogram was not obtained either because the CT scan
convincingly demonstrated the presence of the aortic lesion (16 cases, 26%) or because the clinical condition
was too unstable to allow any further delay to surgery.
For those two patients, the diagnosis was confirmed at
emergency thoracotomy. If an aortogram was the rule
in the early years of this series, it has now been replaced by CT scan and for the last twelve patients no
aortogram was obtained.
The aortic lesion was isolated in only five patients
(8%). All other patients (57±92%) sustained major associated injuries, reflecting the magnitude of the violence
of the accident. The associated injuries are summarized
in Table 32.1. They were responsible for coma in 13
cases (21%), and an emergency laparotomy was performed prior to the aortic repair in 17 cases (28%).
32.2.3 Surgical Treatment
Thirty-seven patients (60%) underwent aortic repair
within 24 h of the accident (Fig. 32.5). Conversely, 25
patients (40%) were treated after a delay extending over
1 month, 23 patients were operated on and two patients
were treated with an endoprosthesis. This delay was
either due to a late diagnosis, the aortic rupture being
obscured by major coexisting lesions in 12 patients, or
was made on purpose for 13 patients because of the
presence of severe associated injuries (four polytraumas
with multiple and severe orthopedic lesions, two ruptured spleens, one liver wound, one coma grade III and
several pulmonary contusions) thought to make the
emergency aortic repair riskier than continued intensive medical therapy.
Sixty patients were operated on by conventional sur-
gery and two were treated with an endoprosthesis (Fig.
32.6).
During surgery, the patients were intubated with a
double-lumen tube in order to allow separate ventilation of the lungs. The isthmic aorta was approached
through a left posterior thoracotomy in the fourth intercostal space in 58 patients (96%). In the remaining two
patients, a sternotomy was carried out for resuscitation

322
https://t.me/med1917
VII. Aortic Injury
purposes. Spinal cord protection and perfusion of distal
organs were achieved by the use of a conventional CPB
whenever possible. This was the case for 57 patients
(95%), the remaining three patients being operated on
either with a Gott shunt (one patient) or with the
clamp-and-sew technique (two patients). The CPB was
established in various manners. The aortic clamping
time ranged from 21 to 110 min (mean, 58 min). There
was no difference in clamping time depending on the
presence or the absence of CPB.
In two cases (3%) the aortic repair had to be carried
out during circulatory arrest at deep hypothermia because of the proximal extension of the aortic tear to the
transverse arch.
The aortic rupture was circumferential in 39 patients
(65%), partial in 20 (33%) and bifocal in one (2%). The
aortic repair could be achieved through direct suture in
26 patients (43%) but required a Dacron prosthesis interposition in the remaining 34 patients (57%).
For the last two cases, because of coexisting lesions
(polytraumatism and lung contusion) and an unstable
aortic lesion, an endoprosthesis was implanted on the
second day after the accident. The immediate outcome
was uneventful.
32.2.4 Results
The overall hospital mortality amounts to 16% (ten patients). Four patients died in the operating theater. Six
patients died during the postoperative course. The time,
circumstances and causes of death are summarized in
Table 32.2.
Several nonfatal complications were observed during
the postoperative course. One patient experienced paraplegia (T-3 level), which appeared 72 h after the surgical procedure and was totally regressive within
3 months (2%). This patient had been operated on with
the aid of CPB with a cross±clamping time of 59 min, a
mean distal arterial pressure of 80 mmHg during CPB
and a total blood loss of 450 ml for the first postoperative 24 h. The only deleterious element could have been
the intraoperative suppression of two pairs of intercostal arteries. However, this delayed spinal cord injury
might have been the result of some reperfusion syndrome with spinal cord edema. This could then explain
the total regression of the neurological deficit in a
rather short time.
Eleven survivors (22%) showed evidence of arterial
hypertension. The mean age of this subgroup of patients was 22.7 Ô 6.4 years and all but two ruptures were
treated by a Dacron tube interposition. No particular
reason could be found; the arterial hypertension was
controlled by medical therapy.
32.3 Technique of Surgical Repair
The patient is placed in the right lateral decubitus position and then the hips are rolled back toward a more
supine position so that the left femoral vessels are accessible (Fig. 32.7) [6, 7].
During surgery, the patient is intubated with a double-lumen tube in order to allow separate ventilation of
the lungs. A catheter is inserted in the patient's right radial artery and another one in the right pedious artery,
opposite to the femoral arterial cannulation, to continuously monitor blood pressure and the distal perfusion.
One or two large-bore needles are positioned securely
in a peripheral vein after placement of a central vein
catheter. A Swan±Ganz catheter might be useful depending on the general condition of the patient (advanced age, cardiac or renal insufficiency). Vesical and
gastric tubes are also inserted.
The isthmic aorta is approached through a wide left
posterior thoracotomy in the fourth intercostal space.
This provides excellent viewing on the aortic isthmus
but allows also access to the aortic arch, the pulmonary
artery, the descending aorta and the left side of the
heart. The arterial cannulation is realized before the
thoracotomy because it allows rapid and massive retransfusion in the case of an aortic rupture occurring
during the thoracotomy, especially when the lung compression on the aortic adventitia is released during dis-
Table 32.2. Circumstances, dates and causes of hospital deaths
Surgery/accident Associated lesions Death/surgery Causes
5th day Brain contusion Day 0 Intracerebral bleeding
11th day Lung contusion Day 0 Pulmonary bleeding
Emergency Resuscitation Day 0 Multiorgan failure +hemorrhage
Emergency Lung contusion Day 0 Pulmonary bleeding
Emergency Brain contusion Day 1 Intracerebral bleeding
Emergency Distal malperfusion Day 1 Multiorgan failure
2nd day Distal malperfusion Day 2 Multiorgan failure
Emergency Preoperative inhalation Day 2 ARDS
Emergency Bronchial rupture + lung contusion Day 10 Septicemia
2nd day endoprothesis Brain lung contusion Day 31 ARDS
ARDS acute respiratory distress syndrome

T. Langanay et al. Chapter 32 Surgical Treatment of an Acute Isthmus Traumatic Rupture
https://t.me/med1917
stable hemodynamic condition during the control of
the aorta. To avoid such a situation, the lung is cautiously retracted and the aorta controlled proximally
and distally before entering the hematoma. Most of the
time, this requires separate control of the distal arch
and the left subclavian artery.
The mediastinal pleura is opened beyond the hematoma over the distal transverse arch, the left subclavian
artery and the upper descending aorta. The dissection
is carried around the vessels, and once the circumferential control has been obtained three tapes are placed, so
that a cross-clamp can be placed immediately in case a
rupture occurs during the dissection of the hematoma
which is conducted step by step toward the tear. The
hematoma is largely removed; the distal clamp is then
moved proximally as far as possible to avoid keeping intercostal arteries in the excluded part of the aorta by
the clamping which would provoke retrograde bleeding
and to allow retrograde flow to go into the intercostal
arteries. The dissection is conducted toward the transection, staying in the periaortic tissue plane. Usually
there is some bleeding into the field from the intercostal arteries between the clamps. They should not be ligated nor oversewn if possible in order to preserve
spinal cord vascularization and the aorta is tailored to
preserve their origins in the repair. The dissection is often more difficult in the case of delayed repair, compared with fresh rupture, because of fibrosis of the hematoma that already exists. In all cases, identification of
the recurrent nerve is difficult, so it might be injured
by the surgical act as well as by the accident itself (a
postoperative recurrent paralysis is not so rare in our
experience) (Fig. 32.8).
A transversal aortotomy is realized in front of the lesion, which is then analyzed; the tear might be circumferential, incomplete with a preserved posterior wall or
more complex with a spiroid tear. Aortic continuity is
reestablished either by a direct end-to-end suture or by
Fig. 32.7. The patient is positioned in the right lateral decubitus
position
section. A cell-saver device is used to suck the blood
out of the thorax so that it permits an autotransfusion
either by the CPB or by the peripheral veins.
A median sternotomy can be preferred in the case of
an unstable hemodynamic state because of the easiest
and fastest realization. It allows the installation of a
CPB and an aortic cross-clamping.
Great care must be taken during the dissection not
to provoke a hemorrhage by disturbing the mediastinal
hematoma, which usually holds back the tear and prevents active bleeding in the pleural space. If this does
occur, the use of the cell-saver and cardiotomy suction
will allow immediate and massive autotransfusion via
the femoral arterial cannula and maintenance of a
a graft interposition. Whenever possible, we prefer to
realize a direct reconstruction, with a continuous running suture with 4-0 (3-0) polypropylene as it permits
us to obtain an ad integrum restitution of the aorta
without any sequelae. To avoid inadequate tractions on
the suture, it might be necessary to mobilize the two
extremities of the aorta by means of a larger dissection.
A direct repair is usually possible when the rupture is
incomplete because the intact part of the aortic wall
prevents the retraction of the two extremities. It might
be more difficult in the case of a spiroid tear concerning a lack of tissue or in the case of delayed surgery. In
such situations, a graft interposition with a pretreated
collagen-woven Dacron tube will be realized (Fig. 32.9).
One must remember that cross-clamping the distal
aortic arch rather than the aorta beyond the left subclavian artery induces a greater increase in left ventricular
afterload and decreases the collateral flow to the lower
part of the body and the spinal cord through the left
323

324
https://t.me/med1917
VII. Aortic Injury
Fig. 32.8. Operative view of the aortic rup-
ture
Fig. 32.9. The aorta is repaired by a di-
rect end-to-end anastomosis or a graft
interposition

T. Langanay et al. Chapter 32 Surgical Treatment of an Acute Isthmus Traumatic Rupture
https://t.me/med1917
325
subclavian artery. So if this can be done, the clamp
should be moved beyond the left subclavian artery.
32.4 Special Situations and Controversies
32.4.1 Update in Natural History
Parmley et al. [8] reported, in their classic autopsy study,
that 89.7% of patients who sustain a traumatic rupture of
the thoracic aorta will die within 6 h following the accident and that only 9% will survive beyond 24 h. Since
1958, therefore, traumatic aortic rupture has been considered as an absolute surgical emergency and the fear
of ªimpending ruptureº has led the surgical community
to rush for aortic repair. It appeared with time and
through increasing reported experiences that this surgical attitude could be debated, as it could be, in some instances, more harmful than useful. Many reports, indeed,
have demonstrated that the aortic lesion is seldom isolated [9, 10]. In a study by Pate et al. [9], only two out
of 59 patients had an isolated rupture of the thoracic aorta. The authors questioned the conclusions of the report
of Parmley et al. emphasizing the fact that it was a retrospective necropsic study implying many selections biases.
Similarly, Williams et al. [11] consider that Parmley et al.
overestimated the risk of delayed rupture of the aorta and
that many patients could undergo laparotomy or orthopedic surgery prior to the aortic repair with very little risk
of sudden rupture of the aortic false aneurysm. In a study
concerning 33 cases of isthmic aortic rupture, Cernaianu
et al. [12] demonstrated a close relationship between the
patients' survival rates and the delay separating the accident and the hospital referral. Conversely, they were unable to establish any relationship between the survival
rate and the delay separating the hospitalization from
the diagnosis, on the one hand, and the diagnosis from
the aortic repair, on the other hand.
32.4.2 Associated Lesions
The literature emphasizes that aortic rupture is seldom
isolated and that associated lesions are responsible for
hospital mortality in the majority of cases (Table 32.3).
This stems from four main reasons:
1. The coexisting lesion can be life-threatening in itself
(e.g., spleen rupture, liver contusion and brain trau-
ma).
2. The number and gravity of the coexisting lesions
may induce an intractable condition of hypovolemic
shock and multiorgan failure.
3. The full systemic heparinization required by the
CPB may adversely affect a brain or pulmonary con-
tusion, leading to fatal hemorrhage.
4. Some lesions (open fractures, voluminous limb he-
matomas) may become septic.
Recent literature [12±14] reports mortality rates ranging
from 5 to 35% and is in accordance with the figures reported by Von Oppell et al. [2] in their meta-analysis.
32.4.3 Postoperative Paraplegia
Paraplegia may complicate the surgical repair in 3±33%
of cases according to the literature [2, 14±16]. In a wellknown meta-analysis, carried out from 87 reports and
including 1,492 patients operated on for acute traumatic
rupture of the aorta, Von Oppell et al. [2] compared the
rates of hospital mortality and paraplegia according to
the surgical technique used during the aortic repair
(Table 32.4). When a distal perfusion system was used,
the risk of paraplegia decreased significantly compared
with that for the simple aortic cross-clamping technique
(6.1 vs 19.2%, p < 0.0001). The difference between ªactiveº and ªpassiveº perfusion systems also appeared significant (2.3 vs 11.1% paraplegias).
Similar data have been reported by several groups.
From a review of the literature including 749 patients,
Zeiger et al. [17] observed 2.9% paraplegias with the
use of CPB vs 20.4% with simple cross-clamping. Kodali
et al. [13] reported a difference of 3.2 vs 28.5% and Pate
et al. a difference of 3.8 vs 26.7% [10].
In contrast, the use of CPB, either total or partial,
requiring full heparinization of the patient, has been
held responsible for an increase in mortality and morbidity. In particular this technique can induce fatal
hemorrhage of brain and pulmonary contusions. This
possibly explains the high mortality observed in the
group of patients operated on with total heparinization
(18.2%) compared with that of those operated on without heparin (11.9%, p<0.01) in the meta-analysis of
Table 32.3. Role of associated lesions in hospital mortality (from the literature)
Katz et al. [15] 35 5 4 80
Mattox et al. [14] 32 6 6 100
Pate et al. [19] 59 6 2 33
Langanay et al. [5] 57 9 5 55
Ruptures (N) Deaths (N) Number of deaths related
to associated lesions
Percentage of deaths related
to associated lesions
Соседние файлы в папке Библиотека им академика М.И. Перельмана
