Lessons learned from midterm follow-up of endovascular repair for traumatic rupture of the aortic isthmus
Article Outline
Objective
The aim of this study was to evaluate the short- and midterm results following endovascular repair of a traumatic rupture of the aortic isthmus.
Methods
Between January 2001 and January 2007, 27 patients underwent endovascular repair for acute traumatic rupture of the aortic isthmus (8 women, 19 men, mean age 40.2 ± 16.7 years [19-78]). All patients underwent a computed tomography scan resulting in the preoperative diagnosis of aortic disruptions. Twenty-one patients were treated within the first 5 days following diagnosis. Follow-up computed tomography scans were performed at 1 week, at 3 and 6 months, and annually thereafter. The median follow-up was 40 months.
Results
All endografts were successfully deployed (Excluder-TAG [16], Talent [10], Zenith [2]). Three patients required common iliac artery access. The morbidity rate was 14.8%: two cases of inadvertent coverage of supra-aortic trunks occurred peroperatively, a proximal type I endoleak was successfully treated by a proximal implantation of a second endograft, and one collapse of an endograft was successfully treated by open repair and explantation. No patient suffered transient or permanent paraplegia, cerebral complication, endograft migration, or secondary endoleak. The overall mortality rate was 3.7%.
Conclusions
Short and midterm results following endovascular treatment for traumatic rupture of the aortic isthmus favor the proposition of endovascular repair as the first-line treatment in hemodynamically unstable patients. In hemodynamically stable patients, the preoperative morphological evaluations aim to assess aortic anatomy and thereby detect possible technical limitations (aortic diameter <20 mm, severe aortic isthmus angulation, short proximal aortic neck <20 mm, conical aorta). In the presence of any one of these technical restrictions, open surgical treatment should be discussed to avoid major per- or postoperative complications related to endovascular repair. Further studies and long-term survival studies are mandatory to determine the efficacy and durability of this technique.
Open operative repair of a thoracic aortic disruption in the presence of other associated injuries correlates with significant mortality approaching 8% to 15%, despite significant improvements in intensive care.1 Paraplegia rates of 2.3% to 14% remain high due to aortic thoracic cross clamping and prolonged distal hypoperfusion in polytraumatized patients despite the use of circulatory assistance,1, 2 In 1994, Dake et al3 reported the first successful endovascular repair of thoracic aorta disease. Currently, endovascular endograft placement represents a valid option with low risk for thoracic aortic aneurysms and complicated type B dissections, especially for patients at high surgical risk.4
For this reason, endovascular repair of acute traumatic rupture of the aortic isthmus has been proposed for those patients with multiple system injuries and therefore considered to be at high surgical risk.5 Here, in this retrospective study, we aim to report our experience6, 7 treating these patients operated on within the last 7 years.
Methods
Patients
At our institution, between January 2001 and January 2007, 27 consecutive patients underwent endograft repair for acute traumatic rupture of the aortic isthmus. All patients admitted for blunt traumatic injury during that time were included. Patients included eight women and 19 men with a mean age of 40.1 ± 16.8 years (range 19 to 78 years). Diagnosis of aortic disruption was achieved by a preprocedural contrast-enhanced computed tomography (CT) scan of all patients, and an arteriography was performed in all cases except two hemodynamically unstable patients (active hemorrhage caused by abdominal injuries) for whom arteriography was contraindicated.
Endograft
Three endovascular devices were used: Excluder TAG (W. L. Gore & Associates, Flagstaff, Ariz), Talent (Medtronic Vascular, Santa Rosa, Calif), and Zenith distal extension cuff (Cook Inc, Bloomington, Ind).
Endovascular repair
Suitable morphology for endograft placement requires a proximal aortic neck length of at least 20 mm between the ostium of the left common carotid artery (LCCA) and the tear. Measurements from preprocedural imaging data were used to select the appropriate diameter and length of the endograft. Devices were oversized by 10% to 20% greater than the minor axis of the aortic neck to provide sufficient radial force for adequate fixation. We decided which commercial endograft to use according to the preoperative sizing of the aortic diameter at the proximal landing zone and according to the minimum diameter available of each commercial endograft to prevent excessive oversizing.
All procedures were performed in the operating room under general anesthesia. Patients were prepared and draped for femoral arteriotomy, potential iliac artery or retroperitoneal aortic approaches, and for emergency thoracotomy. All angiograms were performed through a 5F calibrated pigtail catheter (Cook Australia Pty Ltd, Queensland, Brisbane, Australia) placed percutaneously into the aortic arch via the brachial artery. A 260-cm, 0.035-inch Terumo guidewire (Terumo Medical Corporation, Tokyo, Japan) was placed under fluoroscopic control into the ascending aorta through a sheath in the common femoral artery; a 5F measuring pigtail catheter was advanced into the ascending aorta over the Terumo guide. This pigtail catheter was used to exchange the Terumo guide wire for a 0.035-inch-diameter Lunderquist (Cook Inc, Bloomington, Ind) to guide passage of the 22- to 24F sheath facilitated by application of a small amount of mineral oil. Angiography via a percutaneous brachial artery approach was performed before endograft deployment. Endograft deployment was performed under fluoroscopic control. A control angiography was performed to confirm appropriate position of the device and exclusion of the aortic disruption. In case of endoleak following endograft deployment, the endograft was further expanded with a low-pressure balloon.
Follow-up surveillance was performed with serial CT scans at 1 week, then at 3, 6, and 12 months, and annually thereafter. Outcomes were analyzed using Kaplan-Meier life-table analysis.
Results
The delay between the time of aortic disruption and endovascular treatment was less than 5 days for 21 patients (77.8%) with a mean interval of 9.8 ± 24.8 days. The time between traumatism and diagnosis was always less than 12 hours because these patients were polytraumatized and immediately transferred to our hospital. Diagnosis of aortic disruption was achieved by a contrast-enhanced computed tomography (CT) scan immediately after admission and before endovascular treatment. For six patients, treatment was delayed due to septic state or major cerebral lesions. Twenty-three (85.2%) patients presented with thoracic injuries: lung contusion (13), pneumothorax (6), hemothorax (8) and diaphragmatic rupture (4). Thirteen (48.1%) patients presented with cranial and spinal injuries: intracranial hematoma (10), tetraplegia (1), and spinal fractures (3). Fourteen (51.8%) patients presented with solid abdominal injuries: contusions or rupturing of the spleen (9), liver (10), and kidney (2). Nine (33%) patients presented with major bones fractures: fracture of the pelvis (6), and femur or open fracture of the leg (3). All the patients had multiple system injuries and were considered a high surgical risk. No patient died after admission to hospital and no patients were operated on by the open technique during the same period. The 1-year and 2-year survival rates were 0.92 (SE = 0.02) and 0.88 (SE = 0.03), respectively.
The Excluder TAG endograft (W.L. Gore & Associates, Flagstaff, Ariz) was used in 16 cases, the Talent endograft (Medtronic Vascular, Santa Rosa, Calif) in 10 cases, and Zenith distal extension cuff (Cook Inc, Bloomington, Ind) in two cases. The diameter of the implanted endograft ranged from 18 to 40 mm (mean: 27.3 ± 4.5 mm) and the endograft length from 100 to 150 mm (mean: 101.3 ± 13.8 mm). The choice of the endograft was related to the diameters available in order to prevent an excessive oversizing.
A retroperitoneal iliac approach was necessary in three cases where progression of the sheath by femoral access was impossible. Technical success was achieved in all cases. In three patients, for whom proximal aortic neck length was insufficient, the ostium of the left subclavian artery (LSA) was totally covered deliberately. For one patient in whom the hemodynamic status was unstable at the time of aortic disruption, a LSA to LCCA transposition was secondarily performed to treat vertebrobasilar insufficiency (vertigo and drop attacks). For the two remaining cases whose hemodynamic status was stable at the time of diagnosis, the landing zone was extended by prophylactic LSA to LCCA transposition before endograft repair.
The overall mortality rate was 3.7% (n = 1), and mortality rate related to aortic disruption was 0%. One patient died on the third postoperative day from a traumatic intracranial hematoma.
The morbidity rate was 14.8% (n = 3). No patients have been lost to follow-up, and all have completed each of their scheduled follow-up evaluations and CT scans. Three complications occurred during endovascular repair (Table I). In the first case, a proximal endograft migration occurred, totally covering the LCCA ostium. The endograft was pulled distally by traction from a low-pressure inflated balloon and re-established flow to the LCCA, however, an excessive distal migration led to a proximal type I endoleak. This endoleak was successfully treated by a proximal implantation of a second endograft on the second postoperative day. In the second case, following LSA transposition, the proximal edge of the endograft was placed just distal to the LCCA ostium to preserve common carotid blood flow. Passage of the low-pressure balloon in the endograft led to a proximal endograft jump and proximal migration; peroperative aortography demonstrated complete coverage of the LCCA and of the brachiocephalic trunk (BT). This inadvertent coverage of the LCCA and BT was successfully treated by the stenting of the LCCA across the ostium (Fig 1 and Fig 2) with a nitinol stent (Luminex 8/80 mm Bard Murray Hill, NJ) via a cervical approach. Thus, flow to the LCCA and BT was re-established by transcarotid insertion of a self-expanding stent with a high radial force alongside the thoracic endograft. This stent allowed a widely patent LCCA and BT with aortography demonstrating the exclusion of the aortic disruption, with no evidence of a type I endoleak. For the last case, a partial coverage of the LCCA was due to a covered open stent segment of a TAG device. The LCCA stenosis was nonsignificant (<50%) and a clinical and radiological follow-up was performed associated with antiplatelet medication.
Table I. Complication of graft positioning
| Patients | Anatomy | Type of graft | Complication | Intervention |
|---|---|---|---|---|
| 5 | Severe aortic isthmus angulation | Excluder 2 * 31/100 mm | Proximal endograft migration which totally covering the LCCA ostium | Endograft pulled distally thanks to an inflated low-pressure balloon; excessive distal migration led to a proximal type I endoleak successfully treated by a proximal implantation of a second endograft |
| 21 | Severe aortic isthmus angulation | Tag 26/100 mm | Collapse of an endograft | Open explant and repair by a left thoracotomy |
| 26 | Severe aortic isthmus angulation | Tag 31/100 Mm | Complete coverage of the LCCA and BT | Stenting of the LCCA across the ostium with a nitinol stent Luminex 8/80 mm. |

Fig 1.
Arteriography: flow to the left common carotid artery (LCCA) and brachiocephalic trunk (BT) was re-established by the stenting of the LCCA across the ostium with a bare nitinol stent alongside the thoracic endograft.
A collapse of an endograft (Fig 3 and Fig 4) was revealed at the 30th day following implantation, by a pseudocoarctation syndrome leading to functional renal failure. Open explant and repair by a left thoracotomy was successfully performed. No transient or permanent paraplegia or central neurological complications were observed. No endograft migration or perigraft leak has been observed during follow-up. Median follow-up period was 40 months.

Fig 3.
Arteriography: collapsed endograft. Collapse of the endograft (1) Reperfusion of the posttraumatic false aneurysm (2).
Discussion
Since the first report by Dake et al,3 endovascular management has emerged during the last decade as a valuable treatment modality for thoracic aortic diseases. Semba et al5 reported successful endovascular treatment of thoracic traumatic aortic rupture. Since this initial report, several case reports and institutional reviews reproduced their results; however, these series all include a relatively small number of patients.8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18 A review of reported series, each involving more than 10 patients from 1997 to 2007 (Table II), confirms that endovascular treatment for acute traumatic rupture can be achieved with a high technical success rate (98.8% in 220 patients). For these 220 patients, the overall mortality rate was 5.4% and with an aortic disruption related mortality rate of 1%. Despite significant improvements in medical management, analysis of these data shows that endovascular repair of aortic thoracic disruption correlates with lower rates of mortality rates compared with up to 15% associated with surgical series, as reported in a review of the literature by Jahormi et al.1
Table II. Endovascular treatment: review of literatures of series involving more than 10 patients from 1997 to 2007
| n | Technical success (%) | Mortality | Paraplegia (%) | Follow-up | |||
|---|---|---|---|---|---|---|---|
| Overall (%) | Related to aortic disruption (%) | ||||||
| Lachat8 | 2002 | 12 | 100 | 8 | 8 | 0 | 17 |
| Scheinert10 | 2003 | 10 | 100 | 0 | 0 | 0 | 17 |
| Melnitchouk9 | 2004 | 15 | 100 | 0 | 0 | 6.6 | 34.1 |
| Amabile11 | 2004 | 13 | 100 | 0 | 0 | 0 | 15.1 |
| Doss12 | 2005 | 18 | 100 | 0 | 0 | 0 | 19 |
| Peterson13 | 2005 | 11 | 100 | 0 | 0 | 0 | 21 |
| Marcheix17 | 2006 | 33 | 100 | 0 | 0 | 3 | 28.8 |
| Hoornweg15 | 2006 | 28 | 100 | 14.3 | 0 | 0 | 26.5 |
| Pratesi16 | 2006 | 11 | 100 | 9.1 | 0 | 0 | 18.2 |
| Steingruber14 | 2007 | 22 | 86.3 | 4.5 | 4,5 | 0 | 31.7 |
| Neschis18 | 2007 | 20 | 100 | 20 | 0 | 0 | 23 |
| Montpellier Hospital | 2007 | 27 | 100 | 3.7 | 0 | 0 | 37 |
| Mean | 220 | 98.8 | 5.4 | 1 | 0.9 | 24 | |
At a postoperative rate of 4%, paraplegia remains the main complication of aortic open surgical repair despite the use of circulatory assistance.1 In our series, no patients had paraplegia as a result of endovascular treatment. Melnitchouk et al9 and Marcheix et al17 reported two cases of transient paraparesis both spontaneously and completely regressive. With the avoidance of aortic cross-clamping and prolonged iatrogenic hypotension, results of endovascular repair show lower incidences of paraplegia relative to conventional treatment.
The timing of repair of traumatic injury of the aorta remains controversial. For some authors,19 a delayed treatment is considered appropriate after recovery from associated life-threatening injuries. However, a delayed treatment increases the risks of three major complications:20, 21 (1) an unforeseeable risk of developing delayed free rupture of an initially stable aortic tear; (2) a progressive dilation of the involved aortic segment exerting compression on the trachea and the left main bronchus; and (3) the creation of a fibrous and calcified connective within the aortic wall itself potentially modifying aortic compliance and compromising the success of endovascular treatment. Furthermore, a controlled hypotension may cause cerebral hypoperfusion among patients who have often suffered a cerebral trauma. Melnitchouk et al9 proposed emergency endograft repair to control blood loss in polytraumatized patients and to allow other surgical procedures with patients in a hemodynamically stable condition. Mean delay period before treatment in our series was less than 5 days for 78% of the patients. In a hemodynamically stable condition, a delay in treatment of a few days seems reasonable to treat the associated traumatic lesions. In our institution, we believe that endovascular management as soon as possible offers important advantages over a deliberate wait.
Three patients with an inadequate length of the proximal neck to effectively exclude thoracic aortic lesions had their LSA intentionally overstented. A meta-analysis of Peterson et al22 showed that morbidity relative to LSA revascularization before endograft repair was lower than morbidity in cases of LSA coverage without pre-endograft revascularization (3% vs 23%). In cases of traumatic aortic disruption, patients are generally young. LSA revascularization before endograft repair should be done to prevent neurological complications related to endovascular treatment. Maintaining normal perfusion of the ipsilateral vertebral artery allows the prevention of ischemia of the brainstem. Furthermore, preserving major collaterals of the vertebral artery that contribute to spinal blood flow could protect against spinal cord ischemia when multiple intercostal vessels are covered during thoracic endovascular repair.22 With an aortic transaction located within the proximal neck length necessary for adequate fixation (<20 mm) and a hemodynamically stable patient, our treatment strategy is to extend the landing zone by prophylactic LSA revascularization before endograft repair.
Traumatic aortic disruption represents a different disease process than aneurysm or aortic dissection. Complications and treatment considerations such as the choice of the endograft and its landing zone cannot be extrapolated from larger series reporting treatment of other aortic diseases. In our experience, the main technical limitations of endovascular repair of aortic traumatic disruption is related to the placement of the endograft in the distal portion of aortic arches, near the ostia of the supra-aortic trunks in young patients whose mean aortic diameter is generally less than 20 mm.23 A significant difference between proximal and distal aortic diameter (conical aorta) could be a risk factor of jump or proximal migration of the endograft during endograft placement. Partial or complete coverage of the supra-aortic trunks is a serious complication and requires immediate treatment. As a first attempt, traction of the endograft by a low-pressure balloon should always be tried. In case of failure, transposition or creation of a bypass would be too long and potentially cause ischemic cerebral injuries. Criado24 reported a percutaneous endovascular technique by retrograde puncture of the LCCA to deal with stent graft encroachment and coverage (partial or total) of the origin of the supra-aortic trunks during thoracic endovascular aortic repair. Retrograde catheterization and “interposition” of a bare metal stent between the thoracic endograft and the aortic wall allows preservation of arch branch patency during thoracic endovascular aortic repair and stenting by focally displacing the endograft device. This technique can lead to a rapid restoration of flow in case of inadvertent coverage of the supra-aortic trunks.
Acute aortic isthmus angulation and severely oversized endograft represent two potential anatomic risk factors increasing the probability of endograft collapse. In a multi-institutional retrospective analysis, Muhs et al25 collected computed tomography scans of six patients who had suffered radiologically confirmed TAG endograft collapse. This rare complication may compromise distal flow caused by the collapsed endograft, possibly resulting in acute and potentially lethal high thoracic aortic obstruction. Patients may also show no clinical symptoms of this thoracic aortic obstruction.26 Muhs et al25 reported several factors that may influence this complication: lack of apposition of the endograft to the aortic wall, acute aortic arch angulation, distal aortic diameter and minimum intragraft aortic diameter (aortic diameter perpendicular to the center lumen line at the intragraft landing zone), small diameter aortas, and high percentage of oversizing. The lack of smaller endografts and the small (<20 mm) aortic diameters of young patients does not often allow a moderate oversizing, and the endografts used are consequently severely oversized (>30%). For the patient in our series who experienced endograft collapse, the anatomic factors influencing the collapse, as found by the computed tomography scan performed at the seventh postoperative day, were: an aortic diameter of 20 mm, 30% device oversizing, and a lack of apposition of the endograft to the aortic wall due to the angulation of the proximal neck. Several therapeutic options can be proposed. Most reported cases have been treated by the implantation of a giant Palmaz stent (Cordis, Miami Lakes, Fla) or by the implantation of another endovascular graft within the collapsed endograft. Open endograft explant and repair through a left thoracotomy as performed on our patient is another option. Endovascular repair was not considered in this young patient due to a severely collapsed endograft and a high risk of coverage of supra-aortic trunks due to his extremely angulated aortic arch. The endograft explantation showed a good integration of the distal part of the endograft in the aortic wall after the first postoperative month.
Short and midterm results of endovascular treatment for traumatic rupture of the aortic isthmus suggest that endovascular repair should be proposed as a first-line treatment for hemodynamically unstable patients. For hemodynamically stable patients, the aim of the preoperative morphological evaluations is to assess aortic anatomy and thereby detect possible technical limitations (aortic diameter <20 mm, severe aortic isthmus angulation, short proximal aortic neck <20 mm, conical aorta). In the presence of any one of these technical restrictions, open surgical treatment should be discussed to avoid major per- or postoperative complications related to endovascular repair. Further studies and long-term survival studies are mandatory to determine the efficacy and durability of this technique.
Author contributions
References
- . Traumatic rupture of the thoracic aorta: cohort study and systematic review. J Vasc Surg. 2001;34:1029–1034
- . Traumatic aortic rupture: twenty-year meta-analysis of mortality and risk of paraplegia. Ann Thorac Surg. 1994;58:585–593
- . Transluminal placement of endovascular stent grafts for the treatment of descending thoracic aortic aneurysms. N Engl J Med. 1994;331:1729–1734
- . Endovascular treatment of thoracic aortic disease: four years of experience. Circulation. 2004;110:262–267
- Acute rupture of the descending thoracic aorta: repair with use of endovascular stent grafts. J Vasc Interv Radiol. 1997;8:337–342
- . Endovascular repair for acute traumatic rupture of the thoracic aorta. Ann Thorac Surg. 2003;75:1803–1807
- . Endovascular repair for acute rupture of the descending thoracic aorta. J Endovasc Ther. 2002;9:51–59
- Acute traumatic aortic rupture: early stent graft repair. Eur J Cardiothorac Surg. 2002;21:959–963
- Emergency stent-graft placement for hemorrhage control in acute thoracic aortic rupture. Eur J Cardiothorac Surg. 2004;25:1032–1038
- Endoluminal stent graft placement for acute rupture of the descending thoracic aorta. Eur Heart J. 2004;25:694–700
- . Emergency treatment of acute rupture of the descending thoracic aorta using endovascular stent-grafts. Ann Vasc Surg. 2006;20:723–730
- Surgical versus endovascular treatment of acute thoracic aortic rupture: a single-center experience. Ann Thorac Surg. 2003;76:1465–1469
- . Percutaneous endovascular repair of blunt thoracic aortic transection. J Trauma. 2005;59:1062–1065
- Placement of endovascular stent grafts for emergency repair of acute traumatic aortic rupture: a single-center experience. Eur Radiol. 2007;17:1727–1737
- Endovascular management of traumatic ruptures of the thoracic aorta: a retrospective multicenter analysis of 28 cases in The Netherlands. J Vasc Surg. 2006;43:1096–1102
- Acute traumatic rupture of the descending thoracic aorta: endovascular treatment. Am J Surg. 2006;192:291–295
- Endovascular repair of traumatic rupture of the aortic isthmus: midterm results. J Thorac Cardiovasc Surg. 2006;132:1037–1041
- Twenty consecutive cases of endograft repair of traumatic aortic disruption: lessons learned. J Vasc Surg. 2007;45:487–492
- Delayed treatment of traumatic rupture of the thoracic aorta with endoluminal covered stent. Circulation. 1999;99:498–504
- . The effect of changing presentation and management on the outcome of blunt rupture of the thoracic aorta. J Thorac Cardiovasc Surg. 2006;131:594–600
- Immediate versus delayed endovascular treatment of post-traumatic aortic pseudoaneurysms and type B dissections: retrospective analysis and premises to the upcoming European trial. Circulation. 2002;106:234–240
- . Utility of left subclavian artery revascularization in association with endoluminal repair of acute and chronic thoracic aortic pathology. J Vasc Surg. 2006;43:433–439
- Angiographic description of blunt traumatic injuries to the thoracic aorta with specific relevance to endograft repair. J Endovasc Ther. 2002;9:84–91
- . A percutaneous technique for preservation of arch branch patency during thoracic endovascular aortic repair (TEVAR): retrograde catheterization and stenting. J Endovasc Ther. 2007;14:54–58
- . Anatomic factors associated with acute endograft collapse after Gore TAG treatment of thoracic aortic dissection or traumatic rupture. J Vasc Surg. 2007;45:655–661
- . Collapse of a stent graft following treatment of a traumatic thoracic aortic rupture. J Endovasc Ther. 2005;12:503–507
Competition of interest: none.
PII: S0741-5214(07)02021-6
doi:10.1016/j.jvs.2007.12.008
© 2008 The Society for Vascular Surgery. Published by Elsevier Inc. All rights reserved.


