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R. Fattori, D. Pacini Chapter 31 Traumatic Aortic Rupture
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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.
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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
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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±
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18. Williams JS, Graff JA, Uku JM, Stening JP. Aortic injury in vehicular trauma. Ann Thorac Surg 1994; 57:726±730.
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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.
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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.
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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
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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.
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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
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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
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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
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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
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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
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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