ﺑﺎﺯﮔﺸﺖ ﺑﻪ ﺻﻔﺤﻪ ﻗﺒﻠﯽ
خرید پکیج
تعداد آیتم قابل مشاهده باقیمانده : 3 مورد
نسخه الکترونیک
medimedia.ir

Overview of blunt and penetrating thoracic vascular injury in adults

Overview of blunt and penetrating thoracic vascular injury in adults

INTRODUCTION — Trauma is the fourth leading cause of all civilian deaths in the United States, and the leading cause of death among children and adults under age 45 [1]. Many victims have multiple injuries often involving major vascular structures, which can present acutely as exsanguination or present in a delayed fashion (eg, arteriovenous fistula, post-traumatic aneurysm).

Penetrating trauma and high-energy motor vehicle accidents each contribute to the incidence major chest injury, which can occur in urban or rural environments, but the greatest incidence occurs in urban areas [2]. Better outcomes have been reported for urban compared with rural settings with the difference due to several factors, but mostly related to prolonged transfer times in the rural setting [2].

Advances in diagnosis and management of these injuries are the result of the increasing quality of computed tomographic (CT) angiography for diagnosing injuries, multiplanar CT reconstructions for operative planning, and the increasing availability of appropriately-sized endovascular stent grafts. Modern resuscitation combined with improved operative strategies have also contributed to increased survival. Endovascular management has provided clinicians with options that are generally more rapid and less morbid.

An overview of the management major thoracic vascular injury is reviewed, including surgical and endovascular approaches to treatment and important elements of perioperative care. The management of cardiac injury is reviewed separately. (See "Management of cardiac injury in severely injured patients".)

MECHANISM OF INJURY — Penetrating trauma in combination with an increase in high-energy road traffic accidents may account for the increased incidence of major thoracic vascular injury [2,3]. In one large review, 5760 cardiovascular injuries were sustained in 4459 patients, predominantly in young males, who represented 90 percent of all of penetrating injuries [4]. Truncal (including neck) vascular injuries predominated at 66 percent, with the lower extremity region representing only 19 percent of all vascular injuries. The mechanism of injury varied and included high-velocity weapons (70 to 80 percent), followed by stab wounds (10 to 15 percent) and blunt trauma (5 to 10 percent).

The types of thoracic vascular injuries seen in the civilian population are rarely observed in the military setting. In one study of vascular injuries during wartime, no intrathoracic great vessel injuries were reported [5]. With improvements to body armor, nearly all low-energy penetrating truncal injuries are prevented, and any high kinetic energy missiles that do penetrate the body armor are nearly universally fatal. A similar bimodal pattern might be expected among nonmilitary officers who wear body armor.

Specific anatomic sites

Aorta — Aortic injury is second only to head trauma as a cause of death from blunt trauma. Scene survival following aortic trauma in road traffic accidents is reported to be less than 10 percent, with an overall survival of only 2 percent [6]. For those who reach the hospital for care, survival is poor due to the potential for rapid exsanguination [7,8]. A population-based study of aortic trauma in Scotland demonstrated the rarity of its presentation, comprising 0.3 percent of all trauma admissions [9]. In all, 88 percent of patients with thoracic aortic injury died, with no difference in survival comparing penetrating or blunt trauma as the mechanism of injury. Most (96 percent) patients with thoracic aortic injury had coexistent chest injuries.

Blunt thoracic aortic injury predominates with injury typically located at the aortic isthmus (descending aorta) [10-12]. The majority of aortic transections occur 2 to 3 cm distal to the origin of the left subclavian artery [11]. Among aortic injuries, ascending and transverse aortic injuries are less common and occur in about 10 to 14 percent of cases. Ascending and transverse aortic injuries due to blunt mechanisms are typically lethal. Penetrating injuries involving the ascending aorta are uncommon. In a review of 93 cases, among those who were too hemodynamically unstable for imaging and were taken to the operating room, mortality was very high [13]. Among those with stable vital signs upon arrival who could have imaging and a planned approach, mortality was still 50 percent. It is unusual for patients to survive transport to the hospital with penetrating injuries to the descending thoracic aorta; the literature is composed of only case reports. (See "Clinical features and diagnosis of blunt thoracic aortic injury", section on 'Mechanism of injury'.)

Based on clinical presentation and severity of injury, patients with blunt aortic injury tend to fall into one of three categories: those who die at the scene (70 to 80 percent), those who present alive but hemodynamically unstable (2 to 5 percent, with reported mortality rates of 90 to 98 percent), and those who are hemodynamically stable with a diagnosis made 4 to 18 hours after injury (15 to 25 percent) [14,15]. Overall, 32 to 50 percent of patients presenting to a trauma center with blunt aortic injury will die within 24 hours of initial injury, though most deaths are not directly related to the aortic injury [7,8]. Associated severe brain, lung, and visceral injury directly increase the perioperative risk associated with general anesthesia and a traditional operative approach. For some patients surviving transport to the hospital, concomitant intra-abdominal injury may be the more life-threatening, and may warrant delayed repair of the thoracic aorta [16,17]. The recognition that a group of patients exists who survive several hours to days after admission has led to modification in both type and timing of intervention. Advancement in the use of endovascular techniques in the treatment of blunt aortic injury has been associated with reduced mortality. (See "Initial evaluation and management of blunt thoracic trauma in adults", section on 'Aortic injury'.)

Great vessels — The innominate artery is the second most frequently injured thoracic vessel. With blunt trauma, the injury usually occurs at the vessel origin. These may be associated with sternal fracture or a "seat belt sign" [18].

Left carotid artery injuries usually occur at the vessel origin [19]. Dissection is the most common type of injury. (See "Blunt cerebrovascular injury: Mechanisms, screening, and diagnostic evaluation", section on 'Mechanisms of injury'.)

The subclavian artery and vein (figure 1) are relatively protected by the overlying clavicle, and overall injuries to these vessels are rare. The majority are due to penetrating trauma, but up to 25 percent may be due to blunt mechanisms, which tend to injure the vessel more distally. The fibrous attachments surrounding the subclavian vessels frequently result in a contained extra pleural hematoma, which may extend into the supraclavicular fossa.

Pulmonary vessels — Sudden deceleration due to blunt injury can cause tears at the junction of the pulmonary veins with the left atrium. These injuries are serious though rare occurrences (table 1) [20,21]. Pulmonary arterial and venous pseudoaneurysm, and arteriovenous fistula formation can also occur [22-25].

Thoracic veins — Penetrating injury to the superior vena cava or other great veins is more common than blunt injury, which is associated with high mortality. Blunt injuries tend to occur at the pericardial reflections where the cava is fixed and susceptible to deceleration injury as the mobile heart moves anteriorly [26,27]. (See "Traumatic and iatrogenic injury to the inferior vena cava".)

Associated injuries — Major thoracic vascular injuries occur following significant trauma, are often related to deceleration injury, and are commonly associated with other organ injuries, including other vascular injuries to the trunk or extremities. In a review of vascular injuries, a coexistent chest injury was present in 96 percent of the patients [9]. The median injury severity score was 50, with an interquartile range of 17 to 75. In addition, 65 percent of the patients had a Glasgow coma scale of ≤8. In a review of 5760 civilian cardiovascular truncal injuries (including neck), two or more concurrent vascular injuries occurred in 1057 patients and 32 patients had four or more separate vascular injuries, including lower extremity vascular injuries (19 percent) [4].

Injuries to the major pulmonary vessels may be associated with cardiac and bronchial injuries. Injuries to the vena cava may be associated with hepatic injury. (See "Management of cardiac injury in severely injured patients" and "Identification and management of tracheobronchial injuries due to blunt or penetrating trauma".)

TRAUMA EVALUATION — Acute thoracic vascular injury is a highly lethal injury that can lead to rapid exsanguination and requires prompt identification and management to give the patient the best chance for survival. Delays to definitive hemorrhage control including prolonged prehospital times should be avoided since it is difficult, if not impossible, to stabilize most of these patients.

Management of patients who have suffered potential major, multisystem trauma, either blunt or penetrating, requires a team approach to rapidly identify and address immediately life-threatening conditions. Patients in extremis may require immediate surgical interventions to manage bleeding, which can be continued in the operating room. The diagnostic evaluation and management of the trauma patient with blunt or penetrating chest trauma is based upon protocols from the Advanced Trauma Life Support (ATLS) program, established by the American College of Surgeons Committee on Trauma.

(See "Initial evaluation and management of blunt abdominal trauma in adults".)

(See "Initial evaluation and management of abdominal gunshot wounds in adults".)

(See "Initial evaluation and management of abdominal stab wounds in adults".)

(See "Initial evaluation and management of blunt thoracic trauma in adults".)

History and physical examination — Blunt or penetrating injuries to the major thoracic vessels commonly present acutely (manifesting as bleeding or variable degrees of ischemia), but less extensive injuries may go unrecognized during the evaluation of other acute injuries, and present in a delayed fashion as a post-traumatic pseudoaneurysm or arteriovenous fistula either during the same hospitalization or later after discharge.

The severity and distribution of vascular injury largely depends on the mechanism of injury. Penetrating trauma is often associated with vessel laceration and/or transection, and may result in thrombosis, active bleeding, arteriovenous fistula, and/or pseudoaneurysm. The accurate diagnosis of active hemorrhage versus interrupted perfusion, with or without subsequent ischemia, becomes the cornerstone of management decisions.

Physical examination and determination of hard signs of vascular injury predicts those patients with significant injuries that could benefit from immediate exploration [28]. Hard signs of vascular injury include the following [29]:

Active hemorrhage

Expanding or pulsatile hematoma

Bruit or thrill over wound

Absent distal pulses

Extremity ischemia (pain, pallor, paralysis, cool to touch)

Examination of the chest must be prompt and thorough, as there are many thoracic injuries that can be rapidly lethal. Vital signs should be obtained on arrival, and at regular intervals thereafter. Once the patient's clothing is removed, observe the anterior chest for deformity, ecchymosis, asymmetry, or signs of penetrating injury. A deviated trachea may indicate a developing tension pneumothorax, hemothorax, or great vessel injury. Palpation of the anterior chest can demonstrate crepitus, tenderness, and fractures that were not readily apparent. Listen for decreased breath sounds that may suggest a possible hemothorax and/or pneumothorax. If either is suspected, a tube thoracostomy should be placed to decompress the hemithorax. The patient should be turned while maintaining cervical control and the posterior thorax examined for ecchymoses, or penetrating entry or exit wounds. Once a rapid and thorough examination is completed, routine laboratory tests should be drawn and sent. In hemodynamically stable patients, imaging studies can be performed safely, but should not delay required care as indicated.

A detailed vascular assessment begins with a pulse examination to identify asymmetry or absence of palpable pulses (axillary, brachial, common femoral) that may suggest an aortic or arch vessel injury. Auscultation over the injury site may reveal a bruit that may be indicative of a partially thrombosed or compressed vessel. Distal pulses (ie, radial, ulnar, dorsalis pedis, posterior tibial) should also be documented and marked when identified for future comparison.

Tube thoracostomy — Urgent placement of a large diameter tube thoracostomy should follow the identification of hemothorax or pneumothorax (clinical examination, chest radiograph). Massive hemothorax should be suspected in any trauma patient with shock and absent or decreased breath sounds and dullness to percussion in a hemithorax. (See "Thoracostomy tubes and catheters: Indications and tube selection in adults and children".)

A clamp should be placed on the distal end of the tube until it can be connected to an appropriate suction chamber. This allows for more accurate measurement of the quantity of the hemothorax. If the initial output is greater than 1500 mL or >200 mL/hour for two to four hours, a significant vascular injury is assumed to be present, and the patient should be explored in the operating room [30,31].

Resuscitative thoracotomy — The patient in extremis has likely sustained a lethal injury. A limited number of patients with penetrating injury may be candidates for resuscitative thoracotomy in the emergency department. Resuscitative thoracotomy should only be performed for patients arriving with signs of life with subsequent cardiovascular collapse from exsanguination. Upon performing this maneuver and evacuating the remaining hemothorax, an aortic clamp is placed across the proximal descending thoracic aorta with care taken not to injure the esophagus. A pericardial window should be created if there appears to be hemopericardium. Often, major injuries are identified and should be controlled with either direct compression, if possible, or by packing until the patient can be transported to the operating room. The indications for and outcome of resuscitative thoracotomy are discussed elsewhere. (See "Resuscitative thoracotomy: Technique".)

Control of external hemorrhage — Surgeons should have a good understanding of what exposure is required to control massive hemorrhage from major thoracic vascular injury. The temptation to explore an expanding hematoma prior to obtaining proximal and distal control should be resisted. (See 'Surgical exposures' below.)

Initial control of external hemorrhage can be achieved by a quick skin preparation, wide surgical exposure, and digital occlusion of the bleeding vessel within the wound bed until the patient can be transported to the operating room where formal control and exposure is obtained [32]. If local control is adequate, further surgical exploration, which may cause additional blood loss, should be delayed until the patient is adequately resuscitated. When the injured vessel is exposed, a clamp can be applied, as long as doing so will not exacerbate the existing injury. (See 'Damage control surgery' below.)

DIAGNOSTIC IMAGING

Chest radiography — Plain chest radiography is the most readily available and most common initial imaging evaluation of the chest (algorithm 1). Chest radiography is widely used as a screening study, as it can show life-threatening injuries such as tension pneumothorax, massive hemothorax, or mediastinal hemorrhage, as well as confirm central venous catheter placement. The results of this test are rapidly available and can help direct initial care. Chest radiography can also demonstrate rib fractures, foreign bodies, ballistic fragments, and contusions.

The demonstration of blood on plain radiography is likely to represent significant blood loss since the volume of blood needed to demonstrate hemothorax on upright radiograph can be as much as 400 to 500 mL; twice this amount may be needed to demonstrate hemothorax on a supine radiograph. Differential opacification of the two sites on a supine radiograph should raise concern for the possibility of hemothorax, as the blood will layer posteriorly.

In the setting of penetrating trauma, chest radiography is best performed in the upright position, and radiolucent markers should be placed overlying the skin penetration sites. Major vascular injury is suggested by the presence of a large hemothorax, foreign body (eg, bullet) proximity to the great vessels, or an unusually positioned or a lack of an expected foreign body suggesting possible missile embolization.

In the setting of blunt trauma, the most reliable radiographic finding associated with blunt aortic injury is the loss of the aortic knob contour. Superior mediastinal widening, defined as a width of 8 cm (at the level of the left subclavian artery origin) on an anteroposterior view or a mediastinum to chest width ratio of more than 0.25, is a fairly sensitive (81 to 100 percent), but not a specific (34 to 60 percent), indicator for a traumatic aortic injury [33]. Mediastinal hematoma can be due to causes other than acute traumatic aortic injury (eg, venous bleeding, adjacent spine fracture, sternal fracture). Furthermore, aortic injury can occur with little or no associated mediastinal hematoma. For these reasons, when blunt aortic injury is suspected, we obtain CT angiography. (See 'Vascular imaging' below.)

Injuries to the innominate artery should be suspected if an isolated right-sided widened mediastinum is noted with accompanying leftward tracheal deviation. (See "Clinical features and diagnosis of blunt thoracic aortic injury", section on 'Plain chest film'.)

eFAST exam — Point-of-care ultrasound is well suited for use in the emergency setting in the assessment of hemodynamically unstable trauma patients [34-36]. Portable ultrasound machines with high-resolution imaging allow physicians to diagnose life-threatening conditions and assess the basic hemodynamic status, helping to prioritize and guide appropriate and timely interventions [37]. The focused assessment with sonography for trauma (FAST) examination is a limited four-view ultrasound examination of the abdomen and pericardium. The aim of the study is to rapidly identify life-threatening intra-abdominal bleeding or cardiac tamponade to more quickly implement treatment, though the study is operator dependent. The FAST exam has a sensitivity of 42 to 98 percent and a specificity of 95 to 100 percent, resulting in a positive predictive value between 90 and 95 percent [37]. Extended FAST (eFAST) includes imaging of the anterior lungs bilaterally. In experienced hands for hemodynamically unstable patients, eFAST provides a rapid and sensitive evaluation for hemothorax [31]. However, if there is a high clinical suspicion for injury, a normal eFAST is insufficient to exclude injury. In conjunction with limited cardiac sonogram, eFAST exam can define the nature and extent of associated injuries [38-40]. However, it is important to note that a lack of pericardial fluid on eFAST does not rule out a cardiac injury, as some patients with penetrating injuries may decompress the bleeding from the heart into the pleural space. If there is suspicion of cardiac injury, there should be no hesitation in obtaining formal echocardiography. (See "Initial evaluation and management of blunt cardiac injury", section on 'Echocardiogram' and "Cardiac tamponade".)

Vascular imaging — For hemodynamically stable patients with suspected vascular injury to the aorta or innominate, intrathoracic carotid, or subclavian arteries based on physical examination or plain radiography, we obtain computed tomographic (CT) angiography. Imaging studies can be performed safely but should not delay care required to manage other life-threatening injuries.

CT angiography accurately screens for vascular injury without the embolic risk associated with catheter-based arteriography [41]. Modern software also provides adequate three-dimensional reconstruction to aid in operative planning and the possibility for endovascular repair [42]. Catheter-based angiography is more typically performed in conjunction with endovascular or hybrid repair of vascular injuries. Adjunctive use of intravascular ultrasound may allow adequate endovascular imaging in conjunction with preoperative CT angiography.

CT angiography accurately identifies aortic transection, allowing the initiation of heart rate and blood pressure control and evaluation and timing of therapeutic options. CT angiography can be useful for identifying the location of injury and to evaluate the mediastinum, such as in a patient with a contained hematoma (eg, subclavian artery injury). Initial imaging also provides a baseline for comparison in those who will be initially managed nonoperatively and delineates associated injuries. The presence of metallic fragments or external fixators has not been found to affect the imaging quality obtained by multidetector CT angiography studies in vascular trauma [43].

Vascular injury grading — Multiple schemes have been used to grade aortic injury (predominantly blunt injury). A relatively simple system for grading aortic injury and guiding management is also applicable to other vascular injuries and is shown in the figure and discussed separately (figure 2). (See "Clinical features and diagnosis of blunt thoracic aortic injury", section on 'Aortic injury grading'.)

The American Association for the Surgery of Trauma (AAST) has also published a vascular injury grading scale based on the location of vascular injury [44]. The overall severity of injury is reflected in the thoracic vascular injury scale (table 2). The injury grades correlate with increasing morbidity and mortality, which are lower for smaller vessels and for venous injury compared with arterial injuries of the same size.

Echocardiography — Both transthoracic (TTE) and transesophageal echocardiography (TEE) have well-described uses in thoracic vascular trauma. Both imaging modalities provide good imaging of the pericardium and ventricles. As a result, they both are highly useful for evaluating penetrating cardiac injuries. (See "Management of cardiac injury in severely injured patients".)

The key advantage of TEE in major trauma cases relates to the dual capability of diagnostic information and sophisticated hemodynamic monitoring. The most important diagnostic aspect of TEE relates to the diagnosis of the hemodynamic state relating to cardiac filling and contractility intraoperatively. This guides the use of vasopressors and blood products on a moment-to-moment basis. Specific diagnostic information relating to the heart and great vessels is also possible, particularly cardiac tamponade, segmental wall motion abnormalities, valvular pathology, as well as evaluation of the ascending and descending thoracic aorta.

More detail relating to the use of echocardiography in thoracic vascular trauma can be found in related topics. (See "Clinical features and diagnosis of blunt thoracic aortic injury", section on 'TEE findings' and "Initial evaluation and management of blunt cardiac injury" and "Intraoperative transesophageal echocardiography for noncardiac surgery".)

APPROACH TO MANAGEMENT — Major thoracic vascular injury may be obvious or only suspected based upon trauma mechanism, associated injuries, physical findings, or findings on plain chest radiography. The approach to specific vessel injury and repair in patients depends upon the hemodynamic status of the patient, and the presence of other injuries and medical comorbidities. Urgent operative repair is required for any thoracic vascular injury resulting in hemodynamic instability, ongoing or massive hemorrhage, or a rapidly expanding hematoma. Minimal injuries to the aorta or other major arteries may not be immediately apparent and may present in a delayed fashion due to vessel thrombosis resulting in ischemia, a pseudoaneurysm, or arteriovenous fistula. Injuries to the pulmonary veins can also present in a delayed manner. Such injuries are often identified on follow-up imaging studies.

Hemodynamically unstable — Hemodynamically unstable trauma patients with indications for surgery (eg, positive focused assessment with sonography for trauma [FAST], hard signs of vascular injury) should be taken to the operating room to control the source of hemorrhage, which could be in the chest and/or abdomen. If thoracic vascular injury is identified, but is contained and life-threatening bleeding is identified from another source (eg, spleen, liver, pelvic fracture), then the more severe injury is managed first (ie, damage control approach). (See 'Damage control surgery' below.)

Early surgical planning based upon patient condition is essential. Urgent operative repair is required for any injury resulting in hemodynamic instability, massive or ongoing hemorrhage, or a rapidly expanding hematoma on radiographic studies. Rapid surgical planning and effective communication with the operating room personnel is essential. Information regarding patient condition and urgency for an operating room, patient and table positioning, need for special or preferred instruments, the basic operative plan, body areas to prepare, and other details concerning arteriography or vein harvest should be conveyed to the operating room staff and anesthetic team as early on as possible.

Emergency release of blood products and activation of a massive transfusion protocol should be one of the earliest decisions made in patients with hemodynamic instability or a history of or anticipated massive hemorrhage. This involves a standardized release and early transfusion of packed red blood cells, fresh frozen plasma, cryoprecipitate, and platelets when available. Hesitation to request blood may lead to lag times in resuscitation and delayed care. Vital signs and admission physiology predict mortality, and immediate resuscitation efforts should be directed at correction of the presenting base deficit and coagulopathy [45].

Damage control surgery — Management of traumatic vascular injuries can offer special challenges to experienced surgeons both in combat and in peacetime. A damage control approach may be needed in patients with multiple coexistent injuries and involves rapid control of exsanguinating hemorrhage in an abbreviated initial operative intervention, followed by interval resuscitation, correction of physiologic imbalances, and a scheduled return to the operating room for definitive vascular reconstruction, if the patient survives [32]. Combining the concepts of damage control surgery with a resuscitation strategy that quickly restores physiology may allow patients to survive the major operation required to repair thoracic vascular injuries. Damage control surgery (DCS) has enhanced the survival of severely injured patients in urban trauma centers [46,47]. The essence of DCS is to achieve and conclude the initial operative procedure before the physiologic "point of no return" is reached [46]. DCS was demonstrated to improve survival in critically injured patients who had suffered massive bleeding [47]. Results from wartime conflicts have shown a reduction in mortality compared with previous wars, possibly due to the near uniform application of DCS and principles of damage control resuscitation [48].

Patients with hemodynamic instability with undiagnosed injuries should receive preoperative broad-spectrum antibiotics, be positioned supine, prepared and draped from the neck to the knees, with the most appropriate surgical approach dictated by the anatomy of their injury. A rapid initial intraoperative assessment of the injury and the patient's hemodynamic and physiologic status will help direct the overall goal of the operation in the direction of damage control or definitive repair.

Thoracic damage control can be approached either by abbreviated thoracotomy restoring survivable physiology or by rapid definitive repair [49]. All devitalized tissue should be excised and irrigated under low pressure, with careful evaluation of muscle tissue for viability. The injured segment of artery or vein should be debrided back to normal tissue, as attempts to avoid this step can result in lead to disastrous complications. The level of contamination in the wound should be assessed. Conduit choice can be simplified to saphenous vein for vessels of 5 mm and under, and polytetrafluoroethylene for vessels greater than 5 mm [49]. When injuries are identified to major deep or collecting venous structures, if the patient is not in extremis, they should be repaired to avoid the long-term morbidity associated with ligation [50]. Completion assessments following repair are performed using physical examination, handheld Doppler, or arteriography. Palpable pulses or Doppler signals should be monitored postoperatively to assess continued patency.

Resuscitation — Optimal management of major thoracic vascular injury involves achieving rapid hemostasis, and reversal of metabolic derangements through early use of blood products. Patients who have suffered severe hemorrhage from vascular injuries have an early and profound coagulopathy, acidosis, and hypothermia on admission to the emergency department [51,52]. This lethal triad of hypothermia, acidosis, and coagulopathy is multifactorial in nature, but it is felt that hypoperfusion is at the root of the cause. Hypoperfusion is common in patients with major thoracic vascular injury and is often difficult to assess. As a result, several scoring systems (Trauma Score, Injury Severity Score) have been devised to describe the extent of a patient's injury. However, these scoring systems are descriptive and not helpful in guiding resuscitation of patients who have entered into the lethal triad, but are more useful in post-hoc analysis. (See "Etiology and diagnosis of coagulopathy in trauma patients".)

Early rapid infusion of blood products, high plasma ratios, and minimal crystalloid are beneficial when considering vascular reconstructions in severely injured patients. Resuscitation techniques that use liberal amounts of crystalloid and packed red blood cells can exacerbate coagulopathy. The combination of optimal damage control and resuscitation can allow definitive vascular repairs to be performed and establish normal physiology by the completion of the operation with improved survival in critically injured patients. [32,53-55]. (See "Overview of damage control surgery and resuscitation in patients sustaining severe injury" and "Ongoing assessment, monitoring, and resuscitation of the severely injured patient".)

Many patients with penetrating thoracic vascular injury who require thoracotomy have major bleeding from the pulmonary vascular system [56]. Advanced Trauma Life Support (ATLS) advocates for less aggressive fluid resuscitation and placement of tube thoracostomy in patients with penetrating chest trauma. Animal studies suggest that aggressive crystalloid resuscitation in humans with penetrating chest trauma could increase blood loss and potentially increase mortality [57-60].

Hemodynamically stable — Hemodynamically stable patients without hard signs of vascular injury can undergo definitive imaging to identify the location of injury and evaluate the mediastinum. Specific repair is undertaken as indicated with timing often dictated by the associated injuries. Some thoracic vascular injuries in hemodynamically stable patients may be amenable to a more conservative approach, particularly in the face of multiple other injuries and in high-risk patients. (See 'Vascular imaging' above and 'Management of specific vascular injuries' below.)

Role of endovascular techniques — Endovascular therapy in thoracic vascular trauma offers a less invasive, rapid treatment, and has the added benefit of avoiding the added stress of open surgery, which may otherwise make repair nonsurvivable in some. The application of endovascular techniques to the management of penetrating and blunt traumatic vascular injuries represents a substantial advance in trauma management and has been used with increasing frequency for the management of vascular trauma [61-63]. Interestingly, some of the first covered stents were fashioned and deployed for the treatment of vascular trauma [64-68]. However, while these techniques have been successful for managing the acute injury, there are few long-term data on the use of covered stents for the treatment of vascular injuries. It is extremely important that experienced providers perform these procedures in an environment capable of supporting complex interventions. Protocols for using endovascular techniques for non-aortic vascular trauma continue to evolve. In settings where these circumstances cannot be met, such complex interventions have the potential of causing harm and should not be performed. As such, even in the era of endovascular surgery, surgeons must maintain their familiarity with open approaches to repairing vascular injuries. (See 'Surgical exposures' below.)

Given the high mortality rates associated with blunt thoracic trauma, endovascular management is particularly appealing in the setting of severe concomitant brain and/or lung injuries. When applied in the appropriate setting, the use of endovascular techniques (balloon occlusion, stent-grafting) has the potential to minimize the physiologic burden associated with surgery, particularly in trauma victims, who may lack physiologic reserve. Endovascular techniques can be used to help stabilize a patient by controlling hemorrhage, serve as a bridge to open surgical repair, or be used an alternative to open surgical repair [5,68-76]. As examples:

Covered stent-grafts have expanded the possible treatment options for vessel injury, and potential roles are well described [74-76]. As an example, the majority of pseudoaneurysms from blunt or penetrating trauma can be treated with self-expanding covered stents [69-73].

Endovascular techniques can be used as an adjunct to support the standard open repair of many injuries. Zone I injuries of the neck associated with hard signs of vascular injury (eg, enlarging hematoma at the thoracic inlet, high chest tube output) typically involve the great vessels. Rather than pursuing immediate open surgical exposure, which can be associated with large blood losses, an occlusion balloon can be introduced via the groin to provide proximal vascular control, allowing conduct of a surgical exposure (high anterior thoracotomy, sternotomy, or clavicular resection) in a controlled fashion. With the occlusion balloon in place, intraoperative arteriography can also be performed to locate the injury and aid with operative planning. Once the injury has been exposed, a vascular clamp can be placed to provide control and the occlusion balloon deflated.

The operative mortality rate associated with traditional open repair of blunt aortic injuries is as high as 25 percent related to multisystem organ failure [49], as well as the inability of an already stressed patient with multiple injuries to tolerate the additional stress of open thoracotomy, which requires lateral decubitus positioning and single lung ventilation. However, with advances in endovascular technology, thoracic aortic transection can be treated percutaneously with stent-grafts [77].

There remains concern about the unknown long-term outcome of covered stents for trauma, as minimal long-term follow-up data are available. Stents-grafts placed in thoracic vascular trauma have the possibility for compression and collapse. This raises concern about long-term patency in the young trauma population; it is imperative to follow these patients for late complications. Alternatively, at a later date, when the hematoma and edema have resolved, the stent can be explanted with a formal open repair; this approach would, ideally, reduce the potential for complications that can occur in the acute setting.

Supportive care and monitoring — If extravasation of contrast from the thoracic aorta or other vascular injury is not appreciated on chest CT, other concurrent injuries to the head, abdomen, and extremities can often be repaired while maintaining careful control of heart rate and blood pressure [78]. The optimal timing of vascular repair is not known for certain but should be performed when the patient's physiology has improved.

Monitor chest tube output – Evidence for ongoing bleeding as suggested by a persistent output more than 200 to 250 mL per hour for two to four hours suggests the need for exploration [30]. (See "Thoracostomy tubes and catheters: Indications and tube selection in adults and children" and "Thoracostomy tubes and catheters: Management and removal", section on 'Management of thoracostomy tubes'.)

Control heart rate and blood pressure – For patients who are being managed nonoperatively (eg, minimal vascular injuries), some may benefit from control of heart rate (<100 beats per minute) and blood pressure to maintain a mean arterial pressure in the range of 60 to 70 mmHg. (See 'Thoracic aorta' below.)

Laboratory monitoring – Physiologic variables that can be determined with simple lab work can allow providers to quantify the extent to which the patient's physiology has been altered. Variables that have been shown to discriminate survivors from non-survivors in major vascular trauma include initial pH, base deficit, lactate, anion gap, apparent strong ion difference, and strong ion gap [79]. All these variables are obtainable in a rapid fashion via arterial blood gas analysis with chemistry analysis.

SURGICAL EXPOSURES — A robust body of knowledge of how to perform surgical exposures that allow rapid control of vascular structures for the management of thoracic vascular trauma is extremely important and is available from both civilian and military resources from around the world [5,64,80-95]. The decreasing volume of open vascular surgery makes it even more important that surgeons are familiar with surgical anatomy and various exposures of thoracic vasculature.

In general, the incisions for exposure are placed to obtain vascular control proximal and distal to the site of injury. After obtaining proximal and distal control of the vascular injury, a decision is made as to whether the injury is best repaired primarily, with patch angioplasty, or if the injury needs interposition grafting or bypass.

Through one or more incisions, proximal control of the injured vessel can be obtained before exposing the arterial injury. Injuries to the chest require the surgeon to judge whether the injury involves the proximal left subclavian artery (figure 3). This is usually evident either by the trajectory of the missile or the presence of a hematoma in the left supraclavicular area. Anatomically, the left subclavian artery originates from the distal aortic arch and descends in the posterior mediastinum, which makes vascular control of the proximal left subclavian very difficult through a median sternotomy. Therefore, if the surgeon feels that proximal control of the left subclavian will be necessary, a left anterior thoracotomy through the third intercostal space will be needed. Otherwise, a median sternotomy is the surgical approach of choice for injuries of the heart, ascending aorta, transverse aortic arch, the main pulmonary artery, innominate vein, and intrathoracic vena cava. For injuries to the great vessels, a median sternotomy can be used with the appropriate cervical extension incision.

Five principle incisions are used to provide exposure to the thoracic vasculature. These include the sternotomy, thoracotomy (anterior or posterior), supraclavicular or infraclavicular incision.

Sternotomy — Median sternotomy is the preferred method of exposure for suspected injuries to the heart, ascending aorta, superior vena cava/inferior vena cava, pulmonary hilum, innominate artery or vein, and right or left common carotid artery origins. Other less commonly performed sternal incisions include the hemi-clamshell and clamshell incisions. The hemi-clamshell incision (figure 4), which is similar to trapdoor incision, can be used to further expose the ascending aorta, hilar vessels, and great vessels, but is not usually needed unless there is inadequate exposure through a median sternotomy. The clamshell incision (figure 5) is a transverse sternotomy that can be performed as an extension of a thoracotomy when anterior mediastinal exposure is needed for control of an injury to the heart, or when contralateral chest exposure is needed. (See 'Thoracotomy' below.)

For median sternotomy, an incision is made in the midline of the sternum (figure 6). For injuries to the great vessels, a median sternotomy can be used with the appropriate cervical extension incision (figure 7). The sternum is exposed from the sternal notch to the xiphoid. To either end of the sternum, the dissection is performed bluntly, exposing the sternal notch and the subxiphoid area. The anesthesiologist is asked to hold ventilation, and the sternum is divided in its midline using a sternal saw. The most common technical error is failure to maintain the saw in the midline. Alternatively, the sternum may be divided using a Lipshke knife. The sternum is retracted using a Finochietto retractor (picture 1). The surgeon should look for a hematoma obscuring the great vessels in the superior mediastinum. The hematoma should be explored to identify the left innominate vein, which is a key landmark in the identification of the location of the other vessels. If the field of vision is obscured by hematoma, the surgeon may open the pericardium to find the aortic root. By tracing the aorta as it ascends from the heart, the great vessels can be safely identified. The left innominate vein may be ligated and divided or retracted to provide better exposure of the innominate and carotid arteries (figure 8). Proximal control of injuries to these vessels can usually be achieved at their takeoff from the aortic arch using a vascular clamp. This incision may be combined with a left or right supraclavicular incision for distal vascular control and facilitating arterial repair. (See 'Supraclavicular approach' below.)

Thoracotomy — To obtain proximal vascular control at the distal aortic arch or the left subclavian artery, a left anterior thoracotomy is the incision of choice (figure 3). The need for left subclavian control is usually evident by the trajectory of the missile or the presence of a hematoma in the left supraclavicular region. The left subclavian artery is difficult to control through a median sternotomy.

With the patient in a supine position, the incision is made in the third intercostal space of the anterior surface of the left chest (figure 9). The intercostal musculature is divided on the cephalad aspect of the rib to avoid injury to the intercostal neurovascular bundle. After entering the left chest, a Finochietto retractor is inserted between the ribs to improve exposure. The surgeon should ask the anesthesiologist to stop ventilating the left lung. The left lung is retracted inferiorly and the surgeon should focus his attention medially and cephalad to identify the aortic arch. With a combination of sharp and blunt dissection, the distal aortic arch and the left subclavian origin are exposed. Proximal control of the left subclavian is achieved using a straight vascular clamp (figure 9). The surgeon should identify and protect the vagus nerve as it crosses the aortic arch proximal to the take-off of the left subclavian artery. Once proximal control is obtained, attention is then turned to the supraclavicular region and the subclavian artery is then exposed to obtain distal control.

Injuries to the descending thoracic aorta or distal pulmonary artery or veins are exposed via posterior-lateral thoracotomy (figure 10). Depending on the level of injury to the aorta, the thoracotomy can be extended into a thoraco-abdominal aortic exposure by dividing the diaphragm and performing a retroperitoneal aortic exposure in the usual fashion. (See "Abdominal vascular injury", section on 'Abdominal aorta'.)

Supraclavicular approach — A supraclavicular incision provides exposure to the mid-subclavian artery and common carotid artery in the neck (figure 3). The supraclavicular incision is very useful but requires specific anatomic knowledge to avoid serious injury to important surrounding structures. If a large supraclavicular hematoma exists, the surgeon should hesitate to use this exposure. Rather, obtaining distal control of the subclavian using an infraclavicular incision more laterally may be more appropriate. (See 'Infraclavicular approach' below.)

To obtain supraclavicular exposure of the subclavian vessels, an incision is made one fingerbreadth above the clavicle. The incision is carried down to the level of the platysma, which is divided using electrocautery. Exposure is maintained using self-retaining retractors. The scalene fat pad is identified and divided along its inferior and lateral margins. After retracting the scalene fat pad medially, the surgeon should identify the phrenic nerve as it crosses this region from lateral to medial on the anterior surface of the anterior scalene muscle. Once identified, the phrenic nerve is retracted laterally using a vessel loop and avoiding excessive traction. The anterior scalene muscle is identified and divided from its insertion onto the first rib. The surgeon may need to remove a segment of this muscle to improve exposure of the underlying subclavian artery. The roots of the brachial plexus exit the neck and run laterally to form the cords to innervate the arm, and caution should be used to avoid putting the arm under traction.

A segment of the subclavian artery can usually be mobilized to allow for vascular control. Most branches of the subclavian artery can be ligated, except for the vertebral artery and internal mammary artery (more specifically in patients who have had left internal mammary artery to left anterior descending coronary artery bypass grafting). The vertebral artery should be at the most medial and cephalad portion of the subclavian artery adjacent the internal mammary artery. Again, the surgeon should exercise caution along the medial aspect of this exposure where the thoracic duct resides on the left and large lymphatics reside on the right side (figure 11).

Claviculectomy may be used as an alternate method of exposing distal subclavian artery injuries (figure 12). This exposure is associated with minimal blood loss and permits direct repair of complex injuries of the subclavian artery and veins [96,97]. The procedure is relatively straightforward. An incision is made directly over the clavicle. The dissection is carried down to the level of the periosteum using electrocautery. The periosteum is divided longitudinally along the axis of the clavicle. A Gigli saw or equivalent is used to transect the clavicle medially and laterally; this approach may be more expedient and less morbid than attempting to remove the entire clavicle at the sternum. The underlying scalenus anticus muscle is identified and divided as it inserts on the first rib. The subclavian artery should then be easily exposed and controlled.

Infraclavicular approach — An infraclavicular incision provides exposure to the distal subclavian artery and proximal axillary artery (figure 3). This exposure is normally used either to assist in repairing distal subclavian artery injuries or to gain control of the proximal axillary artery as it exits the thoracic outlet [98].

The incision is made about 1 cm inferior to the clavicle over the lateral aspect of the deltopectoral groove. The fibers of the pectoralis major are split, and the dissection is carried down to the level of the axillary artery. Arterial control can be obtained at this level to provide distal control of subclavian artery injuries or proximal control of vascular injuries more lateral in the arm. The insertion of the pectoralis major and minor can be preserved or divided to provide more exposure as needed. The surgeon should exercise caution to preserve the adjacent axillary nerve and vein.

ENDOVASCULAR APPROACH — Vascular access for an endovascular approach is obtained either at the common femoral (antegrade) or brachial artery (retrograde) in the standard fashion. After placement of a 5 Fr short sheath for access, a diagnostic arteriogram is obtained. The benefit of the retrograde approach is more control over catheters and wires, as the working distance is significantly shorter. Once the lesion has been crossed, catheters and wires should be exchanged in the standard fashion to build a sturdy endovascular platform as a basis for intervention.

When performed from a femoral approach, a guidewire is placed into the aorta and followed by a 4 Fr pigtail catheter. The catheter is advanced to the root of the aorta to perform a diagnostic arch digital subtraction aortogram (injection protocol: 20 mL of contrast injected per second for a total of 40 mL of contrast at 900 psi). Either the innominate artery or left subclavian artery is selected. If unable to select using the pigtail catheter, the surgeon can choose another catheter, such as a 4 Fr angled glide catheter. Selective arteriography should demonstrate the site of the arterial injury.

When performed from a brachial approach, the initial step after obtaining access and identifying the site of injury is crossing the lesion. With placement of a sheath in the brachial artery, there is often no antegrade flow. As a result, diagnostic angiography is performed with low volumes of contrast as in the lower extremity. At our institution, runs are performed through the sidearm of the introducer sheath at volumes of 3 cc/second for a total volume of 6 cc of half-strength contrast. If inadequate images are obtained, either full strength or larger volumes can be used. If contrast is extravasated, further imaging and interventions can be severely hindered. At this point, it should be noted that the surgeon has no proximal control. Often, these lesions do take some effort to cross and, occasionally, the wire will enter into extraluminal planes.

Placement of a covered stent across the injury (figure 13) should provide adequate vascular control to allow stabilization of the patient. Preplacement measurements are made in an attempt to preserve the vertebral artery, and to avoid crossing the sternoclavicular or acromioclavicular joints. We typically will use a 6 to 8 x 24 to 50 cm stent-graft (eg, Viabahn, Fluency). The delivery catheter length on these stent grafts is often limiting at 80 to 110 cm; therefore, brachial artery access may be preferred.

During elective endovascular procedures, the patient is typically systemically anticoagulated. If the patient is stable and has an isolated injury, heparin (50 to 100 units/kg) can be considered. However, if the patient has multisystem injury, is coagulopathic or has suffered large blood loss, no anticoagulation is given.

The selected device is delivered to the zone of injury over the wire and a final positioning digital subtraction arteriogram is obtained. Once placement is confirmed, the device is delivered and a completion arteriogram is performed (image 1). On occasion, to ensure more accurate placement and collateral vessel preservation, one could consider using two shorter stent-grafts and overlap them.

The results of a multicenter trial that evaluated the use of commercially available covered stents for the treatment of first-order branch arteries support the use endovascular stent-grafting compared with open surgery [75]. A limiting factor for this study was that the etiology of injury that prompted the use of stents in this study was not similar to that reported in prior reports on vascular trauma, with 78 percent the result of iatrogenic injury. In this study, 29 percent of the injuries treated were subclavian. With the placement of a covered stent-graft, 85 percent of patients avoided surgery at one year of follow-up. The results of this study should be interpreted with caution, as the etiology of vascular injury is very different from that of true vascular trauma, and as such the results are likely not translatable to real-world vascular trauma.

MANAGEMENT OF SPECIFIC VASCULAR INJURIES

Pulmonary — Intrapericardial pulmonary artery injuries are exposed through a median sternotomy. Anterior injuries can be repaired primarily; however, posterior injuries require cardiopulmonary bypass. Distal pulmonary artery injuries are best exposed through an ipsilateral posterolateral thoracotomy. In patients with major hilar injuries, if primary repair is not feasible or the patient remains in extremis, a lobectomy or pneumonectomy can be performed as life-saving maneuvers. (See "Overview of pulmonary resection", section on 'Traumatic injury'.)

Thoracic aorta

Ascending aorta — Penetrating injuries involving the ascending aorta are uncommon, and in one review, mortality rates among operated patients who were hemodynamically stable upon arrival were 50 percent [13]. While primary repair of lacerations to the anterior ascending aorta can be repaired using a side-biting clamp, more extensive injuries will generally require placing the patient on cardiopulmonary bypass. (See "Overview of open surgical repair of the thoracic aorta" and "Management of cardiac injury in severely injured patients".)

Descending aorta

Penetrating aortic injury — The first published case of placement of a stent-graft in a patient who suffered a gunshot wound to the thoracic aorta was reported in 2006 [99]. The literature is limited to isolated case reports of endovascular management of penetrating thoracic aortic injury, which likely reflects the clinical instability and high mortality in this patient cohort.

Blunt aortic injury — Blunt aortic injury is a life-threatening event often associated with multisystem injury. Among patients who are successfully transported to the hospital, 50 percent die within 24 hours and 90 percent die within the first month if left untreated [6,100]. Various types of blunt trauma, such as a direct blow, a crush injury, or rapid deceleration, may result in varying degrees of injuries ranging from small intimal tears and dissection flaps to a complete transection. (See "Clinical features and diagnosis of blunt thoracic aortic injury", section on 'Aortic injury grading'.)

The majority of aortic transections occur 2 to 3 cm distal to the origin of the left subclavian artery [11]. The aortic adventitia provides the majority of the walls' tensile strength, and there is no evidence to suggest that the adventitia at the aortic isthmus is any weaker than any other part of the aorta. Patients are usually younger, and atherosclerotic disease is generally not present. Thus, deceleration injury may cause arterial wall damage that results in intimal disruption and subsequent thrombosis of small- to medium-caliber vessels, including transection. If the arterial bleeding from the lacerated vessel is contained by the vascular adventitia and/or other surrounding soft tissues, a pseudoaneurysm may result. Clinical manifestations of blunt vascular injury include bleeding and ischemic changes. (See "Clinical features and diagnosis of blunt thoracic aortic injury", section on 'Clinical features'.)

Ninety-five percent of patients with aortic injury have associated injuries and, consequently, it is imperative that a comprehensive trauma evaluation occurs before definitive imaging to rule out aortic injury; however, this process must not be overly delayed. (See "Clinical features and diagnosis of blunt thoracic aortic injury", section on 'Approach to imaging'.)

Most patients presenting with blunt aortic injury should be considered for repair, though patients with minimal injury may be initially managed nonoperatively. The optimal timing of repair of a traumatic contained thoracic aortic transection often comes into question, but repair should be performed when the patient's physiology can tolerate the added stress. (See "Management of blunt thoracic aortic injury", section on 'Approach to management'.)

Patients who are being managed nonoperatively should have heart rate controlled to <100 beats per minute and mean arterial blood pressures maintained in the range of 60 to 70 mmHg (table 3). The need for repair of stable patients with known aortic injuries is not known and, as a result, the duration of antihypertensive therapy and/or the timing and need for aortic repair is not known [63]. Approximately 2 to 5 percent of patients with aortic disruption survive without operation, or even detection, to form chronic pseudoaneurysm [101]. (See "Management of blunt thoracic aortic injury", section on 'Immediate versus delayed' and "Management of blunt thoracic aortic injury", section on 'Anti-impulse therapy' and "Management of blunt thoracic aortic injury", section on 'Nonoperative management of minimal injuries'.)

Prior techniques for treatment involved a thoracotomy for open repair with associated mortality rates ranging between 15 and 28 percent, with associated paraplegia in up to 19 percent of the survivors [7,102,103]. With traditional open repair of blunt aortic injuries, mortality was mostly related to multisystem organ failure [49]. This was often the result of an already stressed patient with multiple injuries, often cerebral and pulmonary, not being able to tolerate the added stress of lateral decubitus positioning, single lung ventilation, and the stress of open surgery. In patients with blunt aortic injury, thoracotomy may worsen associated lung injury and increase mortality [102]. Endovascular management of aortic disease, which has become the standard of care for the management of other descending thoracic aortic pathology (aneurysm, dissection), has been applied to the repair of blunt thoracic aortic injury, resulting in a significant decrease in perioperative morbidity and mortality [74,76,77,99,104-116]. In one review of endovascular treatment of blunt aortic injury, the mortality rate was 6.8 percent at a mean follow-up of 21.7 months; there was one report of postoperative paraplegia [74]. (See "Management of blunt thoracic aortic injury", section on 'Open versus endovascular' and "Surgical and endovascular repair of blunt thoracic aortic injury".)

The commercially available thoracic stent-grafts that were originally designed to treat aneurysmal disease are generally too large. Aggressive over-sizing is known to potentially lead stent-graft infolding inadequate apposition to the lesser curvature of the aortic arch, leading to subsequent endoleak and collapse of the graft [76,99,116]. Lower profile stent-grafts have been designed for use in non-aneurysmal aortas and have been approved for treating blunt aortic rupture. The smallest available aortic devices can treat an aorta with an inner aortic diameter as small as 16 mm. Various other methods of repair have been reported to manage small aortas, all involving devices not specifically approved for this indication, typically using a covered stent (eg, Braun CP). (See "Endovascular devices for thoracic aortic repair", section on 'Thoracic devices' and "Surgical and endovascular repair of blunt thoracic aortic injury".)

Vena cava — Intrathoracic superior vena cava and proximal inferior vena cava injuries are exposed through a median sternotomy. Anterior injuries can be repaired primarily; however, posterior injuries usually require cardiopulmonary bypass. Repairs of these injuries require cardiopulmonary bypass and are performed with pledgeted polypropylene sutures for lacerations. More severe disruptions can be repaired with appropriately sized interposition or patch grafts. (See "Abdominal vascular injury", section on 'Inferior vena cava'.) (See "Traumatic and iatrogenic injury to the inferior vena cava".)

Great vessel injury — Managing injuries to the thoracic outlet (figure 14) often requires incisions that have the potential for serious morbidity. Many injuries in this location are, fortunately, contained hematomas that allow for definitive diagnosis and a tempered approach to treatment. This period of stability creates a window in which successful planning and execution of endovascular interventions can occur.

Several studies have reported successful management of supra-aortic trunk injury to the innominate, carotid, and subclavian arteries without the need to perform thoracotomy or sternotomy [75,117,118]. A review of the literature finds an ever-increasing number of reports on the use of endovascular techniques for the management of upper extremity trauma [5,64,74,118-126]. This is especially important for injuries to the subclavian artery, where exposure is difficult, time consuming, and potentially morbid. In one of the first reports, patency up to 14 months (mean follow-up 6.5 months) was achieved with the use of stent-grafts [64]. The use of stent-grafts was associated with reduced blood loss, a less invasive insertion procedure, reduced requirements for anesthesia, and a limited need for an extensive dissection in the traumatized field. This method of management has been used to treat more devastating military injuries, including acute trauma as well as for the management of late traumatic pseudoaneurysm [5,120].

Subclavian/innominate — Subclavian and innominate vascular injuries can present with signs of injury in the thorax, thoracic outlet, cervical, or upper extremity. In hemodynamically stable patients, preoperative arteriography greatly improves planning. (See "Surgical and endovascular techniques for aortic arch branch and upper extremity revascularization".)

The innominate and right subclavian artery injuries are best exposed though a median sternotomy with a right cervical extension incision, if needed (figure 7 and figure 15). Blunt injuries classically involve the proximal innominate artery, and proximal control needs to be obtained at the level of the transverse aortic arch. Simple penetrating injuries to the innominate artery can be closed with running 4-0 polypropylene, but most injuries will require an ascending aorta to distal innominate artery bypass (figure 8) performed prior to opening and exploring the hematoma and area of injury.

The left subclavian artery is best approached through a combined anterolateral thoracotomy with a separate supraclavicular incision. As a last resort, if further exposure is still required, a "trap-door" thoracotomy can be performed with the addition of a median sternotomy (figure 7). Of note, the subclavian artery is easy to injure, so care should be taken when handling and dissecting this vessel to avoid further blood loss. (See 'Surgical exposures' above.)

Once the subclavian artery is exposed, the surgeon can consider various methods of repair to include: lateral suture, ligation and bypass, interposition graft, patch angioplasty, or subclavian transposition. The surgeon must consider the extent of injury, the overall status of the patient, and the need or availability of conduits to perform the operation. Repair of this vessel usually requires a lateral arteriorrhaphy or graft interposition fashioned in an end-to-side manner if a standard end-to-end anastomosis cannot usually be performed (picture 2). In general, there is no difference in long-term patency rate in the subclavian position whether vein or prosthetic is used. Prosthetic is usually larger than the patient's native vein and may be more resistant to infection in the short term. The authors prefer to use an 8 mm externally supported expanded polytetrafluoroethylene (ePTFE) graft.

Subclavian-to-carotid transposition can be used if a conduit is not available (figure 16). Subclavian-to-carotid transposition is performed by exposing the ipsilateral common carotid through the medial aspect of this same incision. The subclavian artery is divided proximal to the vertebral artery. The subclavian artery stump is over-sewn using a double suture technique (ie, over-sewn plus vertical mattress). Attention is turned to the exposed common carotid artery, taking care to avoid injury to the vagus nerve. Cerebral protection is not normally used when operating on the common carotid arteries. Provided the patient does not have carotid artery disease, the collateral network from the external to the internal carotid artery should suffice (figure 17). After obtaining proximal and distal control, an incision is made in the lateral side of the common carotid and enlarged using a 3 to 4 mm arterial punch. The subclavian artery is then turned up and an end-to-side anastomosis is performed using a running 6-0 Proline suture.

Proximal carotid artery — Carotid injuries in the chest may be associated with other injuries, including injury to other mediastinal structures, such as the other great vessels, esophagus, or trachea. These structures should be inspected and repaired as needed. It should be noted that, if adjacent structures are injured and repaired, the repairs must be separated with local tissue flaps and drained appropriately. Failing to cover and drain adjacent repairs can lead to potentially fatal complications, such as anastomotic dehiscence and exsanguination, fistula formation, and uncontrolled leaks [127,128].

The diagnostic and therapeutic approach for the management of cervical vascular injuries is dictated by their relative location to the anatomic landmarks used to describe the vascular injury. A clear anatomic division of the neck into zones has allowed a selective approach to penetrating neck trauma (figure 18). Zone I lies below the cricoid cartilage, and zone III lies above the angle of the mandible. Zone II lays between zones I and III. In this review, only zone I injuries of the neck (the inferior border being the clavicles and the sternal notch, and the superior border being the cricoid cartilage), also known as the thoracic outlet, are being considered.

Zone I injuries can be subtle (eg, intimal defect, dissection), and frequently require vascular imaging for definitive evaluation. The physical examination can be very helpful when there is a suspected injury. Obvious hard signs of vascular injury may be absent, but soft signs of vascular injury may be observed, such as a palpable thrill, an audible bruit, loss of a carotid pulse with an associated neurologic deficit, hemothorax, or widened mediastinum on chest radiograph (table 4). However, these physical exam findings are overall unreliable for zone I injury, and because of the serious short- and long-term sequelae of missed vascular injuries, we advocate the liberal use of computed tomographic (CT) arteriography. Similarly, any patient with blunt neck trauma presenting with worrisome history or physical exam findings (eg, seat belt sign), should undergo vascular imaging with either multiplanar CT angiography in most cases, or conventional catheter-based four-vessel cerebral angiography [41,129].

Depending upon the patient's clinical course and the availability of a vascular surgeon, proximal control of the great vessels may be performed from a femoral approach with balloon occlusion. Alternatively, if the vessel can be seen from a cervical approach, but not secured with a vascular clamp, a compliant balloon can be passed retrograde for temporary proximal control. Once the vessel is properly exposed, the balloon can be replaced with the appropriate vascular clamp. (See "Surgical exploration for severe neck trauma".)

Surgical exploration of zone I vascular injuries requires a median sternotomy. An alternative technique for proximal carotid exposure and control has been described using a neck incision and placement of a Satinsky clamp in the superior mediastinum [130]; however, we favor a median sternotomy, as it provides maximal exposure and control. Uncontrollable hemorrhage will continue into the thorax until exposure is attained, as most of the proximal vessels are noncompressible. Once initial exposure is obtained, local manual pressure provides adequate hemostasis as more formal proximal and distal control is attained. Depending on the extent of the injury identified, the artery can be repaired primarily with interrupted polypropylene suture, saphenous or ePTFE patch angioplasty, interposition reversed saphenous or PTFE, ligation and transposition, ligation and bypass, or ligation alone. Saphenous vein is preferred over PTFE due to increased patency rates [131].

For patients with penetrating carotid artery injuries and associated neurologic deficit or coma, immediate operative repair is indicated and offers the best and possibly only chance of recovery [132]. Patients presenting with a preoperative Glasgow coma score (GCS) of less than 8 are likely to have adverse outcomes regardless of the management of the carotid injury [133]. If the duration of symptoms has been three or more hours, or has an established deep coma, emergency head CT should be obtained. If the results of the head CT demonstrate an ischemic infarct, revascularization is contraindicated, as it has been shown to have a substantial risk of causing a hemorrhagic transformation of the ischemic region [134]. (See "Surgical exploration for severe neck trauma", section on 'Arterial repair or ligation'.)

The natural history of nonocclusive proximal carotid dissection appears to be resolution in about two-thirds of patients, but approximately one-third will go on to develop pseudoaneurysms and can be a source of thromboembolic disease [135,136]. Many of these lesions are amenable to endovascular treatment, and while there is not a study comparing endovascular repair with open repair, there are several case series demonstrating feasibility and safety with successful interventions. Symptomatic traumatic dissections of the carotid in patients with a contraindication to anticoagulation have been successfully treated with carotid stent placement [137,138]. Thrombosis and thromboembolic events remain a concern after endovascular management of carotid trauma, but this appears to be a rare event. The results of small numbers of case series are difficult to interpret due to the low number of patients and limited follow-up, but it appears that adjuvant anticoagulation in the form of, at a minimum, one antiplatelet agent for at least six weeks is required for stent patency. As a result, patients who have contraindications to anticoagulation may have limited patency when compared with traditional open repair. (See "Blunt cerebrovascular injury: Treatment and outcomes", section on 'Monitoring and complications' and "Blunt cerebrovascular injury: Treatment and outcomes", section on 'Endovascular therapy for inaccessible lesions'.)

POSTOPERATIVE CARE AND FOLLOW-UP — Patients who have undergone repair of major thoracic vascular injury should be followed indefinitely to identify and treat long-term complications.

Annual clinical examination and routine duplex surveillance of bypass grafts will identify stent or graft stenosis that might require secondary intervention. Clinical symptoms and signs of infectious complications should be sought, as these can lead to graft thrombosis, rupture, and potentially death. In addition, pseudoaneurysm formation can be the source of thromboembolism. Most complications can be identified and intervened upon prior development of serious clinical consequences such as thromboembolism or rupture.

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: General issues of trauma management in adults" and "Society guideline links: Thoracic trauma".)

SUMMARY AND RECOMMENDATIONS

Mechanism of injury – Major thoracic vascular injury includes injury to the aorta, brachiocephalic artery, carotid artery, subclavian artery, vena cava, or pulmonary vasculature. Most cases of major thoracic vascular injury are related to penetrating injury (eg, gunshot, stab) or high-energy deceleration injury (eg, traffic accidents). Major thoracic vascular injury is often associated with other organ injuries, including injuries to the heart and airways, as well as other injuries involving the abdomen or extremities. (See 'Mechanism of injury' above.)

Evaluation – Blunt or penetrating injuries to the major thoracic vasculature can present acutely with external bleeding or as an expanding hematoma, hemothorax, or overt exsanguination, or with ischemic symptoms (eg, stroke, upper extremity). Less severe injuries may go unrecognized during the evaluation of other acute injuries and thus present in delayed fashion as an arteriovenous fistula or post-traumatic pseudoaneurysm. The initial diagnostic evaluation and management is based upon protocols from the Advanced Trauma Life Support (ATLS) program focusing on control of external hemorrhage and cardiorespiratory support. A limited number of patients with penetrating thoracic injury may be candidates for resuscitative thoracotomy. (See 'Trauma evaluation' above.)

Physical examination – The physical examination should include a detailed vascular examination with complete bilateral pulse examination, including upper extremity blood pressures and evaluation for hard signs of vascular injury, which predicts those patients with significant injuries that benefit from immediate exploration. Hard signs of vascular injury include the following (see 'History and physical examination' above):

Active hemorrhage

Expanding or pulsatile hematoma

Bruit or thrill over wound

Absent distal pulses

Extremity ischemia (pain, pallor, paralysis, cool to touch)

Clinical evaluation – Major vascular injury is suggested on plain chest radiograph by the presence of hemothorax, foreign body in proximity to a major vessel, widened mediastinum, and loss of aortic knob contour. In hemodynamically unstable patients, the extended focused assessment with sonography for trauma (eFAST) examination provides a rapid and sensitive evaluation for hemothorax and identifies cardiac effusion or tamponade. (See 'Diagnostic imaging' above.)

Hemodynamically unstable – For hemodynamically unstable patients, ongoing or massive hemorrhage, or a rapidly expanding hematoma, urgent exploration and operative repair is necessary to identify the injury and provide the best chance for survival. Optimal management involves achieving rapid hemostasis, and reversal of metabolic derangements through early use of blood products. If thoracic vascular injury is identified, but is contained, and life-threatening bleeding is identified from another source (eg, spleen, liver, pelvic fracture), then the more severe injury is managed first and a damage control approach applied to the thoracic vascular injury (abbreviated thoracotomy restoring survivable physiology, or rapid definitive repair). (See 'Hemodynamically unstable' above.)

Hemodynamically stable – For hemodynamically stable patients with suspected vascular injury to the aorta or great vessels based on physical examination or plain radiography, we obtain computed tomographic (CT) angiography. Catheter-based angiography is more typically performed in conjunction with endovascular or hybrid repair of vascular injuries. Adjunctive use of intravascular ultrasound may allow adequate endovascular imaging in conjunction with preoperative CT angiography. (See 'Hemodynamically stable' above.)

Vascular injury grading – A relatively simple system to grade aortic vascular and guide management is also applicable to other vascular injuries (figure 2). The American Association for the Surgery of Trauma (AAST) thoracic vascular injury scale reflects the overall severity of thoracic vascular injury (table 2) and correlates with increasing morbidity and mortality, which is lower for smaller vessels and for venous injury compared with arterial injuries of the same size. (See 'Vascular injury grading' above.)

Surgical exposures – The main approaches used for surgical exposure of thoracic vascular injuries are sternotomy, thoracotomy, and supraclavicular/infraclavicular incisions. The decision of which to use is based initially on what exposure will provide the best vascular control proximal and distal to the site of injury. Additional exposure by extending the incision or providing a separate incision may be needed. Once the vessel can be controlled proximally and distally, the method of vascular repair is chosen based on the extent of damage (eg, simple repair, patch angioplasty, interposition grafting, bypass). The repair of specific vascular injuries is discussed above. (See 'Surgical exposures' above and 'Management of specific vascular injuries' above.)

Endovascular techniques – Endovascular techniques have been applied to the management of traumatic vascular injuries with increasing frequency and represent a substantial advance in trauma management. Endovascular repair can also be used as an adjunct to support the standard open repair of many injuries, and among patients with thoracic vascular injury, it is particularly appealing for those with severe concomitant brain and/or lung injuries. Long-term data are lacking and protocols for using endovascular techniques for vascular injuries are evolving. (See 'Endovascular approach' above.)

Postoperative care and follow-up – Patients who have undergone repair of major thoracic vascular injury should be followed indefinitely to identify and treat long-term complications (eg, stenosis, pseudoaneurysm). Annual clinical examination and routine duplex surveillance of vascular repairs will identify areas of stenosis that might require repeat intervention. Most complications can be identified and intervened upon prior development of serious clinical consequences such as thromboembolism or rupture. (See 'Postoperative care and follow-up' above.)

  1. Rice DP, MacKenzie EJ, Jones AS, et al. Cost of Injury in the United States: A Report to Congress. Institute for Health & Aging, University of California and Injury Prevention Center, The Johns Hopkins University, 1989.
  2. Gupta R, Rao S, Sieunarine K. An epidemiological view of vascular trauma in Western Australia: a 5-year study. ANZ J Surg 2001; 71:461.
  3. Lim JY, Wolf AS, Flores RM. Thoracic vessel injury. Minerva Chir 2013; 68:251.
  4. Mattox KL, Feliciano DV, Burch J, et al. Five thousand seven hundred sixty cardiovascular injuries in 4459 patients. Epidemiologic evolution 1958 to 1987. Ann Surg 1989; 209:698.
  5. Fox CJ, Gillespie DL, O'Donnell SD, et al. Contemporary management of wartime vascular trauma. J Vasc Surg 2005; 41:638.
  6. Richens D, Kotidis K, Neale M, et al. Rupture of the aorta following road traffic accidents in the United Kingdom 1992-1999. The results of the co-operative crash injury study. Eur J Cardiothorac Surg 2003; 23:143.
  7. von Oppell UO, Dunne TT, De Groot MK, Zilla P. Traumatic aortic rupture: twenty-year metaanalysis of mortality and risk of paraplegia. Ann Thorac Surg 1994; 58:585.
  8. Jamieson WR, Janusz MT, Gudas VM, et al. Traumatic rupture of the thoracic aorta: third decade of experience. Am J Surg 2002; 183:571.
  9. Tambyraja AL, Scollay JM, Beard D, et al. Aortic trauma in Scotland--a population based study. Eur J Vasc Endovasc Surg 2006; 32:686.
  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.
  11. Duhaylongsod FG, Glower DD, Wolfe WG. Acute traumatic aortic aneurysm: the Duke experience from 1970 to 1990. J Vasc Surg 1992; 15:331.
  12. Burkhart HM, Gomez GA, Jacobson LE, et al. Fatal blunt aortic injuries: a review of 242 autopsy cases. J Trauma 2001; 50:113.
  13. Pate JW, Cole FH Jr, Walker WA, Fabian TC. Penetrating injuries of the aortic arch and its branches. Ann Thorac Surg 1993; 55:586.
  14. Karmy-Jones R, Jurkovich GJ. Blunt chest trauma. Curr Probl Surg 2004; 41:211.
  15. Prêtre R, LaHarpe R, Cheretakis A, et al. Blunt injury to the ascending aorta: three patterns of presentation. Surgery 1996; 119:603.
  16. Hudson HM 2nd, Woodson J, Hirsch E. The management of traumatic aortic tear in the multiply-injured patient. Ann Vasc Surg 1991; 5:445.
  17. Atkins MD, Marrocco CJ, Bohannon WT, Bush RL. Stent-graft repair for blunt traumatic aortic injury as the new standard of care: is there evidence? J Endovasc Ther 2009; 16 Suppl 1:I53.
  18. Stover S, Holtzman RB, Lottenberg L, Bass TL. Blunt innominate artery injury. Am Surg 2001; 67:757.
  19. Wall MJ Jr, Hirshberg A, LeMaire SA, et al. Thoracic aortic and thoracic vascular injuries. Surg Clin North Am 2001; 81:1375.
  20. McKeown PP, Rosemurgy A, Conant P. Blunt traumatic rupture of pulmonary vein, left atrium, and bronchus. Ann Thorac Surg 1991; 52:1171.
  21. Fang R, Miller OL, Cai T, et al. Blunt avulsion of the right inferior pulmonary vein. J Trauma 2004; 56:191.
  22. Fuller J, Clark TC. Repair of traumatic aneurysm of the pulmonary artery with arteriovenous fistula. Minn Med 1987; 70:521.
  23. Hubler B, Earls JP, Stevens K. Traumatic pulmonary arterial and venous pseudoaneurysms. AJR Am J Roentgenol 1997; 169:1354.
  24. Mills T, Gupta S, Helmcke F, et al. Posttraumatic pulmonary arteriovenous fistula presenting as multiple embolic strokes. Echocardiography 2007; 24:79.
  25. Ito T, Sakamoto T, Norio H, et al. An arteriovenous fistula between the internal mammary artery and the pulmonary vein following blunt chest trauma. Cardiovasc Intervent Radiol 2005; 28:120.
  26. Couves CM, Heughan C. Laceration of superior vena cava due to blunt trauma: successful surgical management. Can J Surg 1981; 24:402.
  27. Clements RH, Fischer PJ 2nd. Blunt injury of the intrapericardial great vessels. J Trauma 2001; 50:129.
  28. Demetriades D, Charalambides D, Lakhoo M. Physical examination and selective conservative management in patients with penetrating injuries of the neck. Br J Surg 1993; 80:1534.
  29. Nance ML. National Trauma Data Bank Annual Report. 2012. http://www.facs.org/trauma/ntdb/pdf/ntdb-annual-report-2012.pdf (Accessed on October 22, 2013).
  30. ATLS. https://www.facs.org/quality-programs/trauma/atls (Accessed on May 19, 2020).
  31. Mowery NT, Gunter OL, Collier BR, et al. Practice management guidelines for management of hemothorax and occult pneumothorax. J Trauma 2011; 70:510.
  32. Fox CJ, Gillespie DL, Cox ED, et al. Damage control resuscitation for vascular surgery in a combat support hospital. J Trauma 2008; 65:1.
  33. Raptis CA, Hammer MM, Raman KG, et al. Acute traumatic aortic injury: practical considerations for the diagnostic radiologist. J Thorac Imaging 2015; 30:202.
  34. Abdulrahman Y, Musthafa S, Hakim SY, et al. Utility of extended FAST in blunt chest trauma: is it the time to be used in the ATLS algorithm? World J Surg 2015; 39:172.
  35. Schellenberg M, Inaba K, Bardes JM, et al. The combined utility of extended focused assessment with sonography for trauma and chest x-ray in blunt thoracic trauma. J Trauma Acute Care Surg 2018; 85:113.
  36. Lobo V, Hunter-Behrend M, Cullnan E, et al. Caudal Edge of the Liver in the Right Upper Quadrant (RUQ) View Is the Most Sensitive Area for Free Fluid on the FAST Exam. West J Emerg Med 2017; 18:270.
  37. Rippey JC, Royse AG. Ultrasound in trauma. Best Pract Res Clin Anaesthesiol 2009; 23:343.
  38. Plummer D, Brunette D, Asinger R, Ruiz E. Emergency department echocardiography improves outcome in penetrating cardiac injury. Ann Emerg Med 1992; 21:709.
  39. Sisley AC, Rozycki GS, Ballard RB, et al. Rapid detection of traumatic effusion using surgeon-performed ultrasonography. J Trauma 1998; 44:291.
  40. Rozycki GS, Feliciano DV, Ochsner MG, et al. The role of ultrasound in patients with possible penetrating cardiac wounds: a prospective multicenter study. J Trauma 1999; 46:543.
  41. Ofer A, Nitecki SS, Braun J, et al. CT angiography of the carotid arteries in trauma to the neck. Eur J Vasc Endovasc Surg 2001; 21:401.
  42. Scaglione M, Pinto A, Pinto F, et al. Role of contrast-enhanced helical CT in the evaluation of acute thoracic aortic injuries after blunt chest trauma. Eur Radiol 2001; 11:2444.
  43. White PW, Gillespie DL, Feurstein I, et al. Sixty-four slice multidetector computed tomographic angiography in the evaluation of vascular trauma. J Trauma 2010; 68:96.
  44. http://www.aast.org/library/traumatools/injuryscoringscales.aspx (Accessed on April 11, 2019).
  45. Eastridge BJ, Owsley J, Sebesta J, et al. Admission physiology criteria after injury on the battlefield predict medical resource utilization and patient mortality. J Trauma 2006; 61:820.
  46. Fox CJ, Starnes BW. Vascular surgery on the modern battlefield. Surg Clin North Am 2007; 87:1193.
  47. Rotondo MF, Schwab CW, McGonigal MD, et al. 'Damage control': an approach for improved survival in exsanguinating penetrating abdominal injury. J Trauma 1993; 35:375.
  48. Beekley AC, Watts DM. Combat trauma experience with the United States Army 102nd Forward Surgical Team in Afghanistan. Am J Surg 2004; 187:652.
  49. Goaley TJ, Dente CJ, Feliciano DV. Torso vascular trauma at an urban level I trauma center. Perspect Vasc Surg Endovasc Ther 2006; 18:102.
  50. Quan RW, Adams ED, Cox MW, et al. The management of trauma venous injury: civilian and wartime experiences. Perspect Vasc Surg Endovasc Ther 2006; 18:149.
  51. Brohi K, Singh J, Heron M, Coats T. Acute traumatic coagulopathy. J Trauma 2003; 54:1127.
  52. Cosgriff N, Moore EE, Sauaia A, et al. Predicting life-threatening coagulopathy in the massively transfused trauma patient: hypothermia and acidoses revisited. J Trauma 1997; 42:857.
  53. Holcomb JB, Jenkins D, Rhee P, et al. Damage control resuscitation: directly addressing the early coagulopathy of trauma. J Trauma 2007; 62:307.
  54. Fox, CJ, Mehta, SG, Cox, ED, et al. Effect of recombinant factor VIIa as an adjunctive therapy in damage control for wartime vascular injuries: a case control study. J Trauma 2009; 66:112.
  55. Fox CJ, Gillespie DL, Cox ED, et al. The effectiveness of a damage control resuscitation strategy for vascular injury in a combat support hospital: results of a case control study. J Trauma 2008; 64:S99.
  56. Mandal AK, Oparah SS. Unusually low mortality of penetrating wounds of the chest. Twelve years' experience. J Thorac Cardiovasc Surg 1989; 97:119.
  57. Sakles JC, Sena MJ, Knight DA, Davis JM. Effect of immediate fluid resuscitation on the rate, volume, and duration of pulmonary vascular hemorrhage in a sheep model of penetrating thoracic trauma. Ann Emerg Med 1997; 29:392.
  58. Bickell WH, Bruttig SP, Millnamow GA, et al. Use of hypertonic saline/dextran versus lactated Ringer's solution as a resuscitation fluid after uncontrolled aortic hemorrhage in anesthetized swine. Ann Emerg Med 1992; 21:1077.
  59. Kowalenko T, Stern S, Dronen S, Wang X. Improved outcome with hypotensive resuscitation of uncontrolled hemorrhagic shock in a swine model. J Trauma 1992; 33:349.
  60. Capone AC, Safar P, Stezoski W, et al. Improved outcome with fluid restriction in treatment of uncontrolled hemorrhagic shock. J Am Coll Surg 1995; 180:49.
  61. Arthurs ZM, Sohn VY, Starnes BW. Vascular trauma: endovascular management and techniques. Surg Clin North Am 2007; 87:1179.
  62. Cardarelli MG, McLaughlin JS, Downing SW, et al. Management of traumatic aortic rupture: a 30-year experience. Ann Surg 2002; 236:465.
  63. Pate JW, Gavant ML, Weiman DS, Fabian TC. Traumatic rupture of the aortic isthmus: program of selective management. World J Surg 1999; 23:59.
  64. Marin ML, Veith FJ, Panetta TF, et al. Transluminally placed endovascular stented graft repair for arterial trauma. J Vasc Surg 1994; 20:466.
  65. Dotter CT. Transluminally-placed coilspring endarterial tube grafts. Long-term patency in canine popliteal artery. Invest Radiol 1969; 4:329.
  66. Volodos NL, Karpovich IP, Troyan VI, et al. Clinical experience of the use of self-fixing synthetic prostheses for remote endoprosthetics of the thoracic and the abdominal aorta and iliac arteries through the femoral artery and as intraoperative endoprosthesis for aorta reconstruction. Vasa Suppl 1991; 33:93.
  67. Marin ML, Veith FJ, Panetta TF, et al. Percutaneous transfemoral insertion of a stented graft to repair a traumatic femoral arteriovenous fistula. J Vasc Surg 1993; 18:299.
  68. Marin ML, Veith FJ. Clinical application of endovascular grafts in aortoiliac occlusive disease and vascular trauma. Cardiovasc Surg 1995; 3:115.
  69. Coldwell DM, Novak Z, Ryu RK, et al. Treatment of posttraumatic internal carotid arterial pseudoaneurysms with endovascular stents. J Trauma 2000; 48:470.
  70. Duane TM, Parker F, Stokes GK, et al. Endovascular carotid stenting after trauma. J Trauma 2002; 52:149.
  71. Ellis PK, Kennedy PT, Barros D'Sa AA. Successful exclusion of a high internal carotid pseudoaneurysm using the Wallgraft endoprosthesis. Cardiovasc Intervent Radiol 2002; 25:68.
  72. McNeil JD, Chiou AC, Gunlock MG, et al. Successful endovascular therapy of a penetrating zone III internal carotid injury. J Vasc Surg 2002; 36:187.
  73. Wyers MC, Powell RJ. Management of carotid injuries in a hostile neck using endovascular grafts. J Vasc Surg 2004; 39:1335.
  74. Starnes BW, Arthurs ZM. Endovascular management of vascular trauma. Perspect Vasc Surg Endovasc Ther 2006; 18:114.
  75. White R, Krajcer Z, Johnson M, et al. Results of a multicenter trial for the treatment of traumatic vascular injury with a covered stent. J Trauma 2006; 60:1189.
  76. Lin PH, Bush RL, Zhou W, et al. Endovascular treatment of traumatic thoracic aortic injury--should this be the new standard of treatment? J Vasc Surg 2006; 43 Suppl A:22A.
  77. Hoornweg LL, Dinkelman MK, Goslings JC, et al. Endovascular management of traumatic ruptures of the thoracic aorta: a retrospective multicenter analysis of 28 cases in The Netherlands. J Vasc Surg 2006; 43:1096.
  78. Salazar GM, Walker TG. Evaluation and management of acute vascular trauma. Tech Vasc Interv Radiol 2009; 12:102.
  79. Kaplan LJ, Kellum JA. Initial pH, base deficit, lactate, anion gap, strong ion difference, and strong ion gap predict outcome from major vascular injury. Crit Care Med 2004; 32:1120.
  80. Carrick MM, Morrison CA, Pham HQ, et al. Modern management of traumatic subclavian artery injuries: a single institution's experience in the evolution of endovascular repair. Am J Surg 2010; 199:28.
  81. Adar R, Schramek A, Khodadadi J, et al. Arterial combat injuries of the upper extremity. J Trauma 1980; 20:297.
  82. Andreev A, Kavrakov T, Karakolev J, Penkov P. Management of acute arterial trauma of the upper extremity. Eur J Vasc Surg 1992; 6:593.
  83. Bongard F, Dubrow T, Klein S. Vascular injuries in the urban battleground: experience at a metropolitan trauma center. Ann Vasc Surg 1990; 4:415.
  84. Diamond S, Gaspard D, Katz S. Vascular injuries to the extremities in a suburban trauma center. Am Surg 2003; 69:848.
  85. Fitridge RA, Raptis S, Miller JH, Faris I. Upper extremity arterial injuries: experience at the Royal Adelaide Hospital, 1969 to 1991. J Vasc Surg 1994; 20:941.
  86. Graham JM, Feliciano DV, Mattox KL, et al. Management of subclavian vascular injuries. J Trauma 1980; 20:537.
  87. Graham JM, Mattox KL, Feliciano DV, DeBakey ME. Vascular injuries of the axilla. Ann Surg 1982; 195:232.
  88. Hyre CE, Cikrit DF, Lalka SG, et al. Aggressive management of vascular injuries of the thoracic outlet. J Vasc Surg 1998; 27:880.
  89. Katras T, Baltazar U, Rush DS, et al. Subclavian arterial injury associated with blunt trauma. Vasc Surg 2001; 35:43.
  90. Lin PH, Koffron AJ, Guske PJ, et al. Penetrating injuries of the subclavian artery. Am J Surg 2003; 185:580.
  91. Nanobashvili J, Kopadze T, Tvaladze M, et al. War injuries of major extremity arteries. World J Surg 2003; 27:134.
  92. Pillai L, Luchette FA, Romano KS, Ricotta JJ. Upper-extremity arterial injury. Am Surg 1997; 63:224.
  93. Rich NM, Hobson RW, Jarstfer BS, Geer TM. Subclavian artery trauma. J Trauma 1973; 13:485.
  94. Sturm JT, Dorsey JS, Olson FR, Perry JF Jr. The management of subclavian artery injuries following blunt thoracic trauma. Ann Thorac Surg 1984; 38:188.
  95. Weber MA, Fox CJ, Adams E, et al. Upper extremity arterial combat injury management. Perspect Vasc Surg Endovasc Ther 2006; 18:141.
  96. Buscaglia LC, Walsh JC, Wilson JD, Matolo NM. Surgical management of subclavian artery injury. Am J Surg 1987; 154:88.
  97. George SM Jr, Croce MA, Fabian TC, et al. Cervicothoracic arterial injuries: recommendations for diagnosis and management. World J Surg 1991; 15:134.
  98. Wall MJ Jr, Granchi T, Liscum K, Mattox KL. Penetrating thoracic vascular injuries. Surg Clin North Am 1996; 76:749.
  99. Fang TD, Peterson DA, Kirilcuk NN, et al. Endovascular management of a gunshot wound to the thoracic aorta. J Trauma 2006; 60:204.
  100. PARMLEY LF, MATTINGLY TW, MANION WC, JAHNKE EJ Jr. Nonpenetrating traumatic injury of the aorta. Circulation 1958; 17:1086.
  101. Bennett DE, Cherry JK. The natural history of traumatic aneurysms of the aorta. Surgery 1967; 61:516.
  102. Kasirajan K, Heffernan D, Langsfeld M. Acute thoracic aortic trauma: a comparison of endoluminal stent grafts with open repair and nonoperative management. Ann Vasc Surg 2003; 17:589.
  103. Verdant A. Contemporary results of standard open repair of acute traumatic rupture of the thoracic aorta. J Vasc Surg 2010; 51:294.
  104. Kato N, Dake MD, Miller DC, et al. Traumatic thoracic aortic aneurysm: treatment with endovascular stent-grafts. Radiology 1997; 205:657.
  105. Semba CP, Mitchell RS, Miller DC, et al. Thoracic aortic aneurysm repair with endovascular stent-grafts. Vasc Med 1997; 2:98.
  106. Dake MD, Miller DC, Mitchell RS, et al. The "first generation" of endovascular stent-grafts for patients with aneurysms of the descending thoracic aorta. J Thorac Cardiovasc Surg 1998; 116:689.
  107. Mitchell RS, Miller DC, Dake MD, et al. Thoracic aortic aneurysm repair with an endovascular stent graft: the "first generation". Ann Thorac Surg 1999; 67:1971.
  108. Yamane BH, Tefera G, Hoch JR, et al. Blunt thoracic aortic injury: open or stent graft repair? Surgery 2008; 144:575.
  109. Xenos ES, Abedi NN, Davenport DL, et al. Meta-analysis of endovascular vs open repair for traumatic descending thoracic aortic rupture. J Vasc Surg 2008; 48:1343.
  110. Jonker FH, Giacovelli JK, Muhs BE, et al. Trends and outcomes of endovascular and open treatment for traumatic thoracic aortic injury. J Vasc Surg 2010; 51:565.
  111. 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.
  112. Amabile P, Collart F, Gariboldi V, et al. Surgical versus endovascular treatment of traumatic thoracic aortic rupture. J Vasc Surg 2004; 40:873.
  113. Görich J, Asquan Y, Seifarth H, et al. Initial experience with intentional stent-graft coverage of the subclavian artery during endovascular thoracic aortic repairs. J Endovasc Ther 2002; 9 Suppl 2:II39.
  114. Thompson CS, Rodriguez JA, Ramaiah VG, et al. Acute traumatic rupture of the thoracic aorta treated with endoluminal stent grafts. J Trauma 2002; 52:1173.
  115. Karmy-Jones R, Hoffer E, Meissner MH, et al. Endovascular stent grafts and aortic rupture: a case series. J Trauma 2003; 55:805.
  116. Steinbauer MG, Stehr A, Pfister K, et al. Endovascular repair of proximal endograft collapse after treatment for thoracic aortic disease. J Vasc Surg 2006; 43:609.
  117. Becker GJ, Benenati JF, Zemel G, et al. Percutaneous placement of a balloon-expandable intraluminal graft for life-threatening subclavian arterial hemorrhage. J Vasc Interv Radiol 1991; 2:225.
  118. Patel AV, Marin ML, Veith FJ, et al. Endovascular graft repair of penetrating subclavian artery injuries. J Endovasc Surg 1996; 3:382.
  119. Aerts NR, Poli de Figueiredo LF, Burihan E. Emergency room retrograde transbrachial arteriography for the management of axillosubclavian vascular injuries. J Trauma 2003; 55:69.
  120. Clouse WD, Rasmussen TE, Perlstein J, et al. Upper extremity vascular injury: a current in-theater wartime report from Operation Iraqi Freedom. Ann Vasc Surg 2006; 20:429.
  121. Danetz JS, Cassano AD, Stoner MC, et al. Feasibility of endovascular repair in penetrating axillosubclavian injuries: a retrospective review. J Vasc Surg 2005; 41:246.
  122. Dinkel HP, Eckstein FS, Triller J, Do DD. Emergent axillary artery stent-graft placement for massive hemorrhage from an avulsed subscapular artery. J Endovasc Ther 2002; 9:129.
  123. McArthur CS, Marin ML. Endovascular therapy for the treatment of arterial trauma. Mt Sinai J Med 2004; 71:4.
  124. Ohki T, Veith FJ, Kraas C, et al. Endovascular therapy for upper extremity injury. Semin Vasc Surg 1998; 11:106.
  125. Ohki T, Veith FJ, Marin ML, et al. Endovascular approaches for traumatic arterial lesions. Semin Vasc Surg 1997; 10:272.
  126. Valentin MD, Tulsyan N, James K. Endovascular management of traumatic axillary artery dissection--a case report and review of the literature. Vasc Endovascular Surg 2004; 38:473.
  127. Feliciano DV, Bitondo CG, Mattox KL, et al. Combined tracheoesophageal injuries. Am J Surg 1985; 150:710.
  128. Symbas PN, Hatcher CR Jr, Vlasis SE. Esophageal gunshot injuries. Ann Surg 1980; 191:703.
  129. Biffl WL, Moore EE, Offner PJ, Burch JM. Blunt carotid and vertebral arterial injuries. World J Surg 2001; 25:1036.
  130. Feliciano DV. Management of penetrating injuries to carotid artery. World J Surg 2001; 25:1028.
  131. Becquemin JP, Cavillon A, Brunel M, et al. Polytetrafluoroethylene grafts for carotid repair. Cardiovasc Surg 1996; 4:740.
  132. Ramadan F, Rutledge R, Oller D, et al. Carotid artery trauma: a review of contemporary trauma center experiences. J Vasc Surg 1995; 21:46.
  133. Teehan EP, Padberg FT Jr, Thompson PN, et al. Carotid arterial trauma: assessment with the Glasgow Coma Scale (GCS) as a guide to surgical management. Cardiovasc Surg 1997; 5:196.
  134. Murray JA, Demetriades D, Asensio JA. Carotid injury: postrevascularization hemorrhagic infarction. J Trauma 1996; 41:760.
  135. Duke BJ, Ryu RK, Coldwell DM, Brega KE. Treatment of blunt injury to the carotid artery by using endovascular stents: an early experience. J Neurosurg 1997; 87:825.
  136. Prêtre R, Kürsteiner K, Reverdin A, Faidutti B. Blunt carotid artery injury: devastating consequences of undetected pseudoaneurysm. J Trauma 1995; 39:1012.
  137. Cohen JE, Ben-Hur T, Rajz G, et al. Endovascular stent-assisted angioplasty in the management of traumatic internal carotid artery dissections. Stroke 2005; 36:e45.
  138. Kerby JD, May AK, Gomez CR, Rue LW 3rd. Treatment of bilateral blunt carotid injury using percutaneous angioplasty and stenting: case report and review of the literature. J Trauma 2000; 49:784.
Topic 15227 Version 10.0

References

آیا می خواهید مدیلیب را به صفحه اصلی خود اضافه کنید؟