Hypothermic circulatory arrest for repair of injuries of the thoracic aorta and great vessels
http://www.100md.com
《血管的通路杂志》
Department of Cardiovascular and Thoracic Surgery, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas, TX 75390-8879, USA
Presented at the 53rd International Congress of the European Society of Cardiovascular Surgery, Ljubljana, Slovenia, June 2–5, 2004.
Abstract
Traumatic great vessel injuries are frequently lethal events. Expedient diagnosis and prompt repair by clamping and replacing the affected segment of aorta (often with left-heart bypass) can salvage many patients. Rarely, due to the location of the injury or delayed presentation, standard techniques cannot be used and hypothermic circulatory arrest (HCA) is required for access, exposure and repair. The results of surgical reconstruction of acute and chronic traumatic thoracic vascular injuries under these circumstances are not well described. We reviewed all operations on the great vessels at our institution over a 16-year period that had a traumatic etiology and used HCA. Fourteen cases were identified (10 male, 4 female, age 46±4 years), arising from three acute and eleven remote traumatic events. All repairs were performed with cardiopulmonary bypass (mean CPB time was 155±13 min), deep hypothermia, and an interval of circulatory arrest (mean circulatory arrest interval 31±4 min). One patient died in the perioperative period from a stroke (7% 30-day mortality). Another patient exsanguinated from a recurrent pseudoaneurysm 3 months post-repair. No patient developed paraplegia. HCA can be a useful adjunct in managing complex post-traumatic great vessel injuries. Acute injuries of the ascending aorta and transverse arch usually require this technique, but HCA also offers a safe way to manage repair of the descending thoracic aorta when proximal aortic control is compromised.
Key Words: Hypothermic circulatory arrest; Great vessels; Thoracic aorta; Vascular trauma
1. Introduction
Injuries to the thoracic aorta and great vessels are a major cause of mortality in trauma patients. These injuries are most commonly the result of blunt trauma with a rapid deceleration mechanism [1], although they may also arise from penetrating trauma or iatrogenic injury. Most great vessel injuries can be diagnosed with a high degree of accuracy with modern imaging techniques, especially multiplanar arteriography, helical computed tomography (CT), magnetic resonance imaging (MRI) or trans-esophageal echocardiography (TEE).
The most common site of great vessel injury is in the proximal descending thoracic aorta (aortic isthmus) [2]. When diagnosed early, most centers recommend early repair, and a variety of surgical techniques have been advocated including direct suture or interposition graft placement with simple aortic cross-clamping alone [3], with aortic clamping plus left heart bypass for distal perfusion [4], or rarely with aortic clamping and full cardiopulmonary bypass support [5]. More recently, repair with endovascular stent grafts has also been described [6].
Certain situations mandate more complex approaches. In some instances, the injury may not have been diagnosed at the time of the initial traumatic event. Over time, a large pseudoaneurysm can develop which prohibits safe proximal aortic clamping for conventional repair. In other cases, the injury involves the ascending aorta, transverse aortic arch, or the origins of the arch vessels at sites where clamping of the aorta is not feasible or carries a high risk of stroke. Injuries of the thoracic aorta may also present as aortic dissection [7]. In these complex cases, hypothermic circulatory arrest may be required to facilitate surgical exposure and reduce the risk of neurologic injury [8]. The purpose of the current study was to review our experience with circulatory arrest for repair of acute and chronic traumatic thoracic vascular injuries.
2. Materials and methods
This study was approved by the Institutional Review Boards of the University of Texas Southwestern Medical Center at Dallas and the North Texas Veterans Administration Hospital. Surgical and perfusion databases at our affiliated institutions were reviewed between the dates of 1/1/1990–12/31/2005 to identify operations on the great vessels that utilized hypothermic circulatory arrest as an adjunct to surgery. Medical records and radiographic studies of potential cases were then evaluated to identify trauma-related injuries.
Injuries were categorized as ‘definite’ or ‘possible’ vascular trauma based on clinical data. ‘Definite’ cases were defined as great vessel injuries with a significant history of trauma and either no underlying risk factors for the injury or documented negative screening prior to the traumatic event (in the case of aortic aneurysms and dissections). ‘Possible’ traumatic vascular injuries were defined as cases with significant antecedent trauma in patients that had either medical risk factors for the lesion (such as hypertension in patients presenting as aortic dissection) or an atypical lesion diagnosed after significant thoracic trauma.
Injuries were further divided into ‘acute’ and ‘remote’ based on whether the great vessel injury was diagnosed at the initial trauma presentation. Injuries that were suspicious by radiographic or intraoperative appearance, but lacked a documented antecedent history of trauma were specifically excluded. Patients that underwent endovascular repair or repair utilizing conventional cardiopulmonary bypass were also not considered.
In all cases, patient clinical information, presenting symptoms, and injury characteristics were recorded. Details of the operative procedure, including the type of repair, durations of total cardiopulmonary bypass and hypothermic circulatory arrest, perfusion temperatures achieved, and use of cerebral protection techniques were collected. Outcomes of the surgical procedures were also examined. Numerical data are reported as mean±standard error of the mean.
A median sternotomy was performed for lesions involving the ascending aorta and proximal transverse arch. Intermittent retrograde cold blood cardioplegia was utilized in repairs of these proximal injuries and the left ventricle was vented through the right superior pulmonary vein. The heart was de-aired using standard techniques in these patients.
A posterolateral fifth interspace left thoracotomy was utilized to approach injuries of the distal arch and descending aorta. Cardiopulmonary bypass was established with arterial inflow into the common femoral artery or descending thoracic aorta and venous return supplied from a cannula inserted into the common femoral vein and advanced to the right atrium. In some cases the pulmonary artery was cannulated for additional venous return, as we have previously described [9]. For these distal injuries the heart was arrested with a bolus of potassium chloride administered through the cardiopulmonary bypass circuit when ventricular fibrillation occurred during cooling. The left ventricle was not decompressed. The aorta was de-aired by placing the patient in deep Trendelenberg position, gently inflating the lungs, and gradually reinstituting cardiopulmonary bypass after the proximal anastomosis was completed.
Repair of acute injuries was delayed until significant intra-abdominal or intra-cranial injuries had been excluded or stabilized to minimize bleeding risk from heparinization and cardiopulmonary bypass during the aortic reconstruction.
3. Results
From this review, 11 ‘definite’ and 3 ‘possible’ cases (10 male, 4 female, age 46±4 years) were identified. These represented 3 acute and 11 remote injuries. All ‘possible’ cases were remote presentations. Among remote injuries, the average time to diagnosis was 8.5±3 years. The mechanism of injury included one penetrating injury (gun shot wound [GSW]), one iatrogenic injury, and twelve blunt injuries (eleven motor vehicle collisions [MVC], one crush injury).
Three patients had significant antecedent procedures: Patient 2 was diagnosed with a proximal, descending thoracic aortic rupture with dissection into the aortic arch during an attempted percutaneous coarctation balloon angioplasty. Patient 6 had undergone four prior operations for repair of congenital heart disease including repair of a Type B interrupted aortic arch with placement of a descending thoracic aortic homograft. Patient 8 had undergone bilateral thoracotomies for treatment of a gun shot wound to the chest 30 years prior. At least four patients did not seek medical attention after the traumatic event. For eight of the remaining patients, the thoracic vascular injury was not diagnosed during the initial evaluation or hospitalization. One patient had a CT abnormality that was not further worked up until he presented with chest pain 2 years later. Cardiac catheterization was then performed for presumed myocardial ischemia at which time a descending thoracic pseudoaneurysm with dissection into the transverse arch was noted. All remote presentations eventually developed symptoms. See Table 1.
Identified injuries included one proximal left common carotid artery pseudoaneurysm (see Figs. 1 and 2), 1 ascending aortic injury, 8 distal arch/proximal descending aortic aneurysms or pseudoaneurysms (see Figs. 3 and 4), and 4 dissections of the aorta. All patients underwent surgical repair either by direct repair or grafting of the involved segment of aorta or arch vessel using cardiopulmonary bypass with a period of deep hypothermic circulatory arrest (mean circulatory arrest interval 31±4 min). See Fig. 5. In most cases, a systemic temperature of approximately 16 °C was achieved, which resulted in longer intervals of extracorporeal circulatory support for cooling and rewarming (mean CPB time was 155±13 min). Retrograde cerebral protection was used in most cases that were approached via a sternotomy. Operative details are described in Table 2.
One out of fourteen patients (patient 4) died in the perioperative period from a stroke for an in-hospital mortality rate of 7%. This patient had originally presented with right carotodynia due to extension of an ascending aortic dissection into the right common carotid artery. Another patient (patient 9) died from rupture of a recurrent pseudoaneurysm of the aortic arch secondary to a staphylococcal graft infection 3 months postoperatively. This patient likely seeded his aortic graft from an infected thigh polytetrafluoroethylene dialysis graft that was not recognized prior to the arch repair.
Although no patient developed paraplegia, five neurologic complications occurred in the study group. In addition to the stroke mentioned above, two patients developed internuclear ophthalmoplegias that persisted. Another patient sustained a left recurrent laryngeal nerve injury. One patient developed a lateral femoral cutaneous nerve palsy after a common femoral artery cannulation. Pulmonary complications represented the most common postoperative adverse event. Two patients required prolonged mechanical ventilation for respiratory failure. Both were extubated but developed subsequent respiratory insufficiency necessitating reintubation and ultimately tracheostomy. One patient required reoperation for recurrent bleeding. Delirium tremens occurred in an additional patient. See Table 3.
4. Conclusions
Hypothermic circulatory arrest is frequently necessary for repair of aneurysms and dissections involving the ascending aorta, transverse arch and proximal great vessels. It rarely has a role in the management of acute trauma since major vascular injuries among survivors of the major trauma most frequently occur at the isthmus in the descending aorta, a site where access for proximal and distal control can be obtained without resorting to complex circulatory management. Few patients with injuries to the ascending aorta survive to hospital presentation, although this group will frequently require cardiopulmonary bypass with or without circulatory arrest. Of the 14 patients who required hypothermic circulatory arrest for repair of traumatic great vessel injuries in our study, only two presented with acute injuries to the ascending aorta. These patients represent 2.6% of the 76 total acute aortic injuries repaired at our institution over the study period. Autopsy series cite the frequency of proximal aortic injuries as high as 20–40% [2], attesting to the highly lethal nature of these proximal injuries.
Most patients treated with circulatory arrest presented with injuries that were diagnosed at a time remote from the traumatic event (11 of 14). Many of these injuries originated at the typical location in the aortic isthmus but required hypothermic circulatory arrest for repair because of difficulty in obtaining proximal control either due to local inflammation or aortic degeneration with extension of the injury into the distal aortic arch. Several other centers have reported their experience with repair of chronic traumatic aortic injuries, and most have described occasional cases where deep hypothermic circulatory arrest was utilized as an adjunctive therapy to facilitate repair [8]. Fraedrich et al. [10] and McCollum et al. [11] performed repairs under hypothermic circulatory arrest in 2/27 and 1/50 chronic traumatic aortic injuries, respectively. Finkelmeier et al. [12] reviewed over 400 reported cases of chronic traumatic aortic injuries in 1982, and reported the use of hypothermic circulatory arrest in 9% of these patients.
Patients with traumatic aortic injury typically present with multi-system trauma. The injury usually is diagnosed by an abnormal chest X-ray, followed by a more definitive study such as computed tomography of the chest. In some cases, the chest X-ray is normal or patients do not seek medical attention because associated injuries are minimal. Among hemodynamically stable patients, only a small percentage of patients actually die due to rupture in the early postinjury period [5]. However, with longer follow-up, most patients eventually develop symptoms or die of delayed rupture as the pseudoaneurysm expands or the dissection progresses [12,13]. Often many years elapse before the patient becomes symptomatic from the unrecognized thoracic vascular injury [12]. This scenario of delayed presentation represents the majority of the cases in our series.
Dissections of the ascending aorta were diagnosed in four patients with a significant antecedent history of trauma in this series. We classified two of these as ‘possible’ cases as a direct cause-and-effect relationship could not be established although the clinical features were highly suspicious for a traumatic etiology. Trauma not uncommonly leads to dissections in the peripheral arterial system but may be an under-recognized cause of aortic and proximal great vessel dissection [14]. Based on autopsy studies, it is estimated that 1.5 % of all aortic dissections are post-traumatic [15]. In Hunt's review of 144 aortic injuries in a more recent timeframe, 8% of injuries were classic dissections; and perhaps more could be classified as such if intimal flaps at the area of injury (which may progress to local or extensive dissection) are also considered [16].
Endovascular repair is under active investigation as a treatment option for some acute and chronic descending aortic injuries. In the latter years of our series when endografts were available, patients were still treated with open repair mainly because of extensive involvement of the transverse aortic arch, concerns about the quality of the surrounding aortic landing zones, the risk of endoleak, and the requisite obligatory intense imaging follow-up. Further research into this promising mode of therapy is needed.
Some surgeons have advocated expectant management of chronic traumatic aortic injury because frequently a heavily calcified, inflamed, fibrous shell containing the injury within the mediastinum is encountered which intuitively appears unlikely to rupture. Our study experience suggests most of these patients eventually develop symptoms that mandate repair. This is consistent with the report from Finklemeier et al. [12] which found that 41% of patients with traumatic aortic pseudoaneurysms will develop symptoms or sustain an event related to the aneurysm within 5 years, and if untreated, one third will die of the aortic lesion. We, therefore, advocate repair of all these injuries unless the patient is a prohibitive surgical risk with a limited life expectancy. Our experience suggests that satisfactory results can be obtained from an aggressive surgical approach despite the high risk of the disease process.
Management of thoracic great vessel injuries remains a considerable challenge. Most acute and chronic injuries can be repaired with standard open techniques and new endovascular strategies are evolving. For some complex injuries, hypothermic circulatory arrest provides a useful adjunct, particularly when there is involvement of the ascending aorta or transverse arch, and when proximal aortic control is compromised.
References
Richens D, Field M, Neale M, Oakley C. The mechanism of injury in blunt traumatic rupture of the aorta. Eur J Cardiothorac Surg 2002; 21:288–293.
Burkhart HM, Gomez GA, Jacobson LE, Pless JE, Broadie TA. Fatal blunt aortic injuries: a review of 242 autopsy cases. J Trauma 2001; 50:113–115.
Mattox KL, Holzman M, Pickard LR, Beall AC Jr, DeBakey ME. Clamp/repair: a safe technique for treatment of blunt injury to the descending thoracic aorta. Ann Thorac Surg 1985; 40:456–463.
Walls JT, Boley TM, Curtis JJ, Smaltz RA. Experience with four surgical techniques to repair traumatic aortic pseudoaneurysm. J Thorac Cardiovasc Surg 1993; 106:283–287.
Fabian TC, Richardson JD, Croce MA, Smith JS Jr, Rodman G Jr, Kearney PA, Flynn W, Ney AL, Cone JB, Luchette FA, Wisner DH, Scholten DJ, Beaver BL, Conn AK, Coscia R, Hoyt DB, Morris JA Jr, Harviel JD, Peitzman AB, Bynoe RP, Diamond DL, Wall M, Gates JD, Asensio JA, McCarhy MC, Girotti MJ, Van Wijngaarden M, Cogbill TH, Levison MA, Aprahamian C, Sutton JE Jr, Allen CF, Hirsch EF, Nagy K, Bachulis BL, Bales CR, Shapiro MJ, Metzler MH, Conti VR, Baker CC, Bannon MP, Ochsner MG, Thomason MH, Hiatt JR, O'Malley K, Obeid FN, Gray P, Bankey PE, Knudson MM, Dyess DL, Enderson BL. Prospective study of blunt aortic injury: multicenter trial of the American Association for the Surgery of Trauma. J Trauma 1997; 42:374–383.
Ot MC, Stewart TC, Lawlor DK, Gray DK, Forbes TL. Management of blunt thoracic aortic injuries: endovascular stents versus open repair. J Trauma 2004; 56:565–570.
Mimasaka S, Yajima Y, Hashiyada M, Nata M, Oba M, Funayama M. A case of aortic dissection caused by blunt chest trauma. Forensic Sci Int 2003; 132:5–8.
Dumanian AV, Hoeksema TD, Santschi DR, Greenwald JH, Frahm CJ. Profound hypothermia and circulatory arrest in the surgical treatment of traumatic aneurysm of the thoracic aorta. J Thorac Cardiovasc Surg 1970; 59:541–545.
Mull DH, Jessen ME. Alternate surgical approach for posttraumatic thoracic aortic pseudoaneurysm. J Trauma 1997; 42:546–548.
Fraedrich G, Spillner G, Schlosser V, Beyersdorf F. Chirurgische therapie des chronischen traumatischen Aortenaneurysmas. Zentralbl Chir 1996; 121:756–756.
McCollum CH, Graham JM, Noon GP, DeBakey ME. Chronic traumatic aneurysms of the thoracic aorta: an analysis of 50 patients. J Trauma 1979; 19:248–252.
Finkelmeier BA, Mentzer Jr RM, Kaiser DL, Tegtmeyer CJ, Nolan SP. Chronic traumatic thoracic aneurysms. Influence of operative treatment on natural history: an analysis of reported cases, 1950–1980. J Thorac Cardiovasc Surg 1982; 84:257–266.
Bennett DE, Cherry JK. The natural history of traumatic aneurysms of the aorta. Surgery 1967; 61:516–523.
Onoguchi K, Takashi H, Sasaki T, Hashimoto K, Takakura H, Takeuchi S. Chronic dissecting aneurysm of the thoracic aorta following minor blunt trauma. Jpn J Thorac Cardiovasc Surg 2001; 49:635–637.
Wilson SK, Hutchins GM. Aortic dissecting aneurysms. Causative factors in 204 subjects. Arch Pathol Lab Med 1982; 106:175–180.
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.(Matthias Peltz, Debra S. )
Presented at the 53rd International Congress of the European Society of Cardiovascular Surgery, Ljubljana, Slovenia, June 2–5, 2004.
Abstract
Traumatic great vessel injuries are frequently lethal events. Expedient diagnosis and prompt repair by clamping and replacing the affected segment of aorta (often with left-heart bypass) can salvage many patients. Rarely, due to the location of the injury or delayed presentation, standard techniques cannot be used and hypothermic circulatory arrest (HCA) is required for access, exposure and repair. The results of surgical reconstruction of acute and chronic traumatic thoracic vascular injuries under these circumstances are not well described. We reviewed all operations on the great vessels at our institution over a 16-year period that had a traumatic etiology and used HCA. Fourteen cases were identified (10 male, 4 female, age 46±4 years), arising from three acute and eleven remote traumatic events. All repairs were performed with cardiopulmonary bypass (mean CPB time was 155±13 min), deep hypothermia, and an interval of circulatory arrest (mean circulatory arrest interval 31±4 min). One patient died in the perioperative period from a stroke (7% 30-day mortality). Another patient exsanguinated from a recurrent pseudoaneurysm 3 months post-repair. No patient developed paraplegia. HCA can be a useful adjunct in managing complex post-traumatic great vessel injuries. Acute injuries of the ascending aorta and transverse arch usually require this technique, but HCA also offers a safe way to manage repair of the descending thoracic aorta when proximal aortic control is compromised.
Key Words: Hypothermic circulatory arrest; Great vessels; Thoracic aorta; Vascular trauma
1. Introduction
Injuries to the thoracic aorta and great vessels are a major cause of mortality in trauma patients. These injuries are most commonly the result of blunt trauma with a rapid deceleration mechanism [1], although they may also arise from penetrating trauma or iatrogenic injury. Most great vessel injuries can be diagnosed with a high degree of accuracy with modern imaging techniques, especially multiplanar arteriography, helical computed tomography (CT), magnetic resonance imaging (MRI) or trans-esophageal echocardiography (TEE).
The most common site of great vessel injury is in the proximal descending thoracic aorta (aortic isthmus) [2]. When diagnosed early, most centers recommend early repair, and a variety of surgical techniques have been advocated including direct suture or interposition graft placement with simple aortic cross-clamping alone [3], with aortic clamping plus left heart bypass for distal perfusion [4], or rarely with aortic clamping and full cardiopulmonary bypass support [5]. More recently, repair with endovascular stent grafts has also been described [6].
Certain situations mandate more complex approaches. In some instances, the injury may not have been diagnosed at the time of the initial traumatic event. Over time, a large pseudoaneurysm can develop which prohibits safe proximal aortic clamping for conventional repair. In other cases, the injury involves the ascending aorta, transverse aortic arch, or the origins of the arch vessels at sites where clamping of the aorta is not feasible or carries a high risk of stroke. Injuries of the thoracic aorta may also present as aortic dissection [7]. In these complex cases, hypothermic circulatory arrest may be required to facilitate surgical exposure and reduce the risk of neurologic injury [8]. The purpose of the current study was to review our experience with circulatory arrest for repair of acute and chronic traumatic thoracic vascular injuries.
2. Materials and methods
This study was approved by the Institutional Review Boards of the University of Texas Southwestern Medical Center at Dallas and the North Texas Veterans Administration Hospital. Surgical and perfusion databases at our affiliated institutions were reviewed between the dates of 1/1/1990–12/31/2005 to identify operations on the great vessels that utilized hypothermic circulatory arrest as an adjunct to surgery. Medical records and radiographic studies of potential cases were then evaluated to identify trauma-related injuries.
Injuries were categorized as ‘definite’ or ‘possible’ vascular trauma based on clinical data. ‘Definite’ cases were defined as great vessel injuries with a significant history of trauma and either no underlying risk factors for the injury or documented negative screening prior to the traumatic event (in the case of aortic aneurysms and dissections). ‘Possible’ traumatic vascular injuries were defined as cases with significant antecedent trauma in patients that had either medical risk factors for the lesion (such as hypertension in patients presenting as aortic dissection) or an atypical lesion diagnosed after significant thoracic trauma.
Injuries were further divided into ‘acute’ and ‘remote’ based on whether the great vessel injury was diagnosed at the initial trauma presentation. Injuries that were suspicious by radiographic or intraoperative appearance, but lacked a documented antecedent history of trauma were specifically excluded. Patients that underwent endovascular repair or repair utilizing conventional cardiopulmonary bypass were also not considered.
In all cases, patient clinical information, presenting symptoms, and injury characteristics were recorded. Details of the operative procedure, including the type of repair, durations of total cardiopulmonary bypass and hypothermic circulatory arrest, perfusion temperatures achieved, and use of cerebral protection techniques were collected. Outcomes of the surgical procedures were also examined. Numerical data are reported as mean±standard error of the mean.
A median sternotomy was performed for lesions involving the ascending aorta and proximal transverse arch. Intermittent retrograde cold blood cardioplegia was utilized in repairs of these proximal injuries and the left ventricle was vented through the right superior pulmonary vein. The heart was de-aired using standard techniques in these patients.
A posterolateral fifth interspace left thoracotomy was utilized to approach injuries of the distal arch and descending aorta. Cardiopulmonary bypass was established with arterial inflow into the common femoral artery or descending thoracic aorta and venous return supplied from a cannula inserted into the common femoral vein and advanced to the right atrium. In some cases the pulmonary artery was cannulated for additional venous return, as we have previously described [9]. For these distal injuries the heart was arrested with a bolus of potassium chloride administered through the cardiopulmonary bypass circuit when ventricular fibrillation occurred during cooling. The left ventricle was not decompressed. The aorta was de-aired by placing the patient in deep Trendelenberg position, gently inflating the lungs, and gradually reinstituting cardiopulmonary bypass after the proximal anastomosis was completed.
Repair of acute injuries was delayed until significant intra-abdominal or intra-cranial injuries had been excluded or stabilized to minimize bleeding risk from heparinization and cardiopulmonary bypass during the aortic reconstruction.
3. Results
From this review, 11 ‘definite’ and 3 ‘possible’ cases (10 male, 4 female, age 46±4 years) were identified. These represented 3 acute and 11 remote injuries. All ‘possible’ cases were remote presentations. Among remote injuries, the average time to diagnosis was 8.5±3 years. The mechanism of injury included one penetrating injury (gun shot wound [GSW]), one iatrogenic injury, and twelve blunt injuries (eleven motor vehicle collisions [MVC], one crush injury).
Three patients had significant antecedent procedures: Patient 2 was diagnosed with a proximal, descending thoracic aortic rupture with dissection into the aortic arch during an attempted percutaneous coarctation balloon angioplasty. Patient 6 had undergone four prior operations for repair of congenital heart disease including repair of a Type B interrupted aortic arch with placement of a descending thoracic aortic homograft. Patient 8 had undergone bilateral thoracotomies for treatment of a gun shot wound to the chest 30 years prior. At least four patients did not seek medical attention after the traumatic event. For eight of the remaining patients, the thoracic vascular injury was not diagnosed during the initial evaluation or hospitalization. One patient had a CT abnormality that was not further worked up until he presented with chest pain 2 years later. Cardiac catheterization was then performed for presumed myocardial ischemia at which time a descending thoracic pseudoaneurysm with dissection into the transverse arch was noted. All remote presentations eventually developed symptoms. See Table 1.
Identified injuries included one proximal left common carotid artery pseudoaneurysm (see Figs. 1 and 2), 1 ascending aortic injury, 8 distal arch/proximal descending aortic aneurysms or pseudoaneurysms (see Figs. 3 and 4), and 4 dissections of the aorta. All patients underwent surgical repair either by direct repair or grafting of the involved segment of aorta or arch vessel using cardiopulmonary bypass with a period of deep hypothermic circulatory arrest (mean circulatory arrest interval 31±4 min). See Fig. 5. In most cases, a systemic temperature of approximately 16 °C was achieved, which resulted in longer intervals of extracorporeal circulatory support for cooling and rewarming (mean CPB time was 155±13 min). Retrograde cerebral protection was used in most cases that were approached via a sternotomy. Operative details are described in Table 2.
One out of fourteen patients (patient 4) died in the perioperative period from a stroke for an in-hospital mortality rate of 7%. This patient had originally presented with right carotodynia due to extension of an ascending aortic dissection into the right common carotid artery. Another patient (patient 9) died from rupture of a recurrent pseudoaneurysm of the aortic arch secondary to a staphylococcal graft infection 3 months postoperatively. This patient likely seeded his aortic graft from an infected thigh polytetrafluoroethylene dialysis graft that was not recognized prior to the arch repair.
Although no patient developed paraplegia, five neurologic complications occurred in the study group. In addition to the stroke mentioned above, two patients developed internuclear ophthalmoplegias that persisted. Another patient sustained a left recurrent laryngeal nerve injury. One patient developed a lateral femoral cutaneous nerve palsy after a common femoral artery cannulation. Pulmonary complications represented the most common postoperative adverse event. Two patients required prolonged mechanical ventilation for respiratory failure. Both were extubated but developed subsequent respiratory insufficiency necessitating reintubation and ultimately tracheostomy. One patient required reoperation for recurrent bleeding. Delirium tremens occurred in an additional patient. See Table 3.
4. Conclusions
Hypothermic circulatory arrest is frequently necessary for repair of aneurysms and dissections involving the ascending aorta, transverse arch and proximal great vessels. It rarely has a role in the management of acute trauma since major vascular injuries among survivors of the major trauma most frequently occur at the isthmus in the descending aorta, a site where access for proximal and distal control can be obtained without resorting to complex circulatory management. Few patients with injuries to the ascending aorta survive to hospital presentation, although this group will frequently require cardiopulmonary bypass with or without circulatory arrest. Of the 14 patients who required hypothermic circulatory arrest for repair of traumatic great vessel injuries in our study, only two presented with acute injuries to the ascending aorta. These patients represent 2.6% of the 76 total acute aortic injuries repaired at our institution over the study period. Autopsy series cite the frequency of proximal aortic injuries as high as 20–40% [2], attesting to the highly lethal nature of these proximal injuries.
Most patients treated with circulatory arrest presented with injuries that were diagnosed at a time remote from the traumatic event (11 of 14). Many of these injuries originated at the typical location in the aortic isthmus but required hypothermic circulatory arrest for repair because of difficulty in obtaining proximal control either due to local inflammation or aortic degeneration with extension of the injury into the distal aortic arch. Several other centers have reported their experience with repair of chronic traumatic aortic injuries, and most have described occasional cases where deep hypothermic circulatory arrest was utilized as an adjunctive therapy to facilitate repair [8]. Fraedrich et al. [10] and McCollum et al. [11] performed repairs under hypothermic circulatory arrest in 2/27 and 1/50 chronic traumatic aortic injuries, respectively. Finkelmeier et al. [12] reviewed over 400 reported cases of chronic traumatic aortic injuries in 1982, and reported the use of hypothermic circulatory arrest in 9% of these patients.
Patients with traumatic aortic injury typically present with multi-system trauma. The injury usually is diagnosed by an abnormal chest X-ray, followed by a more definitive study such as computed tomography of the chest. In some cases, the chest X-ray is normal or patients do not seek medical attention because associated injuries are minimal. Among hemodynamically stable patients, only a small percentage of patients actually die due to rupture in the early postinjury period [5]. However, with longer follow-up, most patients eventually develop symptoms or die of delayed rupture as the pseudoaneurysm expands or the dissection progresses [12,13]. Often many years elapse before the patient becomes symptomatic from the unrecognized thoracic vascular injury [12]. This scenario of delayed presentation represents the majority of the cases in our series.
Dissections of the ascending aorta were diagnosed in four patients with a significant antecedent history of trauma in this series. We classified two of these as ‘possible’ cases as a direct cause-and-effect relationship could not be established although the clinical features were highly suspicious for a traumatic etiology. Trauma not uncommonly leads to dissections in the peripheral arterial system but may be an under-recognized cause of aortic and proximal great vessel dissection [14]. Based on autopsy studies, it is estimated that 1.5 % of all aortic dissections are post-traumatic [15]. In Hunt's review of 144 aortic injuries in a more recent timeframe, 8% of injuries were classic dissections; and perhaps more could be classified as such if intimal flaps at the area of injury (which may progress to local or extensive dissection) are also considered [16].
Endovascular repair is under active investigation as a treatment option for some acute and chronic descending aortic injuries. In the latter years of our series when endografts were available, patients were still treated with open repair mainly because of extensive involvement of the transverse aortic arch, concerns about the quality of the surrounding aortic landing zones, the risk of endoleak, and the requisite obligatory intense imaging follow-up. Further research into this promising mode of therapy is needed.
Some surgeons have advocated expectant management of chronic traumatic aortic injury because frequently a heavily calcified, inflamed, fibrous shell containing the injury within the mediastinum is encountered which intuitively appears unlikely to rupture. Our study experience suggests most of these patients eventually develop symptoms that mandate repair. This is consistent with the report from Finklemeier et al. [12] which found that 41% of patients with traumatic aortic pseudoaneurysms will develop symptoms or sustain an event related to the aneurysm within 5 years, and if untreated, one third will die of the aortic lesion. We, therefore, advocate repair of all these injuries unless the patient is a prohibitive surgical risk with a limited life expectancy. Our experience suggests that satisfactory results can be obtained from an aggressive surgical approach despite the high risk of the disease process.
Management of thoracic great vessel injuries remains a considerable challenge. Most acute and chronic injuries can be repaired with standard open techniques and new endovascular strategies are evolving. For some complex injuries, hypothermic circulatory arrest provides a useful adjunct, particularly when there is involvement of the ascending aorta or transverse arch, and when proximal aortic control is compromised.
References
Richens D, Field M, Neale M, Oakley C. The mechanism of injury in blunt traumatic rupture of the aorta. Eur J Cardiothorac Surg 2002; 21:288–293.
Burkhart HM, Gomez GA, Jacobson LE, Pless JE, Broadie TA. Fatal blunt aortic injuries: a review of 242 autopsy cases. J Trauma 2001; 50:113–115.
Mattox KL, Holzman M, Pickard LR, Beall AC Jr, DeBakey ME. Clamp/repair: a safe technique for treatment of blunt injury to the descending thoracic aorta. Ann Thorac Surg 1985; 40:456–463.
Walls JT, Boley TM, Curtis JJ, Smaltz RA. Experience with four surgical techniques to repair traumatic aortic pseudoaneurysm. J Thorac Cardiovasc Surg 1993; 106:283–287.
Fabian TC, Richardson JD, Croce MA, Smith JS Jr, Rodman G Jr, Kearney PA, Flynn W, Ney AL, Cone JB, Luchette FA, Wisner DH, Scholten DJ, Beaver BL, Conn AK, Coscia R, Hoyt DB, Morris JA Jr, Harviel JD, Peitzman AB, Bynoe RP, Diamond DL, Wall M, Gates JD, Asensio JA, McCarhy MC, Girotti MJ, Van Wijngaarden M, Cogbill TH, Levison MA, Aprahamian C, Sutton JE Jr, Allen CF, Hirsch EF, Nagy K, Bachulis BL, Bales CR, Shapiro MJ, Metzler MH, Conti VR, Baker CC, Bannon MP, Ochsner MG, Thomason MH, Hiatt JR, O'Malley K, Obeid FN, Gray P, Bankey PE, Knudson MM, Dyess DL, Enderson BL. Prospective study of blunt aortic injury: multicenter trial of the American Association for the Surgery of Trauma. J Trauma 1997; 42:374–383.
Ot MC, Stewart TC, Lawlor DK, Gray DK, Forbes TL. Management of blunt thoracic aortic injuries: endovascular stents versus open repair. J Trauma 2004; 56:565–570.
Mimasaka S, Yajima Y, Hashiyada M, Nata M, Oba M, Funayama M. A case of aortic dissection caused by blunt chest trauma. Forensic Sci Int 2003; 132:5–8.
Dumanian AV, Hoeksema TD, Santschi DR, Greenwald JH, Frahm CJ. Profound hypothermia and circulatory arrest in the surgical treatment of traumatic aneurysm of the thoracic aorta. J Thorac Cardiovasc Surg 1970; 59:541–545.
Mull DH, Jessen ME. Alternate surgical approach for posttraumatic thoracic aortic pseudoaneurysm. J Trauma 1997; 42:546–548.
Fraedrich G, Spillner G, Schlosser V, Beyersdorf F. Chirurgische therapie des chronischen traumatischen Aortenaneurysmas. Zentralbl Chir 1996; 121:756–756.
McCollum CH, Graham JM, Noon GP, DeBakey ME. Chronic traumatic aneurysms of the thoracic aorta: an analysis of 50 patients. J Trauma 1979; 19:248–252.
Finkelmeier BA, Mentzer Jr RM, Kaiser DL, Tegtmeyer CJ, Nolan SP. Chronic traumatic thoracic aneurysms. Influence of operative treatment on natural history: an analysis of reported cases, 1950–1980. J Thorac Cardiovasc Surg 1982; 84:257–266.
Bennett DE, Cherry JK. The natural history of traumatic aneurysms of the aorta. Surgery 1967; 61:516–523.
Onoguchi K, Takashi H, Sasaki T, Hashimoto K, Takakura H, Takeuchi S. Chronic dissecting aneurysm of the thoracic aorta following minor blunt trauma. Jpn J Thorac Cardiovasc Surg 2001; 49:635–637.
Wilson SK, Hutchins GM. Aortic dissecting aneurysms. Causative factors in 204 subjects. Arch Pathol Lab Med 1982; 106:175–180.
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.(Matthias Peltz, Debra S. )