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Gleason TG, Bavaria JE. Trauma to Great Vessels.
In: Cohn LH, Edmunds LH Jr, eds. Cardiac Surgery in the Adult. New York: McGraw-Hill, 2003:12291250.

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Chapter 51

Trauma to Great Vessels

Thomas G. Gleason/ Joseph E. Bavaria

????Natural History
????Clinical Presentation
????Diagnostic Studies
????Nonisthmic Aortic/Arterial Lacerations
????Associated Injuries
????Postoperative Care

Eighty-five percent of traumatic injuries to the great vessels in civilian practices are caused by penetrating trauma.1,2 Fifty-seven percent of penetrating chest injuries are caused by gunshot wounds and 25% by stab wounds.1,2 These injuries have no distinct pattern of anatomic occurrence but should be approached in a manner consistent with Advanced Trauma Life Support (ATLS) guidelines. Among the remaining 15% of great vessel traumatic injuries, the majority are blunt traumatic aortic ruptures. These injuries should be approached in a uniform manner. One percent of patients presenting with signs of blunt chest trauma will have an aortic injury.35 Vesalius was the first to report on a traumatic injury to the aorta manifesting as a posttraumatic aortic aneurysm in 1557.6,7 Aortic rupture was a very uncommon injury until travel by motor vehicles increased in the latter half of the 20th century.

The standard reference reporting on traumatic aortic rupture dates to 1958, when Parmley et al reviewed 296 cases from the Armed Forces Institute of Pathology.6 This injury remains the second leading cause of death from vehicular trauma, representing 15% of motor vehiclecaused deaths.810 Death occurs immediately in 75% to 90% of cases.6,810 Approximately 8% of patients survive more than 4 hours.6 Those who survive aortic transection typically have two or fewer associated serious injuries, while those who die have four or more serious injuries.6,10 For example, according to Parmley's original report, 42% of patients with aortic rupture had an associated cardiac injury.6 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 both peri- and intraoperatively.


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.6,1114 These injuries are primarily caused by motor vehicle accidents or falls. Motor vehicle drivers, passengers, or pedestrians hit by vehicles represent 73% to 92% of all cases.6,10,11,13,14 Falls causing aortic rupture are typically from greater than 3 m.6,1517 Alcohol or other substance abuse is involved in over 40% of motor vehicle accidents.11,13 Ejection from a vehicle doubles the risk of aortic rupture, and seat belt restraint reduces mortality risk by a factor of four.11 More recently, aortic rupture of both the ascending and descending aorta has been attributed to the deployment of an air bag; in some cases the cars were moving at a speed of less than 10 mph.1821 Accidental or suicidal falls, crush injuries, airplane accidents, and rare cave-ins are other causes of aortic rupture.6,10,12,15,16,22 The majority (70%80%) of victims are male with an average age of 39 (range, 388).10 Recent series demonstrate that 80% of cases are caused by motor vehicle accidents (72% head-on, 24% side impact, and 4% rear impact).9,10,23 Of the patients with traumatic aortic rupture who make it to the hospital alive, 75% are hemodynamically stable.10 Compared to autopsy series, these patients have fewer severe associated injuries.6,9,10,12 Forty percent to 92% of patients are transferred from the original hospital to a level I trauma center.10,23,24

Table 51-1 lists the frequency of associated injuries from data accrued from the 1970s to late 1990s in several different series.10,15,2528 Data from the American Association for the Surgery of Trauma (AAST) trial were gathered prospectively from 50 trauma centers throughout the United States and Canada.10 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 demonstrated that the majority of patients have associated cardiac contusion, recent data suggest the incidence is only 4%.10 Orthopedic injuries remain common, occurring in association with aortic rupture in 20% to 35% of cases. Mean Injury Severity Score (ISS) 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.10

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TABLE 51-1 Associated injuries in hospitalized patients with traumatic aortic disruption



In autopsy series aortic disruptions occur in all aortic segments including, rarely, the abdominal aorta. 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 (Fig. 51-1).6,12,29,30 However, surgical series demonstrate that 84% to 100% of ruptures occur at the isthmus, and only 3% to 10% occur in the ascending, arch, or distal descending aorta.9,10,23,26,27,3133 Among patients who survive, it seems evident that the periadventitial tissue around the isthmus provides some protection against free rupture, allowing for short-term survival and transfer to a hospital.

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FIGURE 51-1 Anatomic diagram of the thoracic aorta and major branches.

The aorta is typically transected in a transverse fashion involving all three layers of the aortic wall with the edges often separated by several centimeters (Fig. 51-2).6,12 Noncircumferential and partial aortic wall disruptions do occur and can vary from only a few millimeters to several centimeters.6,12,34,35 Spiral lacerations or longitudinal extensions are uncommon. Intramural hematomas and focal dissections occur with partial thickness disruptions but not transections.6 Partial tears tend to occur posteriorly, involving the intima and media. Aortic wall structure at and around the transection does not differ from uninvolved aorta, and atherosclerotic disease is generally not present.6,11,12 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 area of the aorta.36,37

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FIGURE 51-2 Photograph of a traumatic aortic disruption at the isthmus. (Reproduced with permission from Strassman G: Traumatic rupture of the aorta. Am Heart J 1947; 33:508.)

Blunt trauma can also produce trauma to the other great vessels. Disruption at the base of the innominate is the most common, the base of the left subclavian artery less common, and the base of the left carotid the least often disrupted.38 Central venous injuries are less commonly injured with blunt trauma.1


Approximately 2% to 5% of patients with aortic disruptions survive without operation, or even detection, to form chronic false aneurysms.39 Little is known of the natural history of these chronic pseudoaneurysms. It is likely that an initial false aneurysm with blood flow partially thromboses and organizes to form a fibrous wall. This wall may calcify.3941 It can evolve into a saccular or fusiform aneurysm and late expansion or even rupture may occur. Ninety percent involve the aortic isthmus, presumably reflective of some inherent protection afforded to this area by mediastinal periadventitial tissues at the isthmus.4244 The patients who develop chronic pseudoaneurysms have fewer associated injuries at the time of the traumatic event.4244 In fact, 35% have no other injuries, and 50% have only one.40


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, postulating that a combination of traction, torsion, shear, bending, and bursting forces secondary to differential deceleration of tissues within the mediastinum causes an appropriate stress to rupture the aorta at specific sites, the isthmus being the most common.11,36,37,4552 The ligamentum arteriosum, the left mainstem bronchus, and the paired intercostal arteries limit the mobility of the aorta at the isthmus and just distal to it. Experiments have suggested that the aorta can be displaced in a longitudinal (cranial or caudal) direction sufficient to cause traction tears at the isthmus.47,49 It has also been recognized that deceleration forces can reach several hundred times the force of gravity, which can produce injury without any direct impact on the chest.45,46 Alternatively, a "shoveling mechanism" has been postulated to explain cranially directed traction stresses in drivers and front seat passengers in motor vehicle accidents.53

Contrarily, Crass et al argue that the forces of differential deceleration, torsion, or hydrostatics have inadequate magnitude in vehicular accidents to result in aortic tearing given the inherent properties of the aorta.5456 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 pressure of 2000 mm Hg before bursting.57,58 Crass proposed a new mechanism based on thoracic compression that he coined "the osseous pinch," which was tested in the laboratory. The hypothesis is that anterior thoracic osseous structures (manubrium, first rib, 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 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.54 In comparison, a 38-mph collision produces a force of 198,000 N in a normal-sized adult.54

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.49 Hyperextension of the spine and consequent shearing forces may play a role in the distal descending aorta.54

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. 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. Consequently, it will be difficult to prove the various hypotheses of mechanism in humans.

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 observed that 86% of patients die at the scene, and 11% survive longer than 6 hours.6 The only survivors in the Parmley series were, in fact, operated on. Mortality rates in most recent surgical series range from 11% to 40%, although the attributable mortality rates are not known.9,10,16,23 Several groups have reported small series of patients who were treated conservatively with beta blockade and vasodilators in patients deemed unsuitable candidates for surgery or in cases of apparent minimal aortic injury.3,5961 Those unsuitable for surgery were too old and morbid or had associated injuries that were too severe for them to tolerate operative repair of the aortic rupture initially and thus underwent delayed repair. When surgery has been delayed with blood pressure control for stabilization of other injuries, the interim mortality rate prior to definitive repair is not clearly known but is probably low. Delays of up to 4 months prior to repair have been reported,6168 although in a recent series of patients who were definitively treated nonoperatively for reasons of comorbidity, the mortality rate was 47%.3 None of the deaths, however, was due to aortic rupture. Another series of 5 patients treated nonoperatively because of associated injuries had an average follow-up of 51 months with no mortality.64 We conclude that aortic transection can and probably should be treated nonoperatively or with operative delay in certain 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.41,44,6974 A review of the literature by Finkelmeier et al demonstrated that among survivors like these, over 70% survive greater than 5 years from the time of the injury.40 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.40

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.14,7578 Patients may develop dyspnea, back pain, or differential hypertension in the lower as compared to the upper extremities.56,75,76,7882 Aortic injuries are more commonly identified in the backdrop of a multiple-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 high deceleration forces, the possibility of aortic rupture exists, and it should be ruled out. In cases of motor vehicle trauma, falls, blasts, crush injuries, or other acceleration or deceleration forces, aortic rupture should be considered.3,8,16,60,8386

The initial management of a multiple-trauma patient is no different with or without suspected aortic disruption. The patient's airway, breathing, and circulation are addressed first. Primary and secondary surveys are completed. 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 of the body compartments, perforated viscus, or central neurologic injury take the usual priority. Most patients with aortic disruption also have one or more fractures. These should be stabilized but not definitively treated prior to excluding the diagnosis of aortic rupture or treating an aortic rupture. There are often clues evident in the initial evaluation of a trauma patient that suggest aortic disruption (Table 51-2). In the majority of trauma cases, a supine chest radiograph is obtained as part of the initial evaluation.

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TABLE 51-2 Clues that suggest aortic disruption

Diagnostic Studies


A standard supine anteroposterior (AP) chest x-ray does not have the diagnostic sensitivity to rule out aortic injury.3,5,16,87 Chest x-ray findings are interpreted as normal at the time of initial evaluation of 9% to 40% of patients with aortic rupture in major trauma centers.3,5,16,77,8794 At least fifteen distinct signs on a standard AP chest x-ray are associated with blunt aortic injury or rupture (Table 51-3).87 Unfortunately, none of these signs are sufficiently sensitive, specific, or predictive of aortic rupture. In a series of 188 consecutively evaluated multiple-trauma patients, 10 blunt aortic injuries were identified, and the sensitivities of these plain radiographic findings ranged from 0% to 90%.87 The specificities ranged from 6% to 93%.87

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TABLE 51-3 Chest x-ray findings associated with blunt aortic disruption

In lieu of attaining an upright chest x-ray, which is typically precluded in a multiple-trauma patient, reverse Trendelenburg 45-degree AP chest x-rays have been suggested to be more accurate than supine films at evaluating the mediastinum.95 However, this technique is not used routinely in most trauma centers, especially when computed tomography is available.


Volumetric helical or spiral computed tomography (CT) has become the standard screening tool to rule out aortic rupture.5 The technology was introduced in the early 1990s, and since that time it has become the screening modality used in most institutions.35,16,17,59,66,89,93,94,96106 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 are typically used, and 50 to 60 images with slice thicknesses of 5 to 7 mm can be acquired in less than 1.5 minutes.5 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, and pseudocoarctation.5

Approximately 1% of blunt trauma patients have a thoracic aortic injury identified by helical CT.3,97 In most prospective series the sensitivity and negative predictive value of helical CT in detecting traumatic aortic rupture are 100%.3,16,93,107 Aortography has been the standard against which all diagnostic methods have been compared, with sensitivities and specificities approaching 100% in older series.108 However, in more recent series that have utilized modern imaging techniques of either helical CT or transesophageal echocardiography (TEE), aortography has had sensitivities of only 78% to 92%.3,109 False-positive CT studies do occur. The specificity, accuracy, and positive predictive value of helical CT range from 50% to 89%.3,16,93,107 One uncommon finding that mimics aortic injury is a ductus diverticulum remnant.5 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 either by TEE or aortography 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.3,5,59 These minimal injuries pose another management dilemma. Many of these minor aortic injuries can and probably should be managed medically with antihypertensive medications and wall stressreducing agents (e.g., beta blockers).59

The degree to which thoracic surgeons rely on chest CT to plan repair of thoracic aortic injuries is variable. Our routine practice at the University of Pennsylvania is to obtain a helical chest CT as the initial screen for aortic injury in the hemodynamically stable patient. Studies that unequivocally demonstrate no aortic injury are cleared with CT alone. Studies that show aortic transection with obvious intimal disruption and periaortic hematoma (Fig. 51-3) go to the operating room for definitive repair once other life-threatening injuries have been identified and appropriately addressed. Studies that demonstrate no clear aortic rupture with intimal disruption but show a periaortic, mediastinal hematoma prompt subsequent aortogram. When a patient is hemodynamically unstable due to hemorrhagic shock, the evaluation of thoracic aortic injury is done in the operating room using TEE as described below. The timing of obtaining the chest CT depends on the stability of the patient, associated injuries, and resuscitation issues, but typically will occur at the same time that head and abdominopelvic CTs are obtained.

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FIGURE 51-3 Helical CT of the chest in a 30-year-old male after a high-speed motor vehicle accident. Aortic transection at the isthmus is clearly seen.


The development of multiplanar transesophageal echocardiography (TEE) has revolutionized cardiothoracic surgery such that its use is now necessary to plan and facilitate optimal intraoperative management in many 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 aortic arch, which are obscured by tracheal and bronchial air artifact. Contrarily, transthoracic echocardiography (TTE) cannot accurately evaluate the distal descending aorta. The accuracy of TEE for diagnosing aortic injury is dependent on the operator. Some report its sensitivity and specificity to be approaching 100%,107,109,110 while others demonstrate a sensitivity and specificity as low as 63% and 84%, respectively.111 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.107

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.107,109 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 passage of the probe.

Multiplanar TEE probes permit acquisition of cross-sectional images at different angles along a single rotational axis (Figs. 51-4 to 51-6). The typical 5- or 7-MHz transducer permits adequate resolution of structures as small as 1 to 2 mm. 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 that can aid in identifying intimal flaps (Fig. 51-5).

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FIGURE 51-4 Transesophageal echocardiographic longitudinal cross-sectional image of the aortic isthmus depicting intimal disruption and para-aortic thrombus. (Courtesy of B. Milas, University of Pennsylvania.)


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FIGURE 51-6 Transesophageal echocardiographic cross-sectional image in short axis depicting aortic transection with the distal aortic lumen (AO) appearing within the proximal aortic lumen. This is diagnostic of aortic transection. (Courtesy of B. Milas, University of Pennsylvania.)


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FIGURE 51-5 Transesophageal echocardiographic cross-sectional image in the short axis 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.)

The most common feature of aortic injury identified by TEE is a mural flap (Figs. 51-4 and 51-6). Thickening of the vessel wall can represent a contained rupture or a mural thrombus (Fig. 51-4). Color Doppler flow mapping can demonstrate alterations in flow patterns including turbulence at the site of injury (Fig. 51-5). 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 that transection is the diagnosis.


Aortography is the imaging modality by which all other techniques have been compared for evaluation of aortic injury (Fig. 51-7). Temporally, its technique and role in evaluating aortic injuries or other vascular injuries were established long before any of the other sophisticated imaging methodologies. In experienced hands its sensitivity and specificity both approach 100%.108 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.82,112,113 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 prehelical CT era, 85% to 95% of aortograms were negative, calling into question the cost- and time-effectiveness of the technique.17,76,82,105,108,113 False-positive studies are usually attributed to atheromata or ductal diverticula.

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FIGURE 51-7 Intra-arterial digital subtraction angiogram of an acute traumatic aortic disruption at the isthmus. The linear tear is typical.

The technique of intra-arterial digital subtraction angiography (IADSA) is used by most groups, including our own, and allows for faster generation of images and shorter times in the angiography suite (Fig. 51-7). Intravenous digital subtraction angiography (IVDSA) has been used in the past by some as an even more rapid means of evaluating the aorta in the angiography suite.113 This technique employs IV contrast instillation with time-delayed images of the arch and descending aorta. The time of study can be reduced by up to 4-fold when compared to conventional biplanar angiography. Unfortunately, the diagnostic quality of IVDSA is less than 70%,113 and consequently with the near uniform availability of helical CT, the technique has become obsolete.


Magnetic resonance angiography (MRA) 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.114117 However, its use in the acute trauma patient has not been justified. The time required to attain images and the confining nature of the scanners preclude its use in this patient population. If MR data acquisition time decreases and patient accessibility within a scanner increases in the future, there may become a role for MRA in acute trauma settings. Alternatively, it is reasonable to follow a patient with traumatic aortic rupture long term using MRA, particularly those patients with minimal aortic injury treated nonoperatively. In the rare patient who presents with aortic aneurysm or pseudoaneurysm remote from the time of aortic injury, MRA is certainly a useful technique.



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 in aortic injury.9,10,60 The leading cause of death in patients with aortic injury who make it to the hospital is exsanguinating aortic rupture, which occurs in 20% of patients.10 Among patients who present with an aortic injury and are hemodynamically stable, 4% die in the hospital of aortic rupture prior to surgical repair.10 These data emphasize that a careful, planned, and expeditious team approach toward these patients is mandatory in order to save as many of these patients as possible. Standard ATLS guidelines for trauma evaluation should be followed. These include performing primary and secondary physical examinations with control of the airway, respiration, and hemodynamics, and obtaining a chest x-ray, baseline chemistry, blood gas, and hematologic studies. The first priorities in these and all trauma patients are to control ventilation and stabilize hemodynamics. This may require intubation, insertion of thoracostomy tubes, resuscitation from cardiac arrest, identification and stabilization of head injuries, laparotomy, or even thoracotomy. 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, bypassing time-consuming tests, in order to achieve the best chance of survival.


After initial trauma evaluation, establishment of an airway, and control of ventilation and hemodynamics, 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 lesions occupying intracranial space 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 imaging equipment, and should be coordinated with the evaluation of other life-threatening injuries. The usual scenario of the hemodynamically stable blunt trauma patient dictates leaving the emergency room 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 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 that cannot be accurately defined by these other imaging techniques. Occasionally, thoracoscopy has been used to evaluate traumatic hemothoraces.118 However, there is little role for thoracoscopy in the diagnosis of aortic rupture because, in experienced hands, the sensitivity and specificity of intraoperative TEE are so good.

In the preoperative period, patients with aortic injury should receive beta blockers and vasodilators for control of aortic wall tension and blood pressure.3,60 Reduction of the change in pressure over the change in time ({Delta}P/{Delta}t) reduces the wall stress significantly.119 These measures have been shown to reduce in-hospital aortic rupture rates without adversely affecting the outcome of other injuries.3 These control measures should be employed both in patients going to the operating room and patients undergoing delayed aortic repair for the treatment of other life-threatening injuries.


Immediate thoracotomy and aortic repair are recommended in stable patients without the need for laparotomy, craniotomy, or pelvic stabilization once the diagnosis of aortic injury is made. Intracranial bleeding causing mass effect and thoracic, abdominal, pelvic, or retroperitoneal hemorrhage should all be addressed prior to thoracotomy for contained aortic injury.62,120 Presentation of aortic disruption with aortic bleeding requires immediate surgery; however, this situation is rarely encountered as it is usually immediately fatal. Aortic injury should be monitored by TEE during surgical treatment of intracranial, thoracic, abdominal, or pelvic injuries. Treatment of injuries that are not life-threatening 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, postponing definitive repair of aortic rupture until complete resuscitation and hemodynamic stability are achieved. Care should be taken during this stabilization period to avoid undue aortic wall stress and hypertension with maintenance of short-acting beta blockers.3 Purposeful delay of definitive aortic repair may be a safe option when there is concomitant severe hepatic trauma that carries a significant risk of recurrent or ongoing hemorrhage.121


The technical issues of repairing aortic lacerations are straightforward. While no one method of repair of aortic transection has been proven superior, standards are being established. There remains considerable controversy surrounding the issue of spinal cord protection and which means of protection are optimal.9,10,23,27,31,33,56,60,64,66,77,86,92,122130 There remain two general perspectives: (1) "clamp-and-sew" techniques are sufficient alone, or (2) some form of lower body perfusion provides added spinal cord and visceral protection against the ischemia of the aortic cross-clamp. Regardless of the technical controversies, paraplegia occurs among these patients at an overall rate of approximately 10%.9,10,31,33,77,131 Prospectively acquired data from multiple institutions demonstrate a marked reduction in paraplegia rates with the use of lower body perfusion techniques.3,10,16,60

Preparations Appropriate blood work including complete blood count, coagulation studies, electrolytes, urea nitrogen, and creatinine should be attained. Antihypertensive and beta-blockade therapy should be ongoing prior to induction of anesthesia. Single (right) lung ventilation is optimal and should be secured either by double-lumen endotracheal tube or single-lumen tube with left bronchial balloon blocker. After anesthetic induction, right femoral and right radial arterial lines should be placed for monitoring of upper and lower body perfusion. The left groin should be left alone for access for possible partial left heart bypass. Several large-bore intravenous catheters for infusion and a pulmonary arterial catheter should be placed for ongoing hemodynamic monitoring. A bladder catheter with temperature probe, peripheral arterial oxygen saturation monitor, and electrocardiogram should be placed for continuous monitoring. A nasogastric (NG) tube is inserted, the stomach emptied, and then the NG tube removed to allow insertion of a TEE probe. Subsequently, the patient is placed in the right lateral decubitus position with the table flexed and the hip rotated slightly leftward to facilitate left groin exposure. The patient's skin is prepped and draped from left shoulder to left knee. A cell-saver system is used for red blood cell salvage. Antifibrinolytic drugs (e.g., aprotinin, tranexamic acid, or {epsilon}-amino caproic acid) may offer a reduced incidence of blood transfusion requirements.132

Spinal cord protection Blood flow is supplied to the spinal cord by anterior and posterior spinal arteries that consist of anatomic vascular chains that run the length of the cord.133 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, 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. 51-8). 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 for at least 25% of patients is essential for cord blood supply in this zone.133,134

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FIGURE 51-8 Cross-sectional diagram showing a medullary (radicular) arterial branch to the anterior spinal artery.

Aortic cross-clamping near the aortic isthmus produces profound hypotension in the lower body and spinal cord below this region, and spinal cord injury is proportional to aortic cross-clamp time (Fig. 51-9).135 Clamping the aorta above the takeoff of the left subclavian artery may increase the risk of paraplegia since there are collateral vessels fed by the internal thoracic, vertebral, and subscapular vessels, all emanating from the subclavian.136 Paraplegia has occurred after only 9 minutes of aortic cross-clamping without extracorporeal perfusion of the lower body (J Bavaria, personal case).

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FIGURE 51-9 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 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.)

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 that are often not available to trauma patients.131,137143 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.144147 Selective spinal cord hypothermia and perfusion have been studied in the laboratory, but to date these techniques have not been employed in humans.148,149 Experience with theoretical neuroprotective pharmaceuticals like steroids, lidocaine, or magnesium has 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. Certainly, some groups have had success with low paraplegia rates using exclusively simple cross-clamping technique,9,23 but these results have not been reproducible throughout many institutions, and their results rely on short cross-clamp times (average 20 to 25 minutes). 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.10,125,131 At the University of Pennsylvania all patients undergoing repair of aortic transection receive some form of lower body perfusion during aortic cross-clamping. There have been no cases of paraplegia since this strategy was implemented in 1994 (over 40 patients; unpublished data).

Incisions A standard fourth interspace posterolateral thoracotomy with or without fifth rib removal or 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 are established. Depending on the stability of the patient, the decision of how to achieve lower body perfusion can be made prior to aortic exposure by gaining access to the left groin or after aortic exposure to facilitate left atrial to distal aortic bypass. The left groin is exposed in the standard fashion. The left common femoral artery is encircled with vessel loops, and the left femoral vein is exposed simply on its anterior surface because circumferential exposure may increase the incidence of deep venous thrombosis.


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.10,23,25,27,86,122124,126,127,129,137,150,151 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.3,10 It is important to be well versed in the various lower body perfusion systems because distinct circumstances may require alterations in routine practice.

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.9,10,23 However, the average cross-clamp time reported in the literature is 41.0 minutes.31 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.

Lower body perfusion systems The system used by any one group should be simply applied, reliable, and routine to that group. Distal perfusion pressure should be maintained at 60 to 70 mm Hg.127 Full heparinization is relatively contraindicated in cases of intracranial hemorrhage and lung injury, but is otherwise safely used by many groups.9,10,31,77,127,150,152 The least amount of heparin that can be used for a given circuit is probably best. Use of a Bio-Medicus 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.123,127,152 It is helpful to employ the use of a heat exchanger within extracorporeal circuits in order to maintain core temperatures above 35?C in those patients who cool quickly.

Partial left heart bypass This technique actively shunts blood from the left atrium to the lower body via either the distal thoracic aorta or left femoral artery.127,150 Typically, a two-stage 2020F cannula is placed into the left atrium through the left inferior pulmonary vein to provide inflow to the pump (Fig. 51-10). Arterial cannulation size is determined by body size and site of cannulation. We employ either a high-flow, atraumatic, aortic cannula for distal aortic cannulation or a 16F to 22F straight arterial cannula for femoral cannulation. Distal aortic cannulation has the advantage of convenience and speed. Partial left heart bypass serves several purposes:

  1. Unloads the left heart and controls proximal hypertension at the time of cross-clamping
  2. Maintains lower body perfusion
  3. Allows rapid infusion of volume
  4. Controls intravascular volume
The lower body is perfused at a flow rate of 2 to 3 L/min with lower body mean arterial pressure (MAP) of 60 to 70 mm Hg while maintaining an upper body MAP 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.

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FIGURE 51-10 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.

Right atrial to femoral arterial bypass A long venous catheter (18F-22F) with multiple side holes is passed via the left common femoral vein into the right atrium using a guidewire technique. The left groin is exposed in the usual fashion, and the anterior wall of the common femoral vein is exposed as described above. A purse-string suture is placed within the vein, and the vein is cannulated. The femoral artery is cannulated. This bypass technique can be used with or without an oxygenator like partial left heart bypass, but it can also provide a complete cardiac output and full cardiopulmonary bypass. This becomes relevant if the aortic arch is involved in the aortic injury. When partial heart bypass is utilized, flows in the circuit are maintained at 2 to 3 L/min as in partial left heart bypass circuits. When neither an oxygenator nor a heat exchanger is used, no heparin is required as with left heart bypass.153 In this case, the femoral arterial PaO2 is approximately 40 mm Hg (saturation 45%65%), which is adequate for tissue oxygen needs provided the hemoglobin concentration is maintained above 10 g/dL. The concern that perfusion of the lower body with this reduced blood oxygen saturation might increase the paraplegia rate has not been realized.137

Right atrial to femoral arterial bypass has the distinct advantage of allowing for establishment of partial or complete bypass prior to entering the chest. Additionally, this technique is preferred when there is concomitant right lung contusion in order to assure adequate tissue oxygenation during repair. Rarely, there may be a need to perform a proximal anastomosis under deep hypothermic circulatory arrest (HCA) because of an injury that involves the aortic arch, and right atrial cannulation provides an adequate amount of inflow to the pump to facilitate complete cardiopulmonary bypass while left atrial cannulation alone usually does not. Use of this technique should proceed with caution in a trauma patient and only after other associated injuries have been addressed to avoid bleeding complications. If HCA is required, it is essential to confirm the lack of aortic valvular insufficiency. When HCA is utilized within the left chest, the left ventricle should be vented via the left inferior pulmonary vein.

Passive proximal to distal aortic shunt (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.123 The proximal end is placed in the ascending aorta, the 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, but it was abandoned due to a high rate of ventricular dysrhythmias, reduced shunt flows, and a higher rate of paraplegia.25,123,124,151,154,155 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.151 The Gott shunt is easy to use although it requires a more extensive dissection of either the aortic arch or ascending aorta. It does not offer the left ventricular unloading or loading advantage that partial bypass systems allow, and therefore blood pressure control is left to pharmacology alone.


The decisions about heparinization and method of lower body perfusion should be made prior to incision if feasible. It should be clear that if no heparin is planned, cannulation of vessels must be immediately followed by bypass to allow for immediate flow through the circuit to prevent thrombosis. The order of conduct for contained aortic disruptions should be to establish groin access first, if employing femoral bypass techniques, followed by chest incision and control of the proximal and distal aorta around the site of injury. If cannulation is planned in the chest, proximal and distal aortic control is established first. The left inferior pulmonary vein is dissected after establishing aortic control when planning partial left heart bypass. Excessive compression or traction of the lung should be avoided, particularly when dissecting out the aortic arch, as the pulmonary artery may be easily disrupted.

The mediastinal pleura is incised along the anterior surface of the proximal left subclavian artery. The subclavian artery is then encircled with a tape. 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 are reflected off the aorta with the overlying pleura and are retracted medially by attaching silk suture stays to the pleura just lateral to the vagus nerve. Loops around the nerves themselves should be avoided, because even stretch of these nerves will 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 most 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.

Distal aortic control is established at an adequate distance from the aortic injury to facilitate repair. The overlying pleura is incised, and the aorta encircled with a tape. 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 2020F dual-stage catheter. The circuit for left heart bypass is 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 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.

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.6,12 Less frequently the transection is only partial. Some authors advocate primary repair at this point,25,156 but most surgeons place a short interposition graft after debridement of the torn edges.9,10,23,26,33,81,124,126,128130 Collagen-coated woven Dacron grafts or gelatin-impregnated grafts are used most commonly. Use of intraluminal prostheses has been abandoned by most groups.157 Grafts are sewn using a running 30 or 40 polypropylene suture with the proximal anastomosis performed first, followed by the distal. Generous amounts of adventitial tissue are included in each bite. Pledgeted reinforcing horizontal mattress sutures are placed intra- or extraluminally as necessary. Upon completion of the anastomoses, the distal clamp is removed first, followed by the proximal aortic, and finally the left subclavian arterial. The patient is then weaned off partial bypass. Heparin is reversed, and the bypass cannulae removed. Hemostasis is achieved, and the chest is closed in a standard fashion.

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 to maintain normal or slightly elevated mean arterial pressure during clamping. The aortic repair is done as expeditiously as possible in order to minimize clamp time. Repair sutures are placed accordingly after clamps are removed. Hemostasis is then achieved after continuity of the aorta is reestablished.

Previous left thoracotomy Emergency room thoracotomies are usually done in haste by inexperienced nonthoracic surgeons and are often placed at sites too low 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. 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 and make it less likely to exsanguinate, but they 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 We recommend 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 is controlled after 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 is then 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.

Endoluminal stent grafts There are now reports of the use of endoluminal stent grafts in the setting of acute traumatic aortic disruption.158,159 In each case reported, associated injuries were felt to render a prohibitive operative risk with conventional repair. Significant pulmonary contusions were cited most frequently. Currently, use of endoluminal stent grafts for aortic transection remains experimental. In the future, a defined role for their use may evolve, particularly in patients with prohibitive injuries, life-threatening comorbidities, or advanced age.

Nonisthmic Aortic/Arterial Lacerations

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.19,24,160 Most commonly the proximal ascending aorta at or just above the sinotubular junction is involved.24 There are a few case reports of ascending aortic ruptures associated with the deployment of air bags.19,20 Ascending aortic ruptures require full heparinization and cardiopulmonary bypass for repair. Therefore, these injuries should initially be managed with beta blockade and blood pressure control until a thorough evaluation of all other life-threatening injuries is completed. These injuries are approached through a median sternotomy. The survival among cases reported in the literature of those undergoing repair is about 85%.24 They have been repaired either primarily or with an interposition graft. Rarely, a concomitant aortic valve replacement is required.24

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.38 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 artery 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.86,161,162 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.161 Alternatively, when injuries extend out onto either the left or right subclavian arteries a thoracosternotomy, cervicosternotomy, or cervicosternothoracotomy "trap door" incision each provides good exposure depending on the level of the injury.1 Finally, the transverse anterior thoracosternotomy "clam-shell" incision provides good exposure to the mediastinal structures and both hemithoraces when multiple injuries require repair.1

Aortic injuries of the descending aorta distal to the isthmus to the level of T8 should be approached through a posterolateral thoracotomy in the 4th, 5th, or 6th 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, but 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.

Associated Injuries

Life-threatening intracranial, thoracic, intra-abdominal, or retroperitoneal hemorrhage should be addressed prior to repair of aortic lacerations that are not bleeding.60,62,163 Posterolateral thoracotomy should immediately follow laparotomy provided hemodynamic stability is achieved after control of intra-abdominal injury. Long bone fractures should be stabilized with only temporary splinting during preparation for thoracotomy. Exsanguinating pelvic fractures should be stabilized with external fixation and/or angiographic embolization prior to aortic repair.77,164166 Patients should be carefully monitored throughout these interventions with judicious fluid replacement, avoiding fluid overload and optimizing respiratory, circulatory, and renal function. Body temperature should be controlled to avoid hypothermia.

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. Vital signs, ventricular filling pressures, blood pressures, cardiac output, renal function, chest tube output, nasogastric drainage, body temperature, neurologic status, blood gases, and coagulation function are all monitored closely. Blood products are given as indicated. Chest x-rays are followed serially. Pulmonary toilet is extraordinarily important, and once clinically stable (usually on postoperative day one) an epidural catheter should be placed for narcotic and local anesthetic delivery if not placed preoperatively. This facilitates 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 cc of serous fluid per day.


Complications after aortic repair occur at a rate of 40% to 50%.10,25,27,33,86 Pneumonia is the most common complication and occurs at a rate of 17% to 34%.10,25,27,33,86 Other complications include bacteremia, renal insufficiency, and paraplegia. Rates of frequency for several series are listed in Table 51-4.10,25,27,33,86 Left vocal cord paralysis has been reported to occur at a rate of 4% to 14%, although recurrent nerve injuries are probably underreported. Late complications are rare in these patients. Aortobronchial fistula following repair of transection has been reported.167,168

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TABLE 51-4 Major postoperative complications

Patients who survive an undiagnosed aortic injury may develop a chronic traumatic aortic aneurysm.15,3944,7074 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 mainstem 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.


The mortality rate of patients with aortic rupture who reach the hospital ranges from 7% to 55% depending on whether or not the injury is repaired.9,10,23,31 Among hemodynamically stable patients undergoing planned thoracotomy and repair, the hospital mortality rate is 14% in the modern era.10 The mortality rate of nonoperative patients with associated injuries precluding initial aortic repair was 55% in the AAST trial.10 All patients who either presented in extremis or with free rupture died of aortic rupture. 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.31

Paraplegia or paraparesis occurred in an average of 9.9% of patients in the review by Von Opell.31 However, paraplegia rates vary widely depending on the operative technique utilized with ranges of 0% to 20%.9,10,23,31,33,64,86 Although several groups have reported very low paraplegia rates using the "clamp-and-sew" technique, these results have not been widely reproduced.10,23 Alternatively, use of extracorporeal lower body perfusion systems has facilitated low rates of paraplegia.10 At the University of Pennsylvania, since the practice of partial left heart bypass for all repairs of aortic transection was instituted in 1994 there have been no cases of paraplegia in a series of over 40 patients (unpublished data). It is also clear that increasing cross-clamp time, particularly beyond 30 minutes, increases the rate of paraplegia.10,135 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 (Tables 51-5 and 51-6).10,31

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TABLE 51-5 Incidence of postoperative paraplegia in relation to operative technique: meta-analysis


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TABLE 51-6 Incidence of postoperative paraplegia in relation to operative technique: AAST prospective trial


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. The incidence of injury to the nonaortic great vessels among cases of penetrating thoracic trauma is not known, but the overall incidence of great vessel injury with thoracic gunshot wounds is approximately 5% and with stab wounds is 2%.169 Patients with penetrating injuries to the thorax should all be managed utilizing standard ATLS protocol as outlined above. Wounds penetrating the thoracic "box" bordered between 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 a sub-xiphoid 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 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.

  1. 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]
  2. 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]
  3. 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.[Medline]
  4. 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]
  5. 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.[Medline]
  6. Parmley L, Mattingly T, Manion W: Nonpenetrating traumatic injury of the aorta. Circulation 1958; 17:1086.[Medline]
  7. Sailer S: Dissecting aneurysm of the aorta. Arch Pathol 1942; 23:704.
  8. Williams JS, Graff JA, Uku JM, Steinig JP: Aortic injury in vehicular trauma. Ann Thorac Surg 1994; 57:726.[Abstract]
  9. Razzouk AJ, Gundry SR, Wang N, et al: Repair of traumatic aortic rupture: a 25-year experience. Arch Surg 2000; 135:913.[Abstract/Free?Full?Text]
  10. 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.[Medline]
  11. Greendyke RM: Traumatic rupture of aorta; special reference to automobile accidents. JAMA 1966; 195:527.[Medline]
  12. 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]
  13. Dischinger P, Cowley R, Shankar B: The incidence of ruptured aorta among vehicular fatalities. Proc Assoc Adv Automot Med Conf 1988; 32:15.
  14. Smith RS, Chang FC: Traumatic rupture of the aorta: still a lethal injury. Am J Surg 1986; 152:660.[Medline]
  15. Duhaylongsod FG, Glower DD, Wolfe WG: Acute traumatic aortic aneurysm: the Duke experience from 1970 to 1990. J Vasc Surg 1992; 15:331.[Medline]
  16. 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]
  17. 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]
  18. Pillgram-Larsen J, Geiran O: [Air bags influence the pattern of injury in severe thoracic trauma]. Tidsskr Nor Laegeforen 1997; 117:2437.[Medline]
  19. 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]
  20. deGuzman BJ, Morgan AS, Pharr WF: Aortic transection following air-bag deployment. N Engl J Med 1997; 337:573.[Free?Full?Text]
  21. Brown DK, Roe EJ, Henry TE: A fatality associated with the deployment of an automobile airbag. J Trauma 1995; 39:1204.[Medline]
  22. Pezzella AT: Blunt traumatic injury of the thoracic aorta following commercial airline crashes. Tex Heart Inst J 1996; 23:65.[Medline]
  23. 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.[Abstract/Free?Full?Text]
  24. 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]
  25. Schmidt CA, Wood MN, Razzouk AJ, et al: Primary repair of traumatic aortic rupture: a preferred approach. J Trauma 1992; 32:588.[Medline]
  26. Hilgenberg AD, Logan DL, Akins CW, et al: Blunt injuries of the thoracic aorta. Ann Thorac Surg 1992; 53:233.[Abstract]
  27. 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]
  28. 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]
  29. Arajarvi E, Santavirta S, Tolonen J: Aortic ruptures in seat belt wearers. J Thorac Cardiovasc Surg 1989; 98:355.[Abstract]
  30. Rabinsky I, Sidhu GS, Wagner RB: Mid-descending aortic traumatic aneurysms. Ann Thorac Surg 1990; 50:155.[Abstract]
  31. von Oppell UO, Dunne TT, De Groot MK, Zilla P: Traumatic aortic rupture: twenty-year meta-analysis of mortality and risk of paraplegia. Ann Thorac Surg 1994; 58:585.[Abstract]
  32. Kieny R, Charpentier A: Traumatic lesions of the thoracic aorta: a report of 73 cases. J Cardiovasc Surg (Torino) 1991; 32:613.[Medline]
  33. 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.[Abstract]
  34. 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]
  35. Strassman G: Traumatic rupture of the aorta. Am Heart J 1947; 33:508.
  36. Butcher HJ: The elastic properties of the human aortic intima, media and adventitia: the initial effect of thromboendarterectomy. Ann Surg 1960; 1151:480.
  37. Lundevall J: The mechanism of traumatic rupture of the aorta. Acta Pathol Microbiol Scand 1964; 62:34.[Medline]
  38. Pretre R, Chilcott M, Murith N, Panos A: Blunt injury to the supra-aortic arteries. Br J Surg 1997; 84:603.[Medline]
  39. Bennett DE, Cherry JK: The natural history of traumatic aneurysms of the aorta. Surgery 1967; 61:516.[Medline]
  40. 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, 19501980. J Thorac Cardiovasc Surg 1982; 84:257.[Abstract]
  41. 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]
  42. 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]
  43. Albuquerque FC, Krasna MJ, McLaughlin JS: Chronic, traumatic pseudoaneurysm of the ascending aorta. Ann Thorac Surg 1992; 54:980.[Abstract]
  44. 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]
  45. Stapp J: Human tolerance to deceleration. Am J Surg 1957; 93:734.[Medline]
  46. Marsh C, Moore R: Deceleration trauma. Am J Surg 1957; 93:623.[Medline]
  47. Aldman B: Biodynamic studies on impact protection. Acta Physiol Scand 1962; 56(suppl):192.
  48. Jackson FR, Berkas EM, Roberts VL: Traumatic aortic rupture after blunt trauma. Dis Chest 1968; 53:577.
  49. Sevitt S: The mechanisms of traumatic rupture of the thoracic aorta. Br J Surg 1977; 64:166.[Medline]
  50. Sevitt S: Traumatic ruptures of the aorta: a clinico-pathological study. Injury 1977; 8:159.[Medline]
  51. Gotzen L, Flory PJ, Otte D: Biomechanics of aortic rupture at classical location in traffic accidents. Thorac Cardiovasc Surg 1980; 28:64.[Medline]
  52. 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]
  53. Voigt GE, Wilfort K: Mechanisms of injuries to unrestrained drivers in head-on collisions, in Proceedings of the 30th Stapp Car Crash Conference. New York, New York Society of Automotive Engineers, 1969.
  54. Crass JR, Cohen AM, Motta AO, et al: A proposed new mechanism of traumatic aortic rupture: the osseous pinch. Radiology 1990; 176:645.[Abstract]
  55. 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]
  56. Cohen AM, Crass JR: Traumatic aortic injuries: current concepts. Semin Ultrasound CT MR 1993; 14:71.[Medline]
  57. Zehnder M: Delayed post-traumatic rupture of the aorta in a young healthy individual after closed injury: mechanical-etiological considerations. Angiology 1956; 7:252.
  58. Oppenheim F: Gibt es eine spontanruptur der gesunden aorta und wie kommt sie zustande? Muenchen Med Wochenschr 1918; 65:1234.
  59. Malhotra AK, Fabian TC, Croce MA, et al: Minimal aortic injury: a lesion associated with advancing diagnostic techniques. J Trauma 2001; 51:1042.[Medline]
  60. 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]
  61. Fisher RG, Oria RA, Mattox KL, et al: Conservative management of aortic lacerations due to blunt trauma. J Trauma 1990; 30:1562.[Medline]
  62. Borman KR, Aurbakken CM, Weigelt JA: Treatment priorities in combined blunt abdominal and aortic trauma. Am J Surg 1982; 144:728.[Medline]
  63. 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]
  64. 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]
  65. 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]
  66. 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.[Medline]
  67. 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]
  68. Pezzella AT, Todd EP, Dillon ML, et al: Early diagnosis and individualized treatment of blunt thoracic aortic trauma. Am Surg 1978; 44:699.[Medline]
  69. 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]
  70. 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]
  71. Roques X: [Chronic post-traumatic aneurysms of the thoracic aorta]. Rev Prat 1991; 41:1789.[Medline]
  72. Becker HM, Ramirez J, Echave V, Heberer G: Traumatic aneurysms of the descending thoracic aorta. Ann Vasc Surg 1986; 1:196.[Medline]
  73. 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]
  74. 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]
  75. Clark DE, Zeiger MA, Wallace KL, et al: Blunt aortic trauma: signs of high risk. J Trauma 1990; 30:701.[Medline]
  76. Gundry SR, Williams S, Burney RE, et al: Indications for aortography in blunt thoracic trauma: a reassessment. J Trauma 1982; 22:664.[Medline]
  77. 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]
  78. 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]
  79. Trachiotis GD, Sell JE, Pearson GD, et al: Traumatic thoracic aortic rupture in the pediatric patient. Ann Thorac Surg 1996; 62:724.[Abstract/Free?Full?Text]
  80. Vlahakes GJ, Warren RL: Traumatic rupture of the aorta. N Engl J Med 1995; 332:389.[Free?Full?Text]
  81. Plume S, DeWeese JA: Traumatic rupture of the thoracic aorta. Arch Surg 1979; 114:240.[Abstract]
  82. 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]
  83. Goarin JP, Le Bret F, Riou B, et al: Early diagnosis of traumatic thoracic aortic rupture by transesophageal echocardiography. Chest 1993; 103:618.
  84. 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]
  85. 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]
  86. Kodali S, Jamieson WR, Leia-Stephens M, et al: Traumatic rupture of the thoracic aorta: a 20-year review, 19691989. Circulation 1991; 84:III40.
  87. 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]
  88. 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.[Abstract/Free?Full?Text]
  89. 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]
  90. 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]
  91. Heystraten FM, Rosenbusch G, Kingma LM, et al: Chest radiography in acute traumatic rupture of the thoracic aorta. Acta Radiol 1988; 29:411.[Medline]
  92. Mattox KL: Fact and fiction about management of aortic transection. Ann Thorac Surg 1989; 48:1.[Medline]
  93. Parker MS, Matheson TL, Rao AV, et al: Making the transition: the role of helical CT in the evaluation of potentially acute thoracic aortic injuries. AJR Am J Roentgenol 2001; 176:1267.[Abstract/Free?Full?Text]
  94. Raptopoulos V, Sheiman RG, Phillips DA, et al: Traumatic aortic tear: screening with chest CT. Radiology 1992; 182:667.[Abstract]
  95. Barker DE, Crabtree JD Jr, White JE, et al: Mediastinal evaluation utilizing the reverse Trendelenburg radiograph. Am Surg 1999; 65:484.[Medline]
  96. Agee CK, Metzler MH, Churchill RJ, Mitchell FL: Computed tomographic evaluation to exclude traumatic aortic disruption. J Trauma 1992; 33:876.[Medline]
  97. Gavant ML, Menke PG, Fabian T, et al: Blunt traumatic aortic rupture: detection with helical CT of the chest. Radiology 1995; 197:125.[Abstract]
  98. 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]
  99. 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]
  100. 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.[Medline]
  101. Mirvis SE, Shanmuganathan K, Miller BH, et al: Traumatic aortic injury: diagnosis with contrast-enhanced thoracic CTfive-year experience at a major trauma center. Radiology 1996; 200:413.[Abstract]
  102. 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]
  103. 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]
  104. Pate JW, Minard G: Imaging of traumatic rupture of the aorta. J Thorac Cardiovasc Surg 1995; 109:190.[Free?Full?Text]
  105. 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]
  106. Wilson D, Voystock JF, Sariego J, Kerstein MD: Role of computed tomography scan in evaluating the widened mediastinum. Am Surg 1994; 60:421.[Medline]
  107. Vignon P, Boncoeur MP, Francois B, et al: Comparison of multiplane transesophageal echocardiography and contrast-enhanced helical CT in the diagnosis of blunt traumatic cardiovascular injuries. Anesthesiology 2001; 94:615.[Medline]
  108. Sturm JT, Hankins DG, Young G: Thoracic aortography following blunt chest trauma. Am J Emerg Med 1990; 8:92.[Medline]
  109. 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]
  110. Kearney PA, Smith DW, Johnson SB, et al: Use of transesophageal echocardiography in the evaluation of traumatic aortic injury. J Trauma 1993; 34:696.[Medline]
  111. 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.[Medline]
  112. LaBerge JM, Jeffrey RB: Aortic lacerations: fatal complications of thoracic aortography. Radiology 1987; 165:367.[Abstract]
  113. 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]
  114. 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]
  115. Goldstein SA, Lindsay J Jr, Vasan R: The diagnosis of thoracic aortic dissection by noninvasive imaging procedures. N Engl J Med 1993; 328:1637.[Free?Full?Text]
  116. Hartnell G, Costello P: The diagnosis of thoracic aortic dissection by noninvasive imaging procedures. N Engl J Med 1993; 328:1637.
  117. 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]
  118. Feliciano DV, Rozycki GS: Advances in the diagnosis and treatment of thoracic trauma. Surg Clin North Am 1999; 79:1417.[Medline]
  119. 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]
  120. Hanschen S, Snow NJ, Richardson JD: Thoracic aortic rupture in patients with multisystem injuries. South Med J 1982; 75:653.[Medline]
  121. 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]
  122. Appelbaum A, Karp RB, Kirklin JW: Surgical treatment for closed thoracic aortic injuries. J Thorac Cardiovasc Surg 1976; 71:458.[Abstract]
  123. 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]
  124. 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]
  125. 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]
  126. 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]
  127. 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.[Medline]
  128. 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]
  129. 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]
  130. Wallenhaupt SL, Hudspeth AS, Mills SA, et al: Current treatment of traumatic aortic disruptions. Am Surg 1989; 55:316.[Medline]
  131. 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]
  132. Robinson J, Nawaz S, Beard JD: Randomized, multicentre, double-blind, placebo-controlled trial of the use of aprotinin in the repair of ruptured abdominal aortic aneurysm. On behalf of the Joint Vascular Research Group. Br J Surg 2000; 87:754.[Medline]
  133. Gillian L: The arterial blood supply of the human spinal cord. J Comp Neurol 1958; 110:75.[Medline]
  134. Adams H, Von Geertruyden H: Neurologic complications of aortic surgery. Ann Surg 1956; 144:574.[Medline]
  135. 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]
  136. 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]
  137. 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]
  138. 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]
  139. Laschinger JC, Cunningham JN Jr, Nathan IM, et al: Intraoperative identification of vessels critical to spinal cord blood supplyuse of somatosensory evoked potentials. Curr Surg 1984; 41:107.[Medline]
  140. 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]
  141. 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]
  142. 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]
  143. 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]
  144. 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]
  145. 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.[Abstract/Free?Full?Text]
  146. Kouchoukos NT, Rokkas CK: Hypothermic cardiopulmonary bypass for spinal cord protection: rationale and clinical results. Ann Thorac Surg 1999; 67:1940.[Abstract/Free?Full?Text]
  147. 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]
  148. 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.[Abstract/Free?Full?Text]
  149. 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]
  150. Fullerton DA: Simplified technique for left heart bypass to repair aortic transection. Ann Thorac Surg 1993; 56:579.[Abstract]
  151. 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]
  152. 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]
  153. Turney SZ: Blunt trauma of the thoracic aorta and its branches. Semin Thorac Cardiovasc Surg 1992; 4:209.[Medline]
  154. Pett SB Jr, Wernly JA, Akl BF: Observations on flow characteristics of passive external aortic shunts. J Thorac Cardiovasc Surg 1987; 93:447.[Abstract]
  155. 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]
  156. McBride LR, Tidik S, Stothert JC, et al: Primary repair of traumatic aortic disruption. Ann Thorac Surg 1987; 43:65.[Abstract]
  157. 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]
  158. 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]
  159. 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]
  160. 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]
  161. Kirsh MM, Orringer MB, Behrendt DM, et al: Management of unusual traumatic ruptures of the aorta. Surg Gynecol Obstet 1978; 146:365.[Medline]
  162. Mattox KL, Wall MJR: Traumatic aneurysm of the thoracic aorta, in Najafi H (ed): Chest Surgery Clinics of North America, vol 2. Philadelphia, WB Saunders, 1992; p 413.
  163. Hudson HM 2nd, Woodson J, Hirsch E: The management of traumatic aortic tear in the multiply-injured patient. Ann Vasc Surg 1991; 5:445.[Medline]
  164. Santini F, Gatti G, Cannarella A, Mazzucco A: Diagnosis and early surgical management of traumatic thoracic aortic disruption. G Ital Cardiol 1999; 29:1426.[Medline]
  165. Ochsner MG Jr, Hoffman AP, DiPasquale D, et al: Associated aortic rupture-pelvic fracture: an alert for orthopedic and general surgeons. J Trauma 1992; 33:429.[Medline]
  166. Ochsner MG Jr, Champion HR, Chambers RJ, Harviel JD: Pelvic fracture as an indicator of increased risk of thoracic aortic rupture. J Trauma 1989; 29:1376.[Medline]
  167. Kazerooni EA, Williams DM, Abrams GD, et al: Aortobronchial fistula 13 years following repair of aortic transection. Chest 1994; 106:1590.[Abstract/Free?Full?Text]
  168. Tsai FC, Lin PJ, Wu YC, Chang CH: Traumatic aortic arch transection with supracarinal tracheoesophageal fistula: case report. J Trauma 1999; 46:951.[Medline]
  169. Demetriades D: Penetrating injuries to the thoracic great vessels. J Card Surg 1997; 12:173.[Medline]

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