Advanced Search
umbrella site table of contents purchase content feedback help button home button home button

Gleason T Gi , Bavaria J Ei . Trauma to the Great Vessels.
Cohn Lh, ed. Cardiac Surgery in the Adult. New York: McGraw-Hill, 2008:1333-1354.

This Article
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this book
Right arrow Author home page(s):
Thomas G. Gleason
Joseph E. Bavaria
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Gleason, T. G.
Right arrow Articles by Bavaria, J. E.
Right arrow Search for Related Content
PubMed
Right arrow Articles by Gleason, T. G.
Right arrow Articles by Bavaria, J. E.

CHAPTER 57

Trauma to the Great Vessels

Thomas G. Gleason/ Joseph E. Bavaria

TRAUMATIC AORTIC DISRUPTION
    Epidemiology
    Pathology
    Pathogenesis of Blunt Aortic Injury
    Natural History
    Clinical Presentation
    Diagnostic Studies
        Chest radiograph
        Computed tomography
        Transesophageal echocardiography
        Aortography
        Magnetic resonance angiography
    Patient Assessment
        Initial evaluation
        Timing of operation
    Operative Strategies
        Open repair
        SPECIAL CONSIDERATIONS
        Endovascular stent grafting (EVSG)
    Nonisthmic Aortic/Arterial Disruptions
    Postoperative Care
    Complications
    Results
NONAORTIC GREAT VESSEL INJURY
References

   INTRODUCTION
 Top
 Next
 
Vesalius was the first to report on a traumatic injury to the aorta manifesting as a posttraumatic aortic aneurysm in 1557.1,2 Aortic rupture was a very uncommon injury until the latter half of the 20th century as travel by motor vehicles increased. Based on limited epidemiologic data, 85% of traumatic injuries to the great vessels in civilian practices were previously attributed to penetrating trauma with 57% caused by gunshot wounds and 25% by stab wounds.36 A more recent Scottish population-based study suggests that over 70% of thoracic aortic trauma is caused by blunt trauma.7 One percent of blunt chest trauma patients will have an aortic injury.810


   TRAUMATIC AORTIC DISRUPTION
 Top
 Previous
 Next
 
Epidemiology

Blunt aortic injury remains the second leading cause of death from vehicular trauma, representing 15% of motor vehicle–caused deaths.1113 Death occurs at the accident scene in 75 to 90% of cases.1,1114 Approximately 8% of patients survive more than 4 hours.1 Those who survive aortic transection typically have two other associated serious injuries, while those who die have four or more serious injuries.1,13 According to Parmley’s landmark report published in 1958, 42% of patients with lethal aortic rupture had an associated cardiac injury.1 The short duration of postaccident survival and the high incidence of fatal associated injuries preclude recovery in most of these patients. Recovery of the select few who survive the first few hours after aortic rupture depends on how they are managed in the hospital.

The true incidence of blunt aortic rupture is not known, but based on autopsy series aortic rupture occurs in 12 to 23% of deaths from blunt trauma.1,1518 According to national vehicular crash databases in the United States and the United Kingdom, the incidence of thoracic aortic injury among motor vehicle crash victims is 1.5% and 1.9%, respectively.19 Seventy-three to 92% of all traumatic aortic disruptions involve motor vehicle drivers, passengers, or pedestrians hit by vehicles.1,13,15,17,18 Alcohol or other substance abuse is involved in over 40% of these motor vehicle accidents.15,17 Ejection from a vehicle doubles the risk of aortic rupture, and seat belt restraint reduces mortality risk by a factor of four.15 Data confirm that active restraints (seat belts) are more effective than passive restraints (air bags) in preventing traumatic aortic injury.20 Aortic rupture of both the ascending and descending aorta has been attributed to the deployment of an air bag, in some cases with cars going less than 10 mph.2124 The risk of an aortic injury is at least three times higher among unbelted than belted motor vehicle occupants.19 Frontal and side impact crashes, regardless of the side of impact, have the highest risk.14,19 Accidental or suicidal falls, crush injuries, airplane accidents, and rare cave-ins are among the other causes of aortic rupture.1,13,16,2527 Falls causing aortic rupture typically occur from heights greater than 3 meters.1,25,26,28

Seventy to eighty percent of these injuries occur in males with an average age of 36 to 40 years.7,13,29,30 Seventy-five percent of patients with traumatic aortic rupture who make it to the hospital alive are initially hemodynamically stable,13 but up to 50% die prior to definitive surgery.29,31 Compared to autopsy series, patients who reach the hospital alive have fewer severe associated injuries.1,12,13,16 Forty to 92% of patients are transferred from a hospital to a level I trauma center.13,32,33

Table 57-1 lists the frequency of associated injuries from data accrued throughout the 1970s into the late 1990s.13,26,3437 The most robust database was gathered prospectively from 50 trauma centers throughout the United States and Canada (American Association for the Surgery of Trauma [AAST] trial).13 Fifty-one percent of patients have an associated closed head injury. Forty-six percent have multiple rib fractures, and 38% have pulmonary contusions. Compared to older autopsy series, which had demonstrated that the majority of patients have associated cardiac contusion, recent data suggest that the incidence is only 4%.13 Orthopedic injuries remain common, occurring in 20 to 35% of cases. Mean injury severity score in the AAST trial was 42.1, which is significantly higher than that seen in older retrospective reports, implying that significantly more patients with these types of serious injuries make it to the hospital and are saved in the modern era.13


View this table:
[in this window]
[in a new window]

 
Table 57–1 Associated Injuries in Hospitalized Patients with Traumatic Aortic Disruption

 
Pathology

Aortic disruptions occur in all aortic segments including, rarely, the abdominal aorta, but the most common site among patients who survive is at the aortic isthmus (Fig. 57-1). According to autopsy series, 36 to 54% occur at the aortic isthmus, 8 to 27% involve the ascending aorta, 8 to 18% occur in the arch, and 11 to 21% involve the distal descending aorta.1,16,38,39 Alternatively, surgical series demonstrate that 84 to 97% of ruptures occur at the isthmus, while 3 to 10% occur in the ascending, arch, or distal descending aorta.12,13,32,35,36,4042 Among patients who survive, it is evident that the periadventitial tissues around the isthmus provide some protection against free rupture that allows for short-term survival and transfer to a hospital. The aorta is typically transected in a transverse fashion involving all three layers of the aortic wall with the edges often separated by several centimeters1,16 (Fig. 57-2). Non-circumferential and partial aortic wall disruptions do occur and can vary from only a few millimeters to several centimeters.1,16,43,44 Spiral lacerations or longitudinal extensions are uncommon. Intramural hematomas and focal dissections occur with partialthickness disruptions but not transections.1 Partial tears tend to occur posteriorly, involving the intima and media. Aortic wall structure at and around the transection does not differ from nearby uninvolved aorta, and atherosclerotic disease is generally not present.1,15,16 The aortic adventitia provides the majority of its tensile strength, but there is no evidence to suggest that the adventitia at the aortic isthmus is any weaker than any other part of the aorta.45,46


Figure 1
View larger version (26K):
[in this window]
[in a new window]

 
Figure 57-1 Anatomic diagram of the thoracic aorta and itsmobility of the aorta at the isthmus and just distal to it. major branches.

 

Figure 2
View larger version (117K):
[in this window]
[in a new window]

 
Figure 57-2 Photograph of a traumatic aortic disruption at the isthmus. (Reproduced with permission from Strassman.44)

 
Blunt trauma can also produce trauma to the other great vessels. Aortic disruption at the base of the innominate artery is the most common site of injury after the isthmus, followed by the base of the left subclavian artery, and then the base of the left carotid.47 Central venous injuries are rarely injured with blunt trauma,5 but they do occur with penetrating trauma.48

Approximately 2 to 5% of patients with aortic disruptions survive without operation, or even detection, to form chronic false aneurysms.49 Little is known of the natural history of these chronic pseudoaneurysms because many go undetected. It is likely that an initial false aneurysm with blood flow partially thromboses and organizes to form a fibrous wall. This wall tends to calcify.4951 It can evolve into a saccular or fusiform aneurysm and late expansion or even rupture can occur. Ninety percent involve the aortic isthmus, again presumably reflective of the inherent protection afforded to this area by mediastinal periadventitial tissues around the isthmus.5254 The patients who develop chronic pseudoaneurysms have fewer associated injuries at the time of the traumatic event.5254 In fact, 35% have no other injuries, and 50% have only one.50

Pathogenesis of Blunt Aortic Injury

Despite extensive investigation, analysis, and debate, no consensus or unified understanding of the pathogenesis of aortic transection has emerged. Popular opinion has employed the "whiplash" theory posing that a combination of traction, torsion, shear, bending, and bursting forces secondary to differential deceleration of tissues within the mediastinum cause an appropriate stress to rupture the aorta at specific sites—the isthmus being the most common.15,45,46,5562 The ligamentum arteriosum, the left main stem bronchus, and the paired intercostal arteries limit the Experiments have suggested that the aorta can be displaced in a longitudinal (cranial or caudal) direction sufficient to cause traction tears at the isthmus.57,59 It has also been apparently recognized that deceleration forces can reach several hundred times the force of gravity, producing injury without any direct impact on the chest.55,56 Alternatively, a "shoveling mechanism" has been postulated to explain cranially directed traction stresses in drivers and front seat passengers in motor vehicle accidents.63

Contrarily, Crass and associates argue that the forces of differential deceleration, torsion, or hydrostatics alone have inadequate magnitude in vehicular accidents to result in aortic tearing given the inherent properties of the aorta.6466 Several studies have demonstrated that the gravitational forces of vehicular trauma do not approach the tensile strength of the aorta. Oppenheim and Zehnder showed that a normal aorta can withstand a 2000-mm Hg pressure before bursting.67,68 Crass proposed a new mechanism he coined "the osseous pinch" based on thoracic compression that he tested in the laboratory. The hypothesis was that anterior thoracic osseous structures (manubrium, first rib, and clavicular heads) rotate posteriorly and inferiorly about the axes of the posterior rib attachments. When the force is large enough these anterior bony structures impact the vertebral column, and the portion of the aorta fixed overlying the spine (the isthmus and proximal descending aorta) is pinched between the bones. This causes a direct shearing of the aorta. Crass’ group demonstrated in a canine model that a blunt force as small as 20,000 N transected the intima and media of the aorta.64 In comparison, a 38-mph collision produces a force of 198,000 N in a normal-sized adult.64 Some clinical data support the osseous pinch mechanism.69

Other forces may be important in ascending aortic injuries. The anterior location of the ascending aorta and the weight and ease of displacement of the heart downward and to the left facilitate traction stress on and above the aortic root.59 Hyperextension of the spine and consequent shearing forces may play a role in the distal descending aorta.64

It is likely that the majority of victims of motor vehicle accidents experience some combination of differential deceleration forces and thoracic compression forces, causing aortic disruption.70 It is clear that many different mechanisms of trauma (i.e., front impact, side impact, falls, crushing injury, and blasts) have caused aortic disruption. Each of these situations affords different circumstances and different forces, making it difficult to isolate a specific mechanism.

Natural History

The natural history of aortic transection in a given patient is dependent on many factors, not the least of which is how quickly a diagnosis is made. Our understanding of survival rates is based on data drawn from autopsy series and operative series. Autopsy studies tend to underestimate the rate of long-term survival, while operative studies tend to overestimate it. Parmley and associates observed that 86% of patients die at the scene, and 11% survive longer than 6 hours.1 The only survivors in the Parmley series were in fact operated on. Mortality rates in most recent surgical series range from 0 to 50% variably dependent on the size of the series, although the attributable-mortality rates are not clearly defined.12,13,25,2932,7175

Several groups have reported selective nonoperative or delayed operative management with aggressive anti-impulse therapy (beta-blockade) in patients deemed unsuitable candidates for surgery or in cases of apparent minimal aortic injury.8,29,30,71,7682 Those initially unsuitable for surgery in these series were elderly and morbid or had too severe associated injuries to tolerate operative repair and thus underwent delayed repair. When surgery has been delayed for stabilization of other injuries, the interim mortality rate prior to definitive repair appears to be between 30 and 50%, with the majority of deaths being attributed to head trauma or other complications.79,81,83 Delays of up to 4 months prior to repair have been reported.78,8490 We conclude that aortic transection can be treated nonoperatively or with operative delay in carefully selected patients with severe associated injuries or significant comorbidities.

Numerous anecdotal reports confirm long-term survival in self-selected patients who were not diagnosed at the time of injury.51,54,9196 A review of the literature by Finkelmeier and colleagues demonstrated that among survivors like these, over 70% survive more than 5 years from the time of the injury.50 The inherent survival bias of this group of patients is evident, but it does confirm that some patients can survive long-term without surgery. In Finkelmeier’s review, the 60 patients who did not have operations for chronic traumatic aortic aneurysms had 5-year, 10-year, and 20-year survival rates of 71, 66, and 62%, respectively. Ninety-four percent of chronic traumatic aortic aneurysms were located at the aortic isthmus. Rarely, the arch and ascending aorta were involved.50

Clinical Presentation

The presentation of aortic rupture is protean. Aortic rupture itself manifests in the form of specific signs or symptoms in less than 50% of cases.18,97100 Patients may develop dyspnea, back pain, or differential hypertension in the lower as compared to the upper extremities.66,97,98,100104 Aortic injuries are more commonly identified in the backdrop of a multi-trauma patient, and the diagnosis is made only if it is suspected. Consequently, aortic injury can easily be missed if patients are not appropriately screened. Identifying the character and mechanism of trauma is the critical first step in making the diagnosis of aortic disruption. If speeds or distances fallen suggest severe impact or significant deceleration forces, the possibility of aortic rupture exists, and it should be ruled out. In all cases of motor vehicle crashes, falls, blasts, crush injuries, or other deceleration forces, aortic rupture should be considered.8,11,25,77,105108

The initial management of a multitrauma patient is uniform regardless of whether aortic disruption is suspected. The patient’s airway, breathing, and circulation are addressed first. Primary and secondary surveys are completed, and appropriate venous access is obtained concomitant with initial laboratory and radiographic studies. Priority of injury is based largely on the acute lethal potential of an injury. Exsanguinating hemorrhage in any body compartment, perforated viscus, or central neurologic injury take the usual priority. Most patients with aortic disruption also have one or more bone fractures. Fractures should be stabilized but not definitively treated prior to excluding the diagnosis or treating an aortic rupture. There are often clues evident in the initial evaluation of a trauma patient that suggest aortic disruption (Table 57-2). In the majority of trauma cases, a supine chest radiograph is obtained as part of the initial evaluation, and the constellation of grossly widened mediastinum, hemothorax, and transient hemodynamic instability upon arrival appear to be predictive of early in-hospital death from blunt thoracic aortic injury.109


View this table:
[in this window]
[in a new window]

 
Table 57–2 Clues that Suggest Aortic Disruption

 
Diagnostic Studies

Chest radiograph

A standard supine anteroposterior chest x-ray does not provide the diagnostic sensitivity to rule out aortic injury.8,10,25,110 Nine to 40% of patients with aortic rupture have chest x-ray findings interpreted as normal at the time of initial evaluation in major trauma centers.8,10,25,99,110117 At least fifteen distinct signs on a standard anteroposterior chest x-ray are associated with blunt aortic injury or rupture (Table 57-3).110 Unfortunately, none of these signs are sufficiently sensitive, specific, or predictive of aortic rupture. In a series of 188 consecutively evaluated multi-trauma patients, 10 blunt aortic injuries were identified, and the sensitivities of these plain radiographic findings ranged from 0 to 90%.110 The specificities ranged from 6 to 93%.110 In lieu of obtaining an upright chest x-ray which is typically not possible in a multitrauma patient, reverse Trendelenburg 45° anteroposterior chest x-rays have been suggested to be more accurate than supine films at evaluating the mediastinum.118


View this table:
[in this window]
[in a new window]

 
Table 57–3 Chest X-Ray Findings Associated with Blunt Aortic Disruption

 
Computed tomography

Volumetric helical or spiral computed tomography (CT) has become the standard screening tool to rule out aortic disruption, with sensitivity and negative predictive values of 100%.8,10,25,116,119121 The technology was introduced in the early 1990s, and since that time it has become the screening modality used in most institutions.810,25,28,76,88,112,116,117,119,121132 Its advantages over other sophisticated imaging techniques (e.g., transesophageal echocardiography, magnetic resonance imaging, or aortography) include its wide availability, its speed, its sensitivity, its reasonable cost, and its ease of interpretation.

Nonionic contrast media is typically used, and 50 to 150 images with slice thicknesses of 3 to 5 mm are acquired in less than 1.5 minutes.10 Normal aorta is depicted with homogeneous enhancement. Several findings are indicative of aortic disruption, including wall thickening, extravasation of contrast, filling defects, para-aortic hematoma, intimal flaps, mural thrombi, pseudoaneurysm, or pseudocoarctation (Fig. 57-3).10


Figure 3
View larger version (94K):
[in this window]
[in a new window]

 
Figure 57-3 Helical computed tomography scan of the chest in a 30-year-old male after a high-speed motor vehicle accident. Slice A demonstrates circumferential disruption of the aortic wall just beyond the left subclavian. Slice B demonstrates an intimal flap in the proximal descending thoracic aorta. Both slices demonstrate periaortic hematoma.

 
Approximately 1% of blunt trauma patients have a thoracic aortic injury identified by helical CT.8,123 False-positive CT studies do occur. The specificity, accuracy, and positive predictive value of helical CT range from 50 to 89%.8,25,116,120 One uncommon finding that mimics aortic injury is a ductus diverticulum remnant.10 Unlike an aortic injury, a ductus diverticulum will have no intimal irregularity or mediastinal hematoma. When there is a luminal or mural aortic irregularity without evidence of a periaortic hematoma, or when there is periaortic hematoma without obvious aortic luminal or mural irregularity, additional aortic imaging should be considered prior to intervention. Minimal aortic injuries (defined as small, less than 1-cm, intimal flaps) are being identified at an increasing rate because of the improved resolution of CT imaging and its widespread use.8,10,76 These minimal injuries pose a management dilemma. Many of these minor aortic injuries can and probably should be managed medically with anti-impulse therapy.76

Transesophageal echocardiography

The development of multiplanar transesophageal echocardiography (TEE) has revolutionized cardiothoracic surgery such that its use is now necessary to plan and facilitate intraoperative management in most cardiothoracic surgical procedures. Its use in cases of aortic transection is no exception. TEE reliably images the entire thoracic aorta except the distal ascending aorta and proximal aortic arch, which can be obscured by tracheal and bronchial air artifact. Contrarily, transthoracic echocardiography cannot accurately evaluate the descending aorta. The accuracy of TEE for diagnosing aortic injury is operator-dependent. Some report its sensitivity and specificity to be approaching 100%,120,133,134 while others demonstrate a sensitivity and specificity as low as 63 and 84%, respectively.135 A recent prospective comparison of the use of helical CT to TEE in evaluating blunt aortic injury in 110 consecutive patients demonstrated a sensitivity, specificity, negative predictive value, and positive predictive value of 93, 100, 99, and 100%, respectively, for TEE compared to 73, 100, 95, and 100% for helical CT.120

A major advantage of TEE is its portability. The hemodynamically unstable patient who is taken to the operating room immediately can undergo exploratory laparotomy or other procedures while simultaneously being evaluated by TEE. The major disadvantage of TEE is that it requires an experienced operator. The risk of TEE is low.120,133 It is contraindicated in cases of concomitant cervical spine, oropharyngeal, esophageal, or severe maxillofacial injury, or in patients with esophageal or pharyngeal lesions that would impede or complicate passage of the probe.

Multiplanar TEE probes permit acquisition of cross-sectional images at different angles along a single rotational axis (Fig. 57-4). The typical 5- or 7-MHz transducer permits adequate resolution of structures as small as 1 to 2 mm.


Figure 4
View larger version (83K):
[in this window]
[in a new window]

 
Figure 57-4 Transesophageal echocardiographic cross-sectional image in the shortaxis with color flow Doppler depicting transection of the aortic isthmus. The transection appears as two distinct lumens, the "double-barrel"sign, and there is flow between the separated aorta. (Courtesy of B. Milas, University of Pennsylvania.)

 
Time-resolved imaging allows evaluation of the movement of anatomic structures and enhances the ability to determine the physiologic consequences of structural abnormalities. Doppler echocardiography is used to evaluate abnormal blood flow patterns which can aid in identifying intimal flaps.

The most common feature of aortic injury identified by TEE is a mural flap. Thickening of the vessel wall can represent a contained rupture or a mural thrombus. Color Doppler flow mapping can demonstrate alterations in flow patterns including turbulence at the site of injury. Chronic atheromatous changes can produce false-positive signs of intimal disruption. When aortic disruption is suspected on TEE there usually is a surrounding mediastinal hematoma, and its absence should prompt skepticism of the diagnosis.

Aortography

Aortography is the imaging modality by which all other techniques have been previously compared for evaluation of aortic injury. Its technique and role in evaluating aortic injuries or other vascular injuries was established long before any of the other sophisticated imaging methodologies. In experienced hands its sensitivity and specificity both approach 100%.136 Its major disadvantages are that its use requires a highly skilled interventional radiology team, and it is time consuming, rendering the patient inaccessible during the time of the study. Rates of exsanguination and death of up to 10% in the angiography suite have been reported.104,137,138 Complication rates attributed directly to aortography are low. Contrast reactions, renal insufficiency secondary to contrast material and groin hematomas or pseudoaneurysms do occur. In the pre–helical CT era, 85 to 95% of aortograms were negative, calling into question the cost- and time-effectiveness of the technique.28,98,104,131,136,138 False-positive studies are usually attributed to atheromata or ductal diverticula. Though now only rarely used for diagnosis, aortography is becoming routine to facilitate endovascular stent grafting (EVSG) for traumatic disruptions (Fig. 57-5).


Figure 5
View larger version (112K):
[in this window]
[in a new window]

 
Figure 57-5 Intra-arterial digital subtraction angiogram of an acute traumatic aortic disruption near the isthmus. The left subclavian artery was transposed to the left common carotid artery prior to deployment of a stent graft.

 
The technique of intra-arterial digital subtraction angiography is used by most groups and allows for faster generation of images. Intravenous digital subtraction angiography was used in the past by some as an even more rapid means of evaluating the aorta in the angiography suite.138 This technique employs IV contrast instillation with time-delayed images of the arch and descending aorta. The time of a study can be reduced by up to fourfold when compared to conventional biplanar angiography. Unfortunately, the diagnostic quality of intravenous digital subtraction angiography is less than 70%,138 and consequently with the near uniform availability of helical CT, the technique has become obsolete.

Magnetic resonance angiography

Magnetic resonance angiography provides excellent images of vascular structures, particularly the thoracic aorta, and its utility in the diagnosis and follow-up of complex aortic disease including aortic dissections and aneurysms is firmly established.139142 However, its use in the acute trauma patient has not been broadly justified. The time required to attain images and the confining nature of the scanners preclude its use in this patient population. If in the future magnetic resonance data acquisition time decreases and patient accessibility within a scanner increases, there may be a role for magnetic resonance angiography in acute trauma settings. Alternatively, it is reasonable to use magnetic resonance angiography for posttherapeutic surveillance of traumatic aortic injuries, particularly in those patients with minimal aortic injury who are treated nonoperatively.

Patient Assessment

Initial evaluation

Ninety-five percent of patients with aortic disruption have associated injuries, and consequently it is imperative that a comprehensive trauma evaluation occur prior to definitive imaging to rule out aortic injury.12,13,77 However, the leading cause of death in patients with aortic injury who make it to the hospital remains exsanguinating aortic rupture, which occurs in at least 20% of patients.13 Among patients who present hemodynamically stable with aortic injury, 4% die in the hospital of aortic rupture prior to surgical repair.13 These data emphasize that a careful, planned, and expeditious team approach is mandatory in order to save as many of these patients as possible. The first steps include primary and secondary physical examinations with control of the airway, respiration, and hemodynamics. Intubation, cardiovascular resuscitation, chest x-ray, insertion of thoracostomy tubes, and identification and stabilization of head injuries take priority. Patients with nonlethal associated injuries who are hemodynamically stable should be diverted toward exclusion of aortic injury, and patients who are unstable require immediate direction toward life-saving operative intervention (e.g., laparotomy or thoracotomy), bypassing all time-consuming tests, in order to achieve the best chance of survival.

After initial trauma evaluation, a head CT should be obtained prior to any planned aortic operation in all patients with signs of an open- or closed-head injury. Relief of intracranial space-occupying lesions takes priority over nonbleeding aortic injuries. Hemodynamically unstable patients with signs of exsanguinating hemorrhage should go directly to the operating room for control of hemorrhage, and TEE should be used to evaluate for aortic injury. Identification of blunt aortic injuries in hemodynamically stable patients should be done in the most efficient manner for a given institution, depending on availability of experienced imaging diagnosticians and equipment, and should be coordinated with the evaluation of other life-threatening injuries. The usual scenario of a hemodynamically stable blunt trauma patient dictates leaving the emergency department to undergo head and abdominopelvic CT scan for identification of closed head injury and intra-abdominal injury. Patients with either an abnormal chest x-ray or a mechanism of injury that poses significant risk of aortic injury (e.g., falls greater than 3 m, motor vehicle crashes of greater than 50 km/h, or pedestrians hit by automobiles) should undergo simultaneous helical chest CT at the time of head and/or abdominopelvic CT. In most institutions, aortography is now reserved for use in patients with equivocal helical CT or TEE results or in patients with complex aortic injuries which cannot be accurately defined by these other imaging techniques. Occasionally thoracoscopy has been used to evaluate traumatic hemothoraces.143 However, there is little role for thoracoscopy in the diagnosis of aortic disruption, because in experienced hands, the sensitivity and specificity of intraoperative TEE is so good.

In the preoperative period, patients with aortic injury should receive anti-impulse therapy for control of aortic wall tension and blood pressure.8,77 Reduction of the change in pressure over the change in time ({Delta}P/{Delta}t) reduces wall stress significantly.144 These measures have been shown to reduce in-hospital aortic rupture rates without adversely affecting the outcome of other injuries.8 These control measures should be employed in patients going to the operating room and in patients undergoing delayed aortic repair for the treatment of other life-threatening injuries.

Timing of operation

Immediate aortic repair is recommended once the diagnosis of aortic injury is made in hemodynamically stable patients without severe associated injuries that require emergent laparotomy, craniotomy, or pelvic stabilization. Intracranial bleeding causing mass effect, and significant thoracic, abdominal, pelvic, or retroperitoneal hemorrhage should all be addressed prior to thoracotomy or stent grafting for contained aortic injury.84,145 Contained aortic injuries should be aggressively managed with anti-impulse therapy if delayed aortic management is planned in order to address other life-threatening injuries. Delayed management may be appropriate in carefully selected patients with severe associated injuries or severe comorbidity.2931,71,79-83,146 Presentation of aortic disruption with ongoing aortic bleeding or signs of impending rupture requires immediate surgical intervention. Aortic injuries should be monitored by TEE during the surgical treatment of intracranial, thoracic, or abdominopelvic injuries. Treatment of all non–life-threatening injuries should be delayed until after definitive aortic repair.

Hemodynamically unstable patients should be taken to the operating room immediately, prior to definitive testing. Laparotomy or even thoracotomy may be required to locate and control ongoing hemorrhage. Patients with instability secondary to associated trauma who require laparotomy or thoracotomy for damage control to establish hemodynamic stability may be better served by subsequent immediate transfer to the intensive care unit for further resuscitation prior to definitive repair of contained aortic rupture until complete resuscitation and hemodynamic stability are achieved. Once stabilized, anti-impulse therapy with short-acting beta-blockade should be instituted and aggressively applied to reduce aortic wall stress.8 Determining the optimal extent of delay for definitive aortic repair in patients with severe associated injuries is not clear. In rare cases, particularly extremely comorbid patients, nonoperative management has been extended for long periods of time with acceptable mortality.82,83

Operative Strategies

Conventional open repair of traumatic aortic disruption via interposition grafting for replacement of the injured segment is safe, effective, and durable. Historically, open repair via thoracotomy is the standard to which all other management strategies must be compared. However, as endovascular strategies for treating abdominal and more recently thoracic aortic pathology have evolved, there is growing enthusiasm for endovascular stent grafting (EVSG) of traumatic disruption because of its relative ease, reduced operative time required, and potentially reduced complication rate compared to conventional open repair. Consequently, but despite a lack of prospective clinical trials, recent trends around the world demonstrate a more liberal use of EVSG for acute traumatic aortic disruption, particularly for complicated cases with severe associated injuries. Retrospective reviews of single institutional experiences have demonstrated favorable short-term outcomes with endovascular strategies; however, the reported series are small, ranging from 5 to 29 cases per report.29,30,72,73,80,147151 Currently there are ongoing clinical trials of the use of new EVSG repair for traumatic aortic disruption, but these trials are not randomizing patients to open repair. An important limitation of the use of EVSG for traumatic transection is that the currently available thoracic aortic stent grafts were designed to treat aneurysmal disease, not traumatic disruption. Unlike aneurysms, aortic transection typically occurs in younger patients (average age 36 to 40 years)7,29,30,152 with normal-caliber descending aortas in the range of 18 to 24 mm. The currently available stent grafts are not optimally suited for this size thoracic aorta. Consequently, groups have often resorted to the use of homemade or improvised materials that were originally designed for other purposes like extension cuffs of abdominal stent grafts. The long-term durability of these rudimentary, rigged devices or even the newest available devices designed for the thoracic aorta is not known. Despite these limitations, it is becoming clearer that EVSG can safely be used in a significant percentage of trauma patients. In many cases, simply bridging a patient with a stent graft to a more stable, chronic pseudoaneurysm may have an advantage over thoracotomy in a multitrauma patient. Because EVSG techniques continue to evolve and are not uniformly applicable, surgeons treating thoracic aortic disruption must be comfortable with conventional open repair techniques.

Open repair

The technical aspects of repairing aortic disruptions are straightforward. Although no one method of repair of aortic transection has been proven superior, standards are established. There remains some controversy surrounding the issue of spinal cord protection and what means of protection are optimal.12,13,32,36,40,42,66,77,86,88,99,108,115,153161 There are two general perspectives: (1) that "clamp-and-sew" techniques are sufficiently safe, and (2) that some form of lower body perfusion provides added spinal cord and visceral protection against the ischemia of the aortic cross-clamp. Paraplegia has historically occurred at an overall rate of approximately 10%.12,40,42,99,152,162 More recently, data from multiple institutions demonstrate a marked reduction in paraplegia rates with the use of adjuvant perfusion techniques.8,13,25,77,163

SPINAL CORD PROTECTION: The spinal cord is supplied blood flow by anterior and posterior spinal arteries that consist of anatomic vascular chains that run the length of the cord.164 The anterior spinal artery supplies the anterior two-thirds of the cord and is well developed in the upper thorax. Collateral arterial vessels also feed off of the left subclavian artery, including the vertebral artery, and consequently its occlusion during repair may have added implications toward a heightened risk of spinal cord ischemia. In the lower thorax and upper abdomen the anterior spinal artery is less developed and relies on segmental branches from intercostal and lumbar arteries. The anterior artery is supplied by 7 to 10 unpaired anterior medullary branches that vary in location along the cord (Fig. 57-6). Usually at least two anterior medullary vessels supply the cervical cord, two or three supply the thoracic cord, and two supply the lumbar cord. At the level of the first lumbar vertebra (variations T8 to L4) the anterior spinal artery receives the arteria radicularis magna (or artery of Adamkiewicz), which is essential for cord blood supply in this zone in at least 25% of patients.164,165


Figure 6
View larger version (116K):
[in this window]
[in a new window]

 
Figure 57-6 Cross-sectional diagram showing a medullary (radicular) arterial branch to the anterior spinal artery.

 
Aortic cross-clamping near the aortic isthmus produces profound hypotension to the lower body and spinal cord below this region, and spinal cord injury is proportional to aortic cross-clamp time (Fig. 57-7).166 Clamping the aorta above the takeoff of the left subclavian artery may increase the risk of paraplegia since the collateral vessels fed by the internal thoracic, vertebral, and subscapular vessels all emanate from the subclavian.167 Paraplegia has occurred after only 9 minutes of aortic cross-clamping without extracorporeal perfusion of the lower body.168


Figure 7
View larger version (19K):
[in this window]
[in a new window]

 
Figure 57-7 Probability of paraplegia in relation to aortic cross-clamp time with and without lower body perfusion in patients with traumatic aortic disruption at the isthmus. (Reproduced with permission from Katz et al.166)

 
Several adjuncts have been proposed to reduce the risk of paraplegia in cases of elective repair of thoracic or thoracoabdominal aneurysms, but many of these techniques are not practical in the trauma patient requiring repair of aortic transection. These include monitoring of somatosensory evoked potentials and lumbar cerebrospinal fluid drainage, both of which require added time and expertise in the preoperative setting which is often not available to trauma patients.162,169175 Hypothermia, while attractive as a means of spinal cord protection, is not practical in partial bypass systems which rely on the heart to perfuse the upper body. On rare occasions when aortic injury involves the aortic arch, hypothermic circulatory arrest techniques are required for repair and may actually offer added spinal cord protection.176179 Selective retrograde spinal cord hypothermia and perfusion has been studied in the laboratory, but to date these techniques have not been employed in humans.180,181 Epidural cooling has been used for thoracoabdominal aortic resections, but is not practical in trauma patients.182 Experience with theoretical neuroprotective pharmaceuticals like steroids, lidocaine, or magnesium have not been thoroughly studied in this patient population.

Based on the currently available data from the surgical community as a whole, it appears that cross-clamp times exceeding 30 minutes and utilization of the "clamp-and-sew" technique alone yield higher rates of paraplegia than techniques that include extracorporeal lower body perfusion (Tables 57-4 and 57-5).152,162,163 Certainly there are groups that have had success with low paraplegia rates using exclusively a simple cross-clamping technique,12,32 but these results have not been reproducible throughout many institutions, and their results rely on short cross-clamp times (average 20 to 25 minutes) with little margin for difficult cases. Recent data suggest that the paraplegia rate approaches zero when cross-clamp times are short (less than 30 minutes) and lower body perfusion techniques are employed.13,156,162 We have employed some form of lower body perfusion, typically left heart bypass, during aortic cross-clamping for these injuries since 1994. In our experience, there have been no cases of paraplegia with open repair since this strategy was implemented (over 50 patients, unpublished data).


View this table:
[in this window]
[in a new window]

 
Table 57–4 Incidence of Postoperative Paraplegia in Relation to Surgical Management: Meta-Analysis

 

View this table:
[in this window]
[in a new window]

 
Table 57–5 Incidence of Postoperative Paraplegia in Relation to Surgical Management: AAST Prospective Trial

 
SIMPLE AORTIC CROSS-CLAMPING: Simple aortic cross-clamping probably still has a role in the management of traumatic aortic rupture. The only advantage to this technique is its simplicity. In particular, it may be useful to the general, vascular, or trauma surgeon who is not experienced in the utilization of extracorporeal perfusion circuits or the cannulation of cardiac chambers or great vessels when thoracic surgical expertise is unavailable. It may also be useful in unstable patients who are actively bleeding from the aortic tear; in these patients there may be no time to employ a distal aortic perfusion system.

When aortic cross-clamp times are less than 25 to 30 minutes, low paraplegia rates have been achieved.12,13,32 However, the average cross-clamp time reported in the literature is 41.0 minutes.40 Many cases of aortic transection require more than 30 minutes to repair because of extravasated blood, fragility of the aorta, and difficulty in identifying local anatomy within a large hematoma. This is especially true if the tear extends proximally to involve the orifice of the left subclavian artery. These patients require clamping the aorta proximal to the left subclavian artery, which may increase the incidence of paraplegia in the absence of distal aortic perfusion.

ADJUVANT PERFUSION METHODS: Optimally, both right radial and femoral arterial catheters should be in place to allow for monitoring of upper and lower body perfusion. Both active and passive shunting systems have been successful with both full systemic heparinization and no heparinization.13,32,34,36,108,153155,157,158,160,169,183185 Despite the theoretical risk of bleeding with heparinization in the trauma setting, most groups, including our own, that employ active partial left heart bypass techniques use full systemic heparinization and have not seen bleeding complications.8,13,75 Pulmonary venous cannulation near its confluence with the left atrium has a lower complication rate than cannulation of the left atrial appendage.186 It is important to be well versed in the various lower body perfusion systems because distinct circumstances may require alterations in routine practice.

The system used by any one group should be simply applied, and reliable and routine for that group. Distal perfusion pressure should be maintained at 60 to 70 mm Hg.158 Full heparinization is relatively contraindicated in cases of intracranial hemorrhage and severe lung injury, but is otherwise safely used by many groups.12,13,40,75,99,158,183,187 Use of a centrifugal pump with heparin-bonded tubing and active partial left heart bypass or use of a heparin-bonded passive shunt is an option that does not require systemic heparinization.154,158,185,187 It is helpful to employ the use of a heat exchanger within extracorporeal circuits in order to maintain core temperatures above 35°C in these patients that cool quickly.

PARTIAL LEFT HEART BYPASS: A small single- or dual-stage cannula is placed into the left atrium through the left inferior pulmonary vein to provide inflow to the pump (Fig. 57-8). Arterial cannulation size is determined by body size and site of cannulation. We preferably use a high-flow, atraumatic, aortic cannula in the distal descending aorta or less commonly place a femoral arterial cannula. Distal aortic cannulation has the advantage of convenience and speed. Partial left heart bypass serves several purposes: (1) to unload the left heart and control proximal hypertension at the time of cross-clamping, (2) to maintain lower body perfusion, (3) to allow rapid infusion of volume, and (4) to control (remove) intravascular volume. The lower body is perfused at a flow rate of 2 to 3 L/min with lower body mean arterial pressure of 60 to 70 mm Hg while maintaining an upper body mean arterial pressure of 70 to 80 mm Hg. All field blood is returned to the circuit via a pump reservoir or is accumulated and returned by cell saver.


Figure 8
View larger version (54K):
[in this window]
[in a new window]

 
Figure 57-8 Diagram showing a typical setup for partial left heart bypass in a patient with aortic disruption at the isthmus.

 
Ventricular arrhythmias pose a major risk since the native heart perfuses the upper body. Single-lung ventilation does not increase postoperative pulmonary problems after left heart bypass. If the system is used without systemic heparinization, heat exchangers and oxygenators should be removed from the circuit to minimize surface area and thrombotic risks, but in doing so great care must be taken to reduce heat losses and maintain near-normal temperatures.

FULL OR PARTIAL CARDIOPULMONARY BYPASS: Direct right atrial cannulation at the inferior vena cava–right atrial junction from a left thoracotomy by simple, transverse, inferior pericardiotomy below the left phrenic nerve is straightforward and provides excellent venous drainage. Alternatively, a long venous catheter with multiple side holes via the left common femoral vein into the right atrium can be placed with a guidewire. Right atrial–femoral arterial bypass has been used with or without an oxygenator like partial left heart bypass. When no oxygenator is used blood is returned with a partial arterial oxygen pressure of approximately 40 mm Hg (saturation 45 to 65%), and this has been shown to be adequate for lower body tissue oxygen needs provided the hemoglobin concentration is maintained above 10 g/dL.169,188 Full cardiopulmonary bypass support is most useful in cases in which the aortic arch is involved in the injury to allow for systemic cooling.189,190

Right femoral venous to arterial bypass has the distinct advantage of allowing for establishment of partial or complete bypass prior to entering the chest. This technique may be preferred when there is concomitant right lung contusion in order to ensure adequate tissue oxygenation during repair. Rarely, there may be a need to perform a proximal anastomosis under deep hypothermic circulatory arrest (HCA) because an injury involves the mid-aortic arch. In cases of aortic arch transection in proximity to the innominate or left common carotid, anterior exposure via sternotomy or thoracosternotomy may offer better exposure for total arch replacement.189,190 Use of HCA in trauma patients should proceed with caution and only after other serious associated injuries have been addressed to avoid bleeding complications. If HCA is required, it is essential to confirm the lack of significant aortic valvular insufficiency. When HCA is utilized within the left chest, the left ventricle should be vented, and we typically do this via the left atrium.

PASSIVE (GOTT) SHUNT: Of predominantly historical interest, this technique shunts blood from the proximal aorta to the distal aorta with a tapered, heparin-coated polyvinyl tube.154 The proximal end is placed in the ascending or arch of the aorta or the left subclavian artery and the distal end is placed in the descending aorta or femoral artery. Ventricular cannulation had been used in the past; however, it was abandoned due to a high rate of ventricular dysrhythmias, reduced shunt flows, and a higher rate of paraplegia.34,154,155,184,191,192 The diameter of the shunt is obviously fixed, and therefore flow is passive, unmonitored, and dependent on a pressure gradient. Femoral arterial monitoring, as with all of these techniques, is recommended.184 The Gott shunt is easy to use, although it requires a more extensive dissection of either the aortic arch or ascending aorta. It offers no left ventricular unloading or loading advantage that partial bypass systems do, and therefore blood pressure control is left to pharmacology alone.

OPERATIVE TECHNIQUES: A standard fourth interspace posterolateral thoracotomy with or without fifth rib notching usually provides excellent exposure to the aortic isthmus and proximal descending aorta. The incision should be long enough to facilitate dissection of the descending aorta below the level of the inferior pulmonary vein and dissection of the arch of the aorta between the left common carotid and left subclavian arteries. Dissection near the isthmus or tear should be avoided until both proximal and distal aortic control is established. Depending on the stability of the patient, lower body perfusion can be established prior to aortic exposure by gaining access to the left groin.

If cannulation is planned in the chest, proximal and distal aortic control is established first. The left inferior pulmonary vein–left atrial junction is dissected after gaining aortic control when using left heart bypass. Excessive compression or traction of the lung should be avoided, particularly when dissecting out the aortic arch, because the left pulmonary artery may be easily disrupted at this location (see Fig. 57-8).

The mediastinal pleura is incised along the anterior surface of the proximal left subclavian artery. The subclavian artery is isolated. The pleura overlying the distal aortic arch is incised lateral to the vagus nerve. Great care is taken to avoid injury to either the phrenic or vagus nerves as they pass over the aortic arch, which can be difficult since they are often obscured by the hematoma. They should be reflected off the aorta with the overlying pleura and retracted medially by attaching stay sutures to the pleura just lateral to the vagus nerve. Loops around the nerves themselves should be avoided, as even stretch of these nerves can result in paresis. This reflection exposes the arch of the aorta between the left common carotid and left subclavian arteries, which is the point needed for proximal aortic control in the majority of cases. Inferiorly, the vagus nerve and its branching left recurrent laryngeal nerve are reflected medially as well. This exposes the ligamentum arteriosum which can be sharply divided. The aortic arch between the left carotid and subclavian artery superiorly and medial to the ligamentum inferiorly is encircled with a tape after establishing a plane between the posterior arch and the trachea using a combination of sharp and gentle finger dissection. There should be no dissection distal to either the left subclavian or the ligamentum in order to avoid free disruption of the hematoma.

Distal aortic control is established at an adequate distance from the aortic injury to facilitate repair. The overlying pleura is incised, and the aorta isolated. The left inferior pulmonary vein is dissected out anteriorly. Opening the pericardium just anterior to the vein allows better exposure and a better site of pulmonary venous cannulation. Heparin, if employed, is given. We establish arterial cannulation first. Distal aortic purse-string sutures are fashioned below the distal clamp site, or the femoral artery is cannulated by Seldinger technique with serial dilatation to the desired cannula size. The inferior pulmonary vein is then cannulated with a dual-stage catheter. The circuit for left heart bypass is de-aired and connected. Lower body perfusion is initiated, and once systemic blood pressure is stabilized the left subclavian artery is clamped followed by the proximal aorta, then the distal aorta. We prefer to always clamp the proximal aorta between the left common carotid artery and the left subclavian artery because the tear frequently extends quite close to the ostium of the left subclavian artery. Upper and lower body pressures are stabilized with the bypass circuit to maintain upper body mean arterial pressures of 70 to 80 mm Hg and a lower body pressure of 60 to 70 mm Hg with flows of 2 to 3 L/min (see Fig. 57-8).

The periaortic hematoma is then entered, and the edges of the transected aorta identified. Usually the aorta is completely transected, and the edges are separated by 2 to 4 cm.1,16 Less frequently the transection is partial. Some authors advocate primary repair at this point;34,193 however, we advocate placing a short interposition graft after débridement of the torn edges.12,13,32,35,42,103,155,157,159161 Collagencoated woven polyester grafts or gelatin-impregnated grafts are used most commonly. Use of intraluminal prostheses has been abandoned by most groups.194 Grafts are sewn using a running polypropylene suture with the proximal anastomosis performed first, followed by the distal. Generous amounts of adventitial tissue are included in each bite. If the proximal anastomosis is done under HCA, cardiopulmonary bypass and reperfusion of the arch should be reinstituted immediately after completion of the proximal anastomosis for optimal neurocerebral protection. This requires cannulation of the graft just beyond the proximal anastomosis, and then the distal anastomosis is completed using a dual arterial-inflow perfusion setup perfusing the arch and lower body simultaneously. The left subclavian can either be incorporated into the proximal anastomosis or grafted separately as appropriate.

If the aorta is already ruptured with bleeding into the hemithorax, proximal aortic dissection between the left carotid and subclavian arteries is rapidly performed, and a cross-clamp quickly applied. The descending aorta is then clamped below the injury, and the hematoma opened. No attempt is made to establish lower body perfusion, but every attempt is made at maintaining adequate mean arterial pressure during clamping. The aortic repair is done as expeditiously as possible to minimize clamp time. Repair sutures are placed accordingly after clamps are removed. Hemostasis is achieved after continuity of the aorta is reestablished.

SPECIAL CONSIDERATIONS

PREVIOUS LEFT THORACOTOMY: Emergency department thoracotomies are usually done in haste by inexperienced nonthoracic surgeons and are often placed at sites too inferior to effectively repair an aortic transection. Given this situation it is usually best to enter the chest through a fourth interspace thoracotomy even if this means creating a second intercostal incision (using the same skin incision). When a patient with a history of prior left thoracotomy presents with an aortic injury the associated scarring offers both an advantage and disadvantage to the patient. The adhesions between the lung and mediastinum help contain the rupture making it less likely to exsanguinate, but the adhesions also make the dissection considerably more difficult and time consuming. Optimally, dissection in these cases should be done prior to heparinization.

EXTENSION OF THE TEAR INTO THE LEFT SUBCLAVIAN ARTERY: Traumatic aortic disruptions that occur in close proximity (<1 cm) from the left subclavian artery portend a higher mortality risk and greater operative difficulty than injuries further away from the left subclavian ostium.195 We recommend routinely placing the proximal aortic clamp proximal to the left subclavian artery since most aortic ruptures tear close to it. This allows for an easier, more precise proximal anastomosis. The subclavian should also be controlled by encircling it with a tape just distal to its origin. Occasionally, the aortic tear will extend into the left subclavian orifice, and in this case the proximal clamp may have to partially or totally occlude the left common carotid. The left subclavian can then be completely detached from the aorta, the proximal anastomosis completed, and the clamp then moved distally onto the graft. The left subclavian is then reattached to the aortic graft with an interposition graft after completing the distal aortic anastomosis. The left common carotid artery will usually tolerate occlusion for 10 to 15 minutes without sequelae. The left subclavian interposition graft is fashioned with an end-to-end anastomosis distally and an end-to-side anastomosis proximally.

Endovascular stent grafting (EVSG)

There are now many reports of the efficacy of EVSG in the setting of acute traumatic aortic disruption.2931,72,73,80,147151,196199 Most groups placing EVS grafts for aortic disruption are doing so selectively based on the prediction of higher risk with conventional repair due to severity of illness, age, comorbidity, or associated injuries. Open- or closed-head injury, bleeding abdominal visceral injury, retroperitoneal bleeding, and pulmonary contusions are commonly cited factors that may favor an EVSG approach.2931,72,73,80,149

EVSG for traumatic aortic disruption should be performed in either a hybrid operating room/angiosuite with a fluoroscopy unit designed for endovascular surgery or a conventional operating room with a portable C-arm fluoroscopy unit. The rate of conversion from EVSG to open repair is higher with management of aortic disruption than aneurysms,72 and the operative team involved must be ready and capable of making the conversion immediately. General anesthesia is used most commonly. Aortic access is retrograde via either the femoral or iliac artery. Percutaneous and femoral arterial cutdown or direct iliac arterial puncture or iliac access via a silo graft sewn to the iliac artery have all been used. One theoretical advantage of an endovascular approach may be the use of a very low dose or no heparin in trauma patients. A floppy J-tipped wire is advanced under fluoroscopic and/or TEE guidance, and an aortogram is performed using steep anterior oblique projection with a marked catheter to accurately assess and measure the aortic arch anatomy relative to the site of transection. Diameter of the prosthesis used should be based on aortic measurements obtained preoperatively by CT angiography. Length of graft coverage should be based on intraoperative angiographic measurements. Intravascular ultrasound is likely to improve our ability to accurately determine the extent of coverage and the size of grafts needed in the operating room.200,201 Based on the proximity to the aortic injury, the left subclavian artery may need to be covered, and if covered, it may need to be embolized and bypassed or transposed to the left common carotid artery in order to ensure a proximal EVS graft seal and avoid problems of ischemia to the left arm or vertebrobasilar system (see Fig. 57-5).202205

Stent graft collapse is a problem that can occur in nearly any setting, but EVSG for transection may be particularly prone because of the fact that the available grafts may be relatively oversized for the normal-sized aorta adjacent to an injured segment. There are several unpublished reports of EVS graft collapse during or immediately after deployment for transection including events from our own institutions. Idu and colleagues reported a case of delayed EVS graft collapse that was identified on CT angiogram 3 months after repair of a traumatic transection.206

There is little doubt that as devices are designed better and more suitably for aortic transection, EVSG will become part of the standard of care. Currently we employ a selective strategy whereby most patients that are young and have limited associated injuries are treated by conventional open grafting, recognizing the durability of this approach. Alternatively, elderly, comorbid patients or those with severe associated injuries are treated with EVSG.

Nonisthmic Aortic/Arterial Disruptions

The incidence of acute rupture of the ascending aorta among motor vehicular or other trauma patients is not known, as most of these patients do not survive beyond the site of the accident. However, there are reports of successful repairs of these injuries.22,33,207 Most commonly the proximal ascending aorta at or just above the sinotubular junction is involved.33 There are a few case reports of ascending aortic ruptures associated with the deployment of air bags.22,23 Ascending aortic ruptures require full heparinization and cardiopulmonary bypass for repair. These injuries are approached through a median sternotomy. The survival among cases reported in the literature of those undergoing repair is about 85%.33 They have been repaired either primarily or with an interposition graft. Rarely, a concomitant aortic valve replacement is required.33

Lacerations to the base of the innominate or left common carotid arteries should be approached through a median sternotomy and may require cardiopulmonary bypass depending on the degree of aortic involvement.47 Extension of the incision into the right or left neck including detachment of the sternocleidomastoid from the sternum is usually helpful in obtaining adequate exposure. When the base of the left carotid or innominate is injured, the safest option is to oversew the base and create an interposition graft to the ascending aorta in an end-to-side fashion.108,208,209 Injury to the base of the left subclavian artery can be approached either by sternotomy or left posterolateral thoracotomy, the latter of which typically provides better exposure.208 Alternatively, when injuries extend out onto either the left or right subclavian artery a thoracosternotomy, cervicosternotomy, or cervicosternothoracotomy "trap door" incision provides good exposure depending on the level of the injury.5 Finally, the transverse anterior thoracosternotomy, "clam-shell" incision provides good exposure to the mediastinal structures and both hemithoraces when multiple injuries require repair.5

Aortic injuries of the descending aorta distal to the isthmus to the level of T8 should be approached through a posterolateral thoracotomy in the fourth, fifth, or sixth interspace, depending on the level of injury. These types of aortic injuries from blunt trauma are rare. More commonly, this segment of aorta is injured by penetrating trauma. These patients rarely make it to the hospital alive. When the distal thoracoabdominal aorta is injured below T8, it should be approached by thoracoabdominal incision. This can be done either retroperitoneally or intraperitoneally. An intraperitoneal approach offers the advantage of allowing for abdominal exploration; however, retraction of the abdominal contents with a thoracoabdominal incision and a violated peritoneum can be cumbersome. We use partial left heart bypass with left atrial to femoral arterial or distal aortic cannulation for all thoracoabdominal aortic procedures unless active bleeding precludes its setup, or there is an absolute contraindication to heparinization.

Postoperative Care

Postoperative care after aortic repair is similar to that given patients who have other major cardiothoracic surgery. Immediately following aortic repair in the operating room, patients should undergo flexible bronchoscopy for evacuation of bloody secretions to avoid plugging and atelectasis of the left lung. Respiratory function, ventricular filling pressures, blood pressure, cardiac output, renal function, chest tube output, nasogastric drainage, body temperature, neurologic status, and coagulation function should be monitored closely. Pulmonary toilet is extraordinarily important, and once clinically stable an epidural catheter may be advantageous to facilitate good pulmonary recovery. Antibiotics are given in a standard prophylactic fashion. Patients are extubated as soon as is clinically indicated. Chest tubes are removed when any air leak has stopped and drainage is less than 150 to 200 mL of serous fluid per day.

Complications

Complications after aortic repair occur at a rate of 40 to 50%.13,34,36,42,108 Pneumonia is the most common complication and occurs at a rate of 17 to 34%.13,34,36,42,108 Other complications include bacteremia, renal insufficiency, and paraplegia. Rates of frequency for several series are listed in Table 57-6.13,34,36,42,108 Left vocal cord paralysis has been reported to occur at a rate of 4 to 14% percent, although recurrent nerve injuries are probably underreported. Late complications are rare in these patients. Aortobronchial fistula following repair of transection has been reported.210,211


View this table:
[in this window]
[in a new window]

 
Table 57–6 Major Postoperative Complications

 
Patients who survive an undiagnosed aortic injury may develop a chronic traumatic aortic aneurysm.26,4954,9296 Among those patients with initial pseudoaneurysm formation, most develop progressive dilation with symptoms of pain referable to aneurysmal expansion. Other symptoms include dyspnea or cough secondary to compression of the left main stem bronchus, hoarseness due to stretching of the recurrent nerve, hemoptysis, or dysphagia. These chronic traumatic aortic aneurysms, once discovered, should be repaired regardless of size unless there are contraindications due to age or comorbidity.

Results

The mortality rate of patients with aortic rupture who reach the hospital ranges from 7 to 65% depending on whether or not the injury is repaired.12,13,2932,40 The large discrepancy is likely due to underreporting of patients who make it to the hospital but not to the operating room, as most series only report operative results. Among hemodynamically stable patients undergoing open repair or EVSG repair, the hospital mortality rate ranges from 0 to 20% in the modern era (Tables 57-6 and 57-7).13,29,30,80,163 The mortality rate of nonoperative patients with associated injuries precluding initial aortic repair was 55% in the AAST trial.13 All patients who either presented in extremis or with free rupture died of aortic rupture. A few small series have demonstrated acceptable survival rates of 67 to 72% in select, high-risk patients treated nonoperatively.82,83 In his meta-analysis of 1492 patients, Von Opell reported an average of 7.8% of patients dying during aortic repair, and 13.5% dying in the postoperative period.40


View this table:
[in this window]
[in a new window]

 
Table 57–7 Results of Endovascular Stent Grafting (EVSG) for Aortic Transection (with Comparison to Open Repair)

 
Paraplegia or paraparesis occurred in an average of 9.9% of patients in the meta-analysis.40 However, paraplegia rates vary widely depending on the operative technique utilized, with a range of 0 to 20% (see Tables 57-4 and 57-7).12,13,2932,40,42,72,73,80,86,108,147,149,163,198 Although there are several groups that have reported very low paraplegia rates using the "clamp-and-sew" technique, these results have not been widely reproduced.13,32 It is clear that increasing cross-clamp time, particularly beyond 30 minutes, increases the rate of paraplegia.13,166 Alternatively, use of extracorporeal lower body perfusion systems have facilitated low rates of paraplegia.13,163 Our own institutional data similarly demonstrate that since the practice of partial left heart bypass for all open repairs of aortic transection was instituted in 1994 (over 50 patients), there have been no cases of paraplegia (unpublished data). The preponderance of data suggests that the combination of partial left heart bypass for lower body perfusion with short, less than 30 minutes, cross-clamp time affords the lowest rate of paraplegia.13,40 The early results of EVSG repair suggest that it may reduce the risk of paraplegia further (see Table 57-7), although to date the data are limited and comparisons are retrospective.


   NONAORTIC GREAT VESSEL INJURY
 Top
 Previous
 Next
 
The majority of injuries to the great venous structures and the pulmonary arteries are a result of penetrating trauma. Blunt trauma to these structures is rare, presumably because of their distensibility and low pressure. The incidence of injury to the nonaortic great vessels among cases of penetrating thoracic trauma is not known; however, the overall incidence of great vessel injury with thoracic gunshot wounds is approximately 5% and with stab wounds is 2%.212 Wounds penetrating the thoracic "box" bordered by the midclavicular lines, the thoracic outlet, and xiphoid process should be explored operatively. Chest tubes should be inserted as a diagnostic and therapeutic measure, and an echocardiogram or a subxiphoid pericardial window performed to rule out hemopericardium. Patients with a high index of suspicion of mediastinal great vessel injury or with a confirmed hemopericardium should undergo sternotomy. Patients with central venous or pulmonary arterial rupture will decompensate from pericardial tamponade. Expeditious pericardial decompression will often provide enough stability to facilitate definitive repair. Exsanguination from a venous or pulmonary arterial injury into one of the hemithoraces requires immediate massive volume resuscitation and transfer to the operating room. Choice of incision should be made based on clinical suspicion of site of injury or objective data (arteriography, chest radiograph, or bleeding site). When the site of injury is not clear, median sternotomy provides excellent access to the heart and great vessels, and it can be extended across a hemithorax or up the neck along either sternocleidomastoid to facilitate exposure of any vascular structure in the chest. Most venous injuries and pulmonary arterial injuries when localized and simple can be repaired without cardiopulmonary bypass. Large or complex venous, and particularly pulmonary arterial, injuries are often more easily repaired on full cardiopulmonary bypass with a decompressed heart. When repairing pulmonary venous injuries it is important to safeguard against air embolus, the result of which can be devastating. Therefore, complex pulmonary venous injury may require aortic cross-clamping with cardioplegia to prevent embolus to the brain.


   References
 Top
 

  1. Parmley L, Mattingly T, Manion W: Nonpenetrating traumatic injury of the aorta. Circulation 1958; 17:1086.[Medline]
  2. Sailer S: Dissecting aneurysm of the aorta. Arch Pathol 1942; 23:704.
  3. Inci I, Ozcelik C, Tacyildiz I, et al: Penetrating chest injuries: Unusually high incidence of high-velocity gunshot wounds in civilian practice. World J Surg 1998; 22:438.[Medline]
  4. LoCicero J 3rd, Mattox KL: Epidemiology of chest trauma. Surg Clin North Am 1989; 69:15.[Medline]
  5. Reul GJ Jr., Beall AC Jr, Jordan GL Jr, Mattox KL: The early operative management of injuries to great vessels. Surgery 1973; 74:862.[Medline]
  6. Weaver FA, Suda RW, Stiles GM, Yellin AE: Injuries to the ascending aorta, aortic arch and great vessels. Surg Gynecol Obstet 1989; 169:27.[Medline]
  7. Tambyraja AL, Scollay JM, Beard D, et al: Aortic trauma in Scotland—A population based study. Eur J Vasc Endovasc Surg 2006; 32:686.[Medline]
  8. Fabian TC, Davis KA, Gavant ML, et al: Prospective study of blunt aortic injury: Helical CT is diagnostic and antihypertensive therapy reduces rupture. Ann Surg 1998; 227:666; discussion 676.[Medline]
  9. Gavant ML, Flick P, Menke P, Gold RE: CT aortography of thoracic aortic rupture. AJR Am J Roentgenol 1996; 166:955.[Abstract/Free Full Text]
  10. Gavant ML: Helical CT grading of traumatic aortic injuries. Impact on clinical guidelines for medical and surgical management. Radiol Clin North Am 1999; 37:553, vi.
  11. Williams JS, Graff JA, Uku JM, Steinig JP: Aortic injury in vehicular trauma. Ann Thorac Surg 1994; 57:726.[Abstract]
  12. Razzouk AJ, Gundry SR, Wang N, et al: Repair of traumatic aortic rupture: A 25-year experience. Arch Surg 2000; 135:913; discussion 919.[Abstract/Free Full Text]
  13. 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; discussion 380.[Medline]
  14. McGwin G Jr, Reiff DA, Moran SG, Rue LW 3rd: Incidence and characteristics of motor vehicle collision-related blunt thoracic aortic injury according to age. J Trauma 2002; 52:859; discussion 865.[Medline]
  15. Greendyke RM: Traumatic rupture of aorta; special reference to automobile accidents. JAMA 1966; 195:527.[Abstract/Free Full Text]
  16. Feczko JD, Lynch L, Pless JE, et al: An autopsy case review of 142 nonpenetrating (blunt) injuries of the aorta. J Trauma 1992; 33:846.[Medline]
  17. Dischinger P, Cowley R, Shankar B: The incidence of ruptured aorta among vehicular fatalities. Proc Am Assoc Automot Med 1988; 32:15.
  18. Smith RS, Chang FC: Traumatic rupture of the aorta: Still a lethal injury. Am J Surg 1986; 152:660.[Medline]
  19. Fitzharris M, Franklyn M, Frampton R, et al: Thoracic aortic injury in motor vehicle crashes: The effect of impact direction, side of body struck, and seat belt use. J Trauma 2004; 57:582.[Medline]
  20. Brasel KJ, Quickel R, Yoganandan N, Weigelt JA: Seat belts are more effective than airbags in reducing thoracic aortic injury in frontal motor vehicle crashes. J Trauma 2002; 53:309; discussion 313.[Medline]
  21. Pillgram-Larsen J, Geiran O: [Air bags influence the pattern of injury in severe thoracic trauma]. Tidsskr Nor Laegeforen 1997; 117:2437.[Medline]
  22. Dunn JA, Williams MG: Occult ascending aortic rupture in the presence of an air bag. Ann Thorac Surg 1996; 62:577.[Abstract/Free Full Text]
  23. deGuzman BJ, Morgan AS, Pharr WF: Aortic transection following air-bag deployment. N Engl J Med 1997; 337:573.[Free Full Text]
  24. Brown DK, Roe EJ, Henry TE: A fatality associated with the deployment of an automobile airbag. J Trauma 1995; 39:1204.[Medline]
  25. Demetriades D, Gomez H, Velmahos GC, et al: Routine helical computed tomographic evaluation of the mediastinum in high-risk blunt trauma patients. Arch Surg 1998; 133:1084.[Abstract/Free Full Text]
  26. Duhaylongsod FG, Glower DD, Wolfe WG: Acute traumatic aortic aneurysm: The Duke experience from 1970 to 1990. J Vasc Surg 1992; 15:331; discussion 342.[Medline]
  27. Pezzella AT: Blunt traumatic injury of the thoracic aorta following commercial airline crashes. Tex Heart Inst J 1996; 23:65.[Medline]
  28. Durham RM, Zuckerman D, Wolverson M, et al: Computed tomography as a screening exam in patients with suspected blunt aortic injury. Ann Surg 1994; 220:699.[Medline]
  29. Cook J, Salerno C, Krishnadasan B, et al: The effect of changing presentation and management on the outcome of blunt rupture of the thoracic aorta. J Thorac Cardiovasc Surg 2006; 131:594.[Abstract/Free Full Text]
  30. Rousseau H, Dambrin C, Marcheix B, et al: Acute traumatic aortic rupture: A comparison of surgical and stent-graft repair. J Thorac Cardiovasc Surg 2005; 129:1050.[Abstract/Free Full Text]
  31. Reed AB, Thompson JK, Crafton CJ, et al: Timing of endovascular repair of blunt traumatic thoracic aortic transections. J Vasc Surg 2006; 43:684.[Medline]
  32. Sweeney MS, Young DJ, Frazier OH, et al: Traumatic aortic transections: Eight-year experience with the "clamp-sew" technique. Ann Thorac Surg 1997; 64:384; discussion 387.[Abstract/Free Full Text]
  33. Symbas PJ, Horsley WS, Symbas PN: Rupture of the ascending aorta caused by blunt trauma. Ann Thorac Surg 1998; 66:113.[Abstract/Free Full Text]
  34. Schmidt CA, Wood MN, Razzouk AJ, et al: Primary repair of traumatic aortic rupture: A preferred approach. J Trauma 1992; 32:588.[Medline]
  35. Hilgenberg AD, Logan DL, Akins CW, et al: Blunt injuries of the thoracic aorta. Ann Thorac Surg 1992; 53:233; discussion 238.[Abstract]
  36. Kirsh MM, Behrendt DM, Orringer MB, et al: The treatment of acute traumatic rupture of the aorta: A 10-year experience. Ann Surg 1976; 184:308.[Medline]
  37. Sturm JT, Billiar TR, Dorsey JS, et al: Risk factors for survival following surgical treatment of traumatic aortic rupture. Ann Thorac Surg 1985; 39:418.[Abstract]
  38. Arajarvi E, Santavirta S, Tolonen J: Aortic ruptures in seat belt wearers. J Thorac Cardiovasc Surg 1989; 98:355.[Abstract]
  39. Rabinsky I, Sidhu GS, Wagner RB: Mid-descending aortic traumatic aneurysms. Ann Thorac Surg 1990; 50:155.[Abstract]
  40. 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.[Abstract]
  41. Kieny R, Charpentier A: Traumatic lesions of the thoracic aorta. A report of 73 cases. J Cardiovasc Surg (Torino) 1991; 32:613.[Medline]
  42. Cowley RA, Turney SZ, Hankins JR, et al: Rupture of thoracic aorta caused by blunt trauma. A fifteen-year experience. J Thorac Cardiovasc Surg 1990; 100:652; discussion 660.[Abstract]
  43. Katz S, Mullin R, Berger RL: Traumatic transection associated with retrograde dissection and rupture of the aorta: Recognition and management. Ann Thorac Surg 1974; 17:273.[Medline]
  44. Strassman G: Traumatic rupture of the aorta. Am Heart J 1947; 33:508.[Medline]
  45. Butcher HJ: The elastic properties of the human aortic intima, media and adventitia: The initial effect of thromboendarterectomy. Ann Surg 1960; 1151:480.
  46. Lundevall J: The mechanism of traumatic rupture of the aorta. Acta Pathol Microbiol Scand 1964; 62:34.[Medline]
  47. Pretre R, Chilcott M, Murith N, Panos A: Blunt injury to the supra-aortic arteries. Br J Surg 1997; 84:603.[Medline]
  48. Wall MJ Jr, Mattox KL, Debakey ME: Injuries to the azygos venous system. J Trauma 2006; 60:357.[Medline]
  49. Bennett DE, Cherry JK: The natural history of traumatic aneurysms of the aorta. Surgery 1967; 61:516.[Medline]
  50. Finkelmeier BA, Mentzer RM Jr, Kaiser DL, et al: Chronic traumatic thoracic aneurysm. Influence of operative treatment on natural history: An analysis of reported cases, 1950–1980. J Thorac Cardiovasc Surg 1982; 84:257.[Abstract]
  51. John LC, Hornick P, Edmondson SJ: Chronic traumatic aneurysm of the aorta: To resect or not. The role of exploration operation. J Cardiovasc Surg (Torino) 1992; 33:106.[Medline]
  52. 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.[Medline]
  53. Albuquerque FC, Krasna MJ, McLaughlin JS: Chronic, traumatic pseudoaneurysm of the ascending aorta. Ann Thorac Surg 1992; 54:980.[Abstract]
  54. Prat A, Warembourg H Jr, Watel A, et al: Chronic traumatic aneurysms of the descending thoracic aorta (19 cases). J Cardiovasc Surg (Torino) 1986; 27:268.[Medline]
  55. Stapp J: Human tolerance to deceleration. Am J Surg 1957; 93:734.[Medline]
  56. Marsh C, Moore R: Deceleration trauma. Am J Surg 1957; 93:623.[Medline]
  57. Aldman B: Biodynamic studies on impact protection. Acta Physiol Scand 1962; 56:Suppl 192.
  58. Jackson FR, Berkas EM, Roberts VL: Traumatic aortic rupture after blunt trauma. Dis Chest 1968; 53:577.[Medline]
  59. Sevitt S: The mechanisms of traumatic rupture of the thoracic aorta. Br J Surg 1977; 64:166.[Medline]
  60. Sevitt S: Traumatic ruptures of the aorta: A clinico-pathological study. Injury 1977; 8:159.[Medline]
  61. Gotzen L, Flory PJ, Otte D: Biomechanics of aortic rupture at classical location in traffic accidents. Thorac Cardiovasc Surg 1980; 28:64.[Medline]
  62. Coermann R, Dotzauer G, Lange W, Voigt GE: The effects of the design of the steering assembly and the instrument panel on injuries (especially aortic rupture) sustained by car drivers in head-on collision. J Trauma 1972; 12:715.[Medline]
  63. Voigt GE, Wilfort K: Mechanisms of injuries to unrestrained drivers in head-on collisions, in Proceedings 30th Stapp Car Crash Conference. New York. Society of Automotive Engineers; 1969:295.
  64. Crass JR, Cohen AM, Motta AO, et al: A proposed new mechanism of traumatic aortic rupture: The osseous pinch. Radiology 1990; 176:645.[Abstract/Free Full Text]
  65. Cohen AM, Crass JR, Thomas HA, et al: CT evidence for the "osseous pinch" mechanism of traumatic aortic injury. AJR Am J Roentgenol 1992; 159:271.[Abstract/Free Full Text]
  66. Cohen AM, Crass JR: Traumatic aortic injuries: Current concepts. Semin Ultrasound CT MR 1993; 14:71.[Medline]
  67. Zehnder M: Delayed post-traumatic rupture of the aorta in a young healthy individual after closed injury: Mechanical-etiological considerations. Angiology 1956; 7:252.[Free Full Text]
  68. Oppenheim F: Gibt es eine spontanruptur der gesunden aorta und wie kommt sie zustande? Muenchen Med Wochenschr 1918; 65:1234.
  69. Javadpour H, O’Toole JJ, McEniff JN, et al: Traumatic aortic transection: Evidence for the osseous pinch mechanism. Ann Thorac Surg 2002; 73:951.[Abstract/Free Full Text]
  70. 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.[Abstract/Free Full Text]
  71. Langanay T, Verhoye JP, Corbineau H, et al: Surgical treatment of acute traumatic rupture of the thoracic aorta: A timing reappraisal? Eur J Cardiothorac Surg 2002; 21:282.[Abstract/Free Full Text]
  72. Andrassy J, Weidenhagen R, Meimarakis G, et al: Stent versus open surgery for acute and chronic traumatic injury of the thoracic aorta: A single-center experience. J Trauma 2006; 60:765; discussion 771.[Medline]
  73. Morishita K, Kurimoto Y, Kawaharada N, et al: Descending thoracic aortic rupture: Role of endovascular stent-grafting. Ann Thorac Surg 2004; 78:1630.[Abstract/Free Full Text]
  74. Doss M, Balzer J, Martens S, et al: Surgical versus endovascular treatment of acute thoracic aortic rupture: A single-center experience. Ann Thorac Surg 2003; 76:1465; discussion 1469.[Abstract/Free Full Text]
  75. Santaniello JM, Miller PR, Croce MA, et al: Blunt aortic injury with concomitant intra-abdominal solid organ injury: Treatment priorities revisited. J Trauma 2002; 53:442; discussion 445.[Medline]
  76. Malhotra AK, Fabian TC, Croce MA, et al: Minimal aortic injury: A lesion associated with advancing diagnostic techniques. J Trauma 2001; 51:1042.[Medline]
  77. Nagy K, Fabian T, Rodman G, et al: Guidelines for the diagnosis and management of blunt aortic injury: An EAST Practice Management Guidelines Work Group. J Trauma 2000; 48:1128.[Medline]
  78. Fisher RG, Oria RA, Mattox KL, et al: Conservative management of aortic lacerations due to blunt trauma. J Trauma 1990; 30:1562.[Medline]
  79. Symbas PN, Sherman AJ, Silver JM, et al: Traumatic rupture of the aorta: Immediate or delayed repair? Ann Surg 2002; 235:796.[Medline]
  80. 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.[Abstract/Free Full Text]
  81. 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; discussion S1892.[Abstract/Free Full Text]
  82. Hirose H, Gill IS, Malangoni MA: Nonoperative management of traumatic aortic injury. J Trauma 2006; 60:597.[Medline]
  83. Holmes JHT, Bloch RD, Hall RA, et al: Natural history of traumatic rupture of the thoracic aorta managed nonoperatively: A longitudinal analysis. Ann Thorac Surg 2002; 73:1149.[Abstract/Free Full Text]
  84. Borman KR, Aurbakken CM, Weigelt JA: Treatment priorities in combined blunt abdominal and aortic trauma. Am J Surg 1982; 144:728.[Medline]
  85. Camp PC, Shackford SR: Outcome after blunt traumatic thoracic aortic laceration: Identification of a high-risk cohort. Western Trauma Association Multicenter Study Group. J Trauma 1997; 43:413.[Medline]
  86. Akins CW, Buckley MJ, Daggett W, et al: Acute traumatic disruption of the thoracic aorta: A ten-year experience. Ann Thorac Surg 1981; 31:305.[Abstract]
  87. Bodily K, Perry JF Jr, Strate RG, Fischer RP: The salvageability of patients with post-traumatic rupture of the descending thoracic aorta in a primary trauma center. J Trauma 1977; 17:754.[Medline]
  88. Camp PC Jr, Rogers FB, Shackford SR, et al: Blunt traumatic thoracic aortic lacerations in the elderly: An analysis of outcome. J Trauma 1994; 37:418; discussion 423.[Medline]
  89. 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.[Medline]
  90. Pezzella AT, Todd EP, Dillon ML, et al: Early diagnosis and individualized treatment of blunt thoracic aortic trauma. Am Surg 1978; 44:699.[Medline]
  91. Weimann S, Balogh D, Furtwangler W, et al: Graft replacement of post-traumatic thoracic aortic aneurysm: Results without bypass or shunting. Eur J Vasc Surg 1992; 6:381.[Medline]
  92. Roques X, Bourdeaud’hui A, Collet D, et al: Traumatic rupture and aneurysm of the aortic isthmus: Late results of repair by direct suture. Ann Vasc Surg 1989; 3:47.[Medline]
  93. Roques X: [Chronic post-traumatic aneurysms of the thoracic aorta]. Rev Prat 1991; 41:1789.[Medline]
  94. Becker HM, Ramirez J, Echave V, Heberer G: Traumatic aneurysms of the descending thoracic aorta. Ann Vasc Surg 1986; 1:196.[Medline]
  95. Russo P, Orszulak TA, Arnold PG, et al: Concomitant repair of a chronic traumatic aortic aneurysm with tracheal erosion. Ann Thorac Surg 1987; 43:559.[Abstract]
  96. Heystraten FM, Rosenbusch G, Kingma LM, Lacquet LK: Chronic posttraumatic aneurysm of the thoracic aorta: Surgically correctable occult threat. AJR Am J Roentgenol 1986; 146:303.[Abstract/Free Full Text]
  97. Clark DE, Zeiger MA, Wallace KL, et al: Blunt aortic trauma: Signs of high risk. J Trauma 1990; 30:701.[Medline]
  98. Gundry SR, Williams S, Burney RE, et al: Indications for aortography in blunt thoracic trauma: A reassessment. J Trauma 1982; 22:664.[Medline]
  99. Kram HB, Appel PL, Wohlmuth DA, Shoemaker WC: Diagnosis of traumatic thoracic aortic rupture: A 10-year retrospective analysis. Ann Thorac Surg 1989; 47:282.[Abstract]
  100. Sturm JT, Perry JF Jr, Olson FR, Cicero JJ: Significance of symptoms and signs in patients with traumatic aortic rupture. Ann Emerg Med 1984; 13:876.[Medline]
  101. Trachiotis GD, Sell JE, Pearson GD, et al: Traumatic thoracic aortic rupture in the pediatric patient. Ann Thorac Surg 1996; 62:724; discussion 731.[Abstract/Free Full Text]
  102. Vlahakes GJ, Warren RL: Traumatic rupture of the aorta. N Engl J Med 1995; 332:389.[Free Full Text]
  103. Plume S, DeWeese JA: Traumatic rupture of the thoracic aorta. Arch Surg 1979; 114:240.[Abstract/Free Full Text]
  104. Kram HB, Wohlmuth DA, Appel PL, Shoemaker WC: Clinical and radiographic indications for aortography in blunt chest trauma. J Vasc Surg 1987; 6:168.[Medline]
  105. Goarin JP, Le Bret F, Riou B, et al: Early diagnosis of traumatic thoracic aortic rupture by transesophageal echocardiography. Chest 1993; 103:618.[Medline]
  106. Hengster P, Furtwangler W, Pernthaler H: Transesophageal echocardiography for the diagnosis of traumatic injury of the thoracic aorta. J Thorac Cardiovasc Surg 1994; 107:638.[Free Full Text]
  107. Hartford JM, Fayer RL, Shaver TE, et al: Transection of the thoracic aorta: assessment of a trauma system. Am J Surg 1986; 151:224.[Medline]
  108. Kodali S, Jamieson WR, Leia-Stephens M, et al: Traumatic rupture of the thoracic aorta. A 20-year review: 1969–1989. Circulation 1991; 84:III40.[Medline]
  109. Simon BJ, Leslie C: Factors predicting early in-hospital death in blunt thoracic aortic injury. J Trauma 2001; 51:906; discussion 911.[Medline]
  110. Cook AD, Klein JS, Rogers FB, et al: Chest radiographs of limited utility in the diagnosis of blunt traumatic aortic laceration. J Trauma 2001; 50:843.[Medline]
  111. Burney RE, Gundry SR, Mackenzie JR, et al: Chest roentgenograms in diagnosis of traumatic rupture of the aorta. Observer variation in interpretation. Chest 1984; 85:605.[Medline]
  112. Cigarroa JE, Isselbacher EM, DeSanctis RW, Eagle KA: Diagnostic imaging in the evaluation of suspected aortic dissection. Old standards and new directions. N Engl J Med 1993; 328:35.[Free Full Text]
  113. Gundry SR, Burney RE, Mackenzie JR, et al: Assessment of mediastinal widening associated with traumatic rupture of the aorta. J Trauma 1983; 23:293.[Medline]
  114. Heystraten FM, Rosenbusch G, Kingma LM, et al: Chest radiography in acute traumatic rupture of the thoracic aorta. Acta Radiol 1988; 29:411.[Medline]
  115. Mattox KL: Fact and fiction about management of aortic transection. Ann Thorac Surg 1989; 48:1.[Medline]
  116. Parker MS, Matheson TL, Rao AV, et al: Making the transition: The role of helical CT in the evaluation of potentially acute tho-racic aortic injuries. AJR Am J Roentgenol 2001; 176:1267.[Abstract/Free Full Text]
  117. Raptopoulos V, Sheiman RG, Phillips DA, et al: Traumatic aortic tear: screening with chest CT. Radiology 1992; 182:667.[Abstract/Free Full Text]
  118. Barker DE, Crabtree JD Jr, White JE, et al: Mediastinal evaluation utilizing the reverse Trendelenburg radiograph. Am Surg 1999; 65:484.[Medline]
  119. Dyer DS, Moore EE, Ilke DN, et al: Thoracic aortic injury: How predictive is mechanism and is chest computed tomography a reliable screening tool? A prospective study of 1,561 patients. J Trauma 2000; 48:673; discussion 682.[Medline]
  120. Vignon P, Boncoeur MP, Francois B, et al: Comparison of multi-plane transesophageal echocardiography and contrast-enhanced helical CT in the diagnosis of blunt traumatic cardiovascular injuries. Anesthesiology 2001; 94:615; discussion 5A.[Medline]
  121. Bruckner BA, DiBardino DJ, Cumbie TC, et al: Critical evaluation of chest computed tomography scans for blunt descending thoracic aortic injury. Ann Thorac Surg 2006; 81:1339.[Abstract/Free Full Text]
  122. Agee CK, Metzler MH, Churchill RJ, Mitchell FL: Computed tomographic evaluation to exclude traumatic aortic disruption. J Trauma 1992; 33:876.[Medline]
  123. Gavant ML, Menke PG, Fabian T, et al: Blunt traumatic aortic rupture: Detection with helical CT of the chest. Radiology 1995; 197:125.
  124. Ishikawa T, Nakajima Y, Kaji T: The role of CT in traumatic rupture of the thoracic aorta and its proximal branches. Semin Roentgenol 1989; 24:38.[Medline]
  125. McLean TR, Olinger GN, Thorsen MK: Computed tomography in the evaluation of the aorta in patients sustaining blunt chest trauma. J Trauma 1991; 31:254.[Medline]
  126. Miller FB, Richardson JD, Thomas HA, et al: Role of CT in diagnosis of major arterial injury after blunt thoracic trauma. Surgery 1989; 106:596; discussion 602.[Medline]
  127. Mirvis SE, Shanmuganathan K, Miller BH, et al: Traumatic aortic injury: diagnosis with contrast-enhanced thoracic CT—Five-year experience at a major trauma center. Radiology 1996; 200:413.[Abstract/Free Full Text]
  128. Mirvis SE, Shanmuganathan K, Buell J, Rodriguez A: Use of spiral computed tomography for the assessment of blunt trauma patients with potential aortic injury. J Trauma 1998; 45:922.[Medline]
  129. Morgan PW, Goodman LR, Aprahamian C, et al: Evaluation of traumatic aortic injury: Does dynamic contrast-enhanced CT play a role? Radiology 1992; 182:661.[Abstract/Free Full Text]
  130. Pate JW, Minard G: Imaging of traumatic rupture of the aorta. J Thorac Cardiovasc Surg 1995; 109:190.[Free Full Text]
  131. Richardson P, Mirvis SE, Scorpio R, Dunham CM: Value of CT in determining the need for angiography when findings of mediastinal hemorrhage on chest radiographs are equivocal. AJR Am J Roentgenol 1991; 156:273.[Abstract/Free Full Text]
  132. Wilson D, Voystock JF, Sariego J, Kerstein MD: Role of computed tomography scan in evaluating the widened mediastinum. Am Surg 1994; 60:421.[Medline]
  133. Smith MD, Cassidy JM, Souther S, et al: Transesophageal echocardiography in the diagnosis of traumatic rupture of the aorta. N Engl J Med 1995; 332:356.[Abstract/Free Full Text]
  134. Kearney PA, Smith DW, Johnson SB, et al: Use of transesophageal echocardiography in the evaluation of traumatic aortic injury. J Trauma 1993; 34:696; discussion 701.[Medline]
  135. Saletta S, Lederman E, Fein S, et al: Transesophageal echocardiography for the initial evaluation of the widened mediastinum in trauma patients. J Trauma 1995; 39:137; discussion 141.[Medline]
  136. Sturm JT, Hankins DG, Young G: Thoracic aortography following blunt chest trauma. Am J Emerg Med 1990; 8:92.[Medline]
  137. LaBerge JM, Jeffrey RB: Aortic lacerations: Fatal complications of thoracic aortography. Radiology 1987; 165:367.[Abstract/Free Full Text]
  138. Eddy AC, Nance DR, Goldman MA, et al: Rapid diagnosis of thoracic aortic transection using intravenous digital subtraction angiography. Am J Surg 1990; 159:500.[Medline]
  139. Nienaber CA, von Kodolitsch Y, Brockhoff CJ, et al: Comparison of conventional and transesophageal echocardiography with magnetic resonance imaging for anatomical mapping of thoracic aortic dissection. A dual noninvasive imaging study with anatomical and/or angiographic validation. Int J Card Imaging 1994; 10:1.[Medline]
  140. Goldstein SA, Lindsay J Jr, Vasan R: The diagnosis of thoracic aortic dissection by noninvasive imaging procedures. N Engl J Med 1993; 328:1637.[Medline]
  141. Hartnell G, Costello P: The diagnosis of thoracic aortic dissection by noninvasive imaging procedures. N Engl J Med 1993; 328:1637; discussion 1638.[Free Full Text]
  142. Nienaber CA, von Kodolitsch Y, Nicolas V, et al: The diagnosis of thoracic aortic dissection by noninvasive imaging procedures. N Engl J Med 1993; 328:1.[Abstract/Free Full Text]
  143. Feliciano DV, Rozycki GS: Advances in the diagnosis and treatment of thoracic trauma. Surg Clin North Am 1999; 79:1417.[Medline]
  144. Williams MJ, Low CJ, Wilkins GT, Stewart RA: Randomised comparison of the effects of nicardipine and esmolol on coronary artery wall stress: Implications for the risk of plaque rupture. Heart 2000; 84:377.[Abstract/Free Full Text]
  145. Hanschen S, Snow NJ, Richardson JD: Thoracic aortic rupture in patients with multisystem injuries. South Med J 1982; 75:653.[Medline]
  146. Klena JW, Shweiki E, Woods EL, Indeck M: Purposeful delay in the repair of a traumatic rupture of the aorta with coexistent liver injury. Ann Thorac Surg 1998; 66:950.[Abstract/Free Full Text]
  147. Peterson BG, Matsumura JS, Morasch MD, West MA, Eskandari MK: Percutaneous endovascular repair of blunt thoracic aortic transection. J Trauma 2005; 59:1062.[Medline]
  148. Dunham MB, Zygun D, Petrasek P, et al: Endovascular stent grafts for acute blunt aortic injury. J Trauma 2004; 56:1173.[Medline]
  149. Ott MC, Stewart TC, Lawlor DK, et al: Management of blunt thoracic aortic injuries: Endovascular stents versus open repair. J Trauma 2004; 56:565.[Medline]
  150. Karmy-Jones R, Hoffer E, Meissner MH, et al: Endovascular stent grafts and aortic rupture: A case series. J Trauma 2003; 55:805.[Medline]
  151. Orford VP, Atkinson NR, Thomson K, et al: Blunt traumatic aortic transection: The endovascular experience. Ann Thorac Surg 2003; 75:106; discussion 111.[Abstract/Free Full Text]
  152. 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; discussion 380.[Medline]
  153. Appelbaum A, Karp RB, Kirklin JW: Surgical treatment for closed thoracic aortic injuries. J Thorac Cardiovasc Surg 1976; 71:458.[Abstract]
  154. Donahoo JS, Brawley RK, Gott VL: The heparin-coated vascular shunt for thoracic aortic and great vessel procedures: a ten-year experience. Ann Thorac Surg 1977; 23:507.[Abstract]
  155. Merrill WH, Lee RB, Hammon JW Jr, et al: Surgical treatment of acute traumatic tear of the thoracic aorta. Ann Surg 1988; 207:699.[Medline]
  156. Pate JW, Gavant ML, Weiman DS, Fabian TC: Traumatic rupture of the aortic isthmus: Program of selective management. World J Surg 1999; 23:59.[Medline]
  157. Stavens B, Hashim SW, Hammond GL, et al: Optimal methods of repair of descending thoracic aortic transection and aneurysms. Am J Surg 1983; 145:508.[Medline]
  158. Szwerc MF, Benckart DH, Lin JC, et al: Recent clinical experience with left heart bypass using a centrifugal pump for repair of traumatic aortic transection. Ann Surg 1999; 230:484; discussion 490.[Medline]
  159. Turney SZ, Attar S, Ayella R, et al: Traumatic rupture of the aorta. A five-year experience. J Thorac Cardiovasc Surg 1976; 72:727.[Abstract]
  160. Zeiger MA, Clark DE, Morton JR: Reappraisal of surgical treatment of traumatic transection of the thoracic aorta. J Cardiovasc Surg (Torino) 1990; 31:607.[Medline]
  161. Wallenhaupt SL, Hudspeth AS, Mills SA, et al: Current treatment of traumatic aortic disruptions. Am Surg 1989; 55:316.[Medline]
  162. von Oppell UO, Dunne TT, De Groot KM, Zilla P: Spinal cord protection in the absence of collateral circulation: Meta-analysis of mortality and paraplegia. J Card Surg 1994; 9:685.[Medline]
  163. Crestanello JA, Zehr KJ, Mullany CJ, et al: The effect of adjuvant perfusion techniques on the incidence of paraplegia after repair of traumatic thoracic aortic transections. Mayo Clin Proc 2006; 81:625.[Abstract/Free Full Text]
  164. Gillian L: The arterial blood supply of the human spinal cord. J Comp Neurol 1958; 110:75.[Medline]
  165. Adams H, Von Geertruyden H: Neurologic complications of aortic surgery. Ann Surg 1956; 144:574.[Medline]
  166. Katz NM, Blackstone EH, Kirklin JW, Karp RB: Incremental risk factors for spinal cord injury following operation for acute traumatic aortic transection. J Thorac Cardiovasc Surg 1981; 81:669.[Abstract]
  167. Wadouh F, Arndt CF, Oppermann E, et al: The mechanism of spinal cord injury after simple and double aortic cross-clamping. J Thorac Cardiovasc Surg 1986; 92:121.[Abstract]
  168. Bavaria J. Personal case.
  169. Grossi EA, Krieger KH, Cunningham JN Jr, et al: Venoarterial bypass: A technique for spinal cord protection. J Thorac Cardiovasc Surg 1985; 89:228.[Abstract]
  170. Laschinger JC, Cunningham JN Jr, Catinella FP, et al: Detection and prevention of intraoperative spinal cord ischemia after cross-clamping of the thoracic aorta: Use of somatosensory evoked potentials. Surgery 1982; 92:1109.[Medline]
  171. Laschinger JC, Cunningham JN Jr, Nathan IM, et al: Intraoperative identification of vessels critical to spinal cord blood supply— Use of somatosensory evoked potentials. Curr Surg 1984; 41:107.[Medline]
  172. Laschinger JC, Cunningham JN Jr, Isom OW, et al: Definition of the safe lower limits of aortic resection during surgical procedures on the thoracoabdominal aorta: Use of somatosensory evoked potentials. J Am Coll Cardiol 1983; 2:959.[Abstract]
  173. Laschinger JC, Cunningham JN Jr, Nathan IM, et al: Experimental and clinical assessment of the adequacy of partial bypass in maintenance of spinal cord blood flow during operations on the thoracic aorta. Ann Thorac Surg 1983; 36:417.[Abstract]
  174. Laschinger JC, Cunningham JN Jr, Cooper MM, et al: Prevention of ischemic spinal cord injury following aortic cross-clamping: Use of corticosteroids. Ann Thorac Surg 1984; 38:500.[Abstract]
  175. McCullough JL, Hollier LH, Nugent M: Paraplegia after thoracic aortic occlusion: Influence of cerebrospinal fluid drainage. Experimental and early clinical results. J Vasc Surg 1988; 7:153.[Medline]
  176. Kouchoukos NT, Wareing TH, Izumoto H, et al: Elective hypothermic cardiopulmonary bypass and circulatory arrest for spinal cord protection during operations on the thoracoabdominal aorta. J Thorac Cardiovasc Surg 1990; 99:659.[Abstract]
  177. Kouchoukos NT, Masetti P, Rokkas CK, et al: Safety and efficacy of hypothermic cardiopulmonary bypass and circulatory arrest for operations on the descending thoracic and thoracoabdominal aorta. Ann Thorac Surg 2001; 72:699; discussion 707.[Abstract/Free Full Text]
  178. Kouchoukos NT, Rokkas CK: Hypothermic cardiopulmonary bypass for spinal cord protection: Rationale and clinical results. Ann Thorac Surg 1999; 67:1940; discussion 1953.[Abstract/Free Full Text]
  179. Rokkas CK, Kouchoukos NT: Profound hypothermia for spinal cord protection in operations on the descending thoracic and thoracoabdominal aorta. Semin Thorac Cardiovasc Surg 1998; 10:57.[Medline]
  180. Parrino PE, Kron IL, Ross SD, et al: Spinal cord protection during aortic cross-clamping using retrograde venous perfusion. Ann Thorac Surg 1999; 67:1589; discussion 1594.[Abstract/Free Full Text]
  181. Parrino PE, Kron IL, Ross SD, et al: Retrograde venous perfusion with hypothermic saline and adenosine for protection of the ischemic spinal cord. J Vasc Surg 2000; 32:171.[Medline]
  182. Black JH, Davison JK, Cambria RP: Regional hypothermia with epidural cooling for prevention of spinal cord ischemic complications after thoracoabdominal aortic surgery. Semin Thorac Cardiovasc Surg 2003; 15:345.[Medline]
  183. Fullerton DA: Simplified technique for left heart bypass to repair aortic transection. Ann Thorac Surg 1993; 56:579.[Abstract]
  184. Verdant A, Page A, Cossette R, et al: Surgery of the descending thoracic aorta: Spinal cord protection with the Gott shunt. Ann Thorac Surg 1988; 46:147.[Abstract]
  185. Jamieson WR, Janusz MT, Gudas VM, et al: Traumatic rupture of the thoracic aorta: Third decade of experience. Am J Surg 2002; 183:571.[Medline]
  186. Karmy-Jones R, Carter Y, Meissner M, Mulligan MS: Choice of venous cannulation for bypass during repair of traumatic rupture of the aorta. Ann Thorac Surg 2001; 71:39; discussion 41.[Abstract/Free Full Text]
  187. Hess PJ, Howe HR Jr, Robicsek F, et al: Traumatic tears of the thoracic aorta: Improved results using the Bio-Medicus pump. Ann Thorac Surg 1989; 48:6.[Abstract]
  188. Turney SZ: Blunt trauma of the thoracic aorta and its branches. Semin Thorac Cardiovasc Surg 1992; 4:209.[Medline]
  189. Leshnower BG, Litt HI, Gleason TG: Anterior approach to traumatic mid aortic arch transection. Ann Thorac Surg 2006; 81:343.[Abstract/Free Full Text]
  190. Carter YM, Karmy-Jones RC, Oxorn DC, Aldea GS: Traumatic disruption of the aortic arch. Eur J Cardiothorac Surg 2001; 20:1231.[Free Full Text]
  191. Pett SB Jr., Wernly JA, Akl BF: Observations on flow characteristics of passive external aortic shunts. J Thorac Cardiovasc Surg 1987; 93:447.[Abstract]
  192. Marvasti MA, Meyer JA, Ford BE, Parker FB Jr: Spinal cord ischemia following operation for traumatic aortic transection. Ann Thorac Surg 1986; 42:425.[Abstract]
  193. McBride LR, Tidik S, Stothert JC, et al: Primary repair of traumatic aortic disruption. Ann Thorac Surg 1987; 43:65.[Abstract]
  194. Ablaza SG, Ghosh SC, Grana VP: Use of a ringed intraluminal graft in the surgical treatment of dissecting aneurysms of the thoracic aorta. A new technique. J Thorac Cardiovasc Surg 1978; 76:390.[Abstract]
  195. Carter Y, Meissner M, Bulger E, et al: Anatomical considerations in the surgical management of blunt thoracic aortic injury. J Vasc Surg 2001; 34:628.[Medline]
  196. Mattison R, Hamilton IN Jr, Ciraulo DL, Richart CM: Stent-graft repair of acute traumatic thoracic aortic transection with intentional occlusion of the left subclavian artery: case report. J Trauma 2001; 51:326.[Medline]
  197. Singh MJ, Rohrer MJ, Ghaleb M, Kim D: Endoluminal stent-graft repair of a thoracic aortic transection in a trauma patient with multiple injuries: Case report. J Trauma 2001; 51:376.[Medline]
  198. Lachat M, Pfammatter T, Witzke H, et al: Acute traumatic aortic rupture: Early stent-graft repair. Eur J Cardiothorac Surg 2002; 21:959.[Abstract/Free Full Text]
  199. Czermak BV, Waldenberger P, Perkmann R, et al: Placement of endovascular stent-grafts for emergency treatment of acute disease of the descending thoracic aorta. AJR Am J Roentgenol 2002; 179:337.[Abstract/Free Full Text]
  200. Greenberg R: Treatment of aortic dissections with endovascular stent grafts. Semin Vasc Surg 2002; 15:122.[Medline]
  201. Herold U, Piotrowski J, Baumgart D, et al: Endoluminal stent graft repair for acute and chronic type B aortic dissection and atherosclerotic aneurysm of the thoracic aorta: An interdisciplinary task. Eur J Cardiothorac Surg 2002; 22:891.[Abstract/Free Full Text]
  202. Gorich J, Asquan Y, Seifarth H, et al: Initial experience with intentional stent-graft coverage of the subclavian artery during endovascular thoracic aortic repairs. J Endovasc Ther 2002; 9(Suppl 2):II39.
  203. Czerny M, Zimpfer D, Fleck T, et al: Initial results after combined repair of aortic arch aneurysms by sequential transposition of the supra-aortic branches and consecutive endovascular stent-graft placement. Ann Thorac Surg 2004; 78:1256.[Abstract/Free Full Text]
  204. Peterson BG, Eskandari MK, Gleason TG, Morasch MD: Utility of left subclavian artery revascularization in association with endoluminal repair of acute and chronic thoracic aortic pathology. J Vasc Surg 2006; 43:433.[Medline]
  205. Rehders TC, Petzsch M, Ince H, et al: Intentional occlusion of the left subclavian artery during stent-graft implantation in the thoracic aorta: Risk and relevance. J Endovasc Ther 2004; 11:659.[Medline]
  206. Idu MM, Reekers JA, Balm R, et al: Collapse of a stent-graft following treatment of a traumatic thoracic aortic rupture. J Endovasc Ther 2005; 12:503.[Medline]
  207. Marzelle J, Nottin R, Dartevelle P, et al: Combined ascending aorta rupture and left main bronchus disruption from blunt chest trauma. Ann Thorac Surg 1989; 47:769.[Abstract]
  208. Kirsh MM, Orringer MB, Behrendt DM, et al: Management of unusual traumatic ruptures of the aorta. Surg Gynecol Obstet 1978; 146:365.[Medline]
  209. Mattox KL, Wall MJR: Traumatic Aneurysm of the Thoracic Aorta. Philadelphia, WB Saunders, 1992.
  210. Kazerooni EA, Williams DM, Abrams GD, et al: Aortobronchial fistula 13 years following repair of aortic transection. Chest 1994; 106:1590.[Medline]
  211. Tsai FC, Lin PJ, Wu YC, Chang CH: Traumatic aortic arch transection with supracarinal tracheoesophageal fistula: case report. J Trauma 1999; 46:951.[Medline]
  212. Demetriades D: Penetrating injuries to the thoracic great vessels. J Card Surg 1997; 12:173; discussion 179.[Medline]




This Article
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this book
Right arrow Author home page(s):
Thomas G. Gleason
Joseph E. Bavaria
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Gleason, T. G.
Right arrow Articles by Bavaria, J. E.
Right arrow Search for Related Content
PubMed
Right arrow Articles by Gleason, T. G.
Right arrow Articles by Bavaria, J. E.