Matthew J. Wall, Jr., Peter Tsai, and Kenneth L. Mattox
The heart and its tributaries are encased in the chest cavity, composed of the manubrium, sternum, clavicle, rib cage, and vertebral bodies. This rigid chassis, for the most part, provides adequate protection against small impacts/injuries. Severe trauma requiring intervention occurs by penetrating or blunt mechanisms. Firearms often result in direct injury to the heart and great vessels, in the path of destruction.
The bony structures, interestingly, can also provide unique forms of injuries as they cause a ricocheting of bullets or alter vectors of the original direction of penetration. Blunt forces can lead to crushing, traction, and torsion injuries to the heart from deceleration forces. Penetrating trauma to the great vessels can lead to immediate exsanguination or pattern of injury similar to blunt trauma including pseudoaneurysm, partial transection with intimal flap, thrombosis, and propagation.
Cardiac injury may account for 10% of deaths from gunshot wounds.1 Penetrating cardiac trauma is a highly lethal injury, with relatively few victims surviving long enough to reach the hospital. In a series of 1,198 patients with penetrating cardiac injuries in South Africa, only 6% of patients reached the hospital with any signs of life.2 With improvements in organized emergency medical transport systems, up to 45% of those who sustain significant heart injury may reach the emergency department with signs of life. It is somewhat frustrating however to note the overall mortality for penetrating trauma has not changed much even in the major trauma centers.3
Blunt cardiac injuries have been reported less frequently than penetrating injuries.1 The actual incidence of cardiac injury is unknown because of the diverse causes and classifications. Thoracic trauma is responsible for 25% of the deaths from vehicular accidents of which 10–70% of this subgroup may have been the result of blunt cardiac rupture. There continues to be tremendous confusion as the term blunt cardiac injury/cardiac contusion is applied to a wide spectrum of pathology.
Penetrating Cardiac Injury
Penetrating trauma is a common mechanism for cardiac injury, with the predominant etiology being from firearms and knives4 (Table 26-1). The location of injury to the heart is associated with the location of injury on the chest wall. Because of an anterior location, the cardiac chambers at greatest risk for injury are the right and left ventricles. In a review of 711 patients with penetrating cardiac trauma, this series noted 54% sustained stab wounds and 42% had gunshot wounds. The right ventricle was injured in 40% of the cases, the left ventricle in 40%, the right atrium in 24%, and the left atrium in 3%. The overall mortality was 47%. This series noted one third of cardiac injuries involved multiple cardiac structures.4 More complicated intracardiac injuries involved the coronary arteries, valvular apparatus, and intracardiac fistulas (such as ventricular septal defects). Only 2% of patients surviving the initial injury required reoperation for a residual defect. The majority of these repairs were performed on a semielective basis.4 Thus, the majority of injuries are to the myocardium, and are readily managed by the general/trauma or acute care surgeon.
TABLE 26-1 Etiology of Traumatic Heart Diseases
Intrapericardial and intracardiac foreign bodies can cause complications of acute suppurative pericarditis, chronic constrictive pericarditis, foreign body reaction, and hemopericardium.5 Needles and other foreign bodies have been noted after deliberate insertion by patients with psychiatric diagnoses. A report by LeMaire et al.5 recommended removal of intrapericardial foreign bodies that are greater than 1 cm in size, that are contaminated, or that produce symptoms.
Intracardiac missiles are embedded in the myocardium, retained in the trabeculations of the endocardial surface, or free in a cardiac chamber. These result from direct penetrating thoracic injury or injury to a peripheral venous structure with embolization to the heart. Observation might be considered when the missile is small, right sided, embedded completely in the wall, contained within a fibrous covering, not contaminated, and producing no symptoms. Right-sided missiles can embolize to the pulmonary artery, where they can be removed if large. In rare cases they can embolize through a patent foramen ovale or atrial septal defect. Left-sided missiles can manifest as systemic embolization shortly after the initial injury.
Blunt Cardiac Injury
Blunt cardiac trauma has replaced the term “cardiac contusion” and describes injury ranging from insignificant bruises of the myocardium to cardiac rupture. Pathology can be caused by direct energy transfer to the heart or by a mechanism of compression of the heart between the sternum and the vertebral column at the time of the accident. Cardiac rupture during external cardiac massage as part of cardiopulmonary resuscitation (CPR) can occur. Blunt cardiac injuries can thus manifest as a spectrum of free septal rupture, free wall rupture, coronary artery thrombosis, cardiac failure, complex and simple dysrhythmias, and rupture of chordae tendineae or papillary muscles.5 The specific mechanisms include motor vehicle accidents, vehicular–pedestrian accidents, falls, crush injuries, blast/explosion, assaults, CPR, and recreational events. Blunt injury may be associated with sternal or rib fractures. In one report a fatal cardiac dysrhythmia occurred when the sternum was struck by a baseball, which may be a form of commotio cordis.6
True cardiac rupture carries a significant risk of mortality. The biomechanics of this injury include (1) direct transmission of increased intrathoracic pressure to the chambers of the heart; (2) a hydraulic effect from a large force applied to the abdominal or extremity veins, causing the force to be transmitted to the right atrium; (3) a decelerating force between fixed and mobile areas, explaining atriocaval tears; (4) a direct force causing myocardial contusion, necrosis, and delayed rupture; and (5) penetration from a broken rib or fractured sternum.1 From autopsy data, blunt cardiac trauma with chamber rupture occurs most often to the left ventricle. In contrast, in patients who arrive alive to the hospital, right atrial disruption is more common. These are seen at the SVC–atrial junction, IVC–atrial junction, or the right atrial appendage. Blunt rupture of the cardiac septum occurs most frequently near the apex of the heart. Multiple ruptures as well as disruption of the conduction system have been reported. Injury to only the membranous portion of the septum is the least common blunt VSD. Traumatic rupture of the thoracic aorta is also associated with lethal cardiac rupture in almost 25% of cases.
Pericardial tears secondary to increased intra-abdominal pressure or lateral decelerative forces can occur. These can occur on the left side, usually parallel to the phrenic nerve; to the right side of the pericardium; to the diaphragmatic surface of the pericardium; and finally to the mediastinum. Cardiac herniation with cardiac dysfunction can occur in conjunction with these tears. The heart may be displaced into either pleural cavity or even the abdomen depending on the tear. In the circumstance of right pericardial rupture, the heart can become twisted, leading to the surprising discovery of an “empty” pericardial cavity at resuscitative left anterolateral thoracotomy. With a left-sided cardiac herniation through a pericardial tear, a trapped apex of the heart prevents the heart from returning to the pericardium and the term strangulated heart has been applied. Unless the heart is returned to its normal position, hypotension and cardiac arrest can occur.7 One clue to the presence of cardiac herniation in a patient with blunt thoracic injury is sudden loss of pulse when the patient is repositioned, such as when moved or placed on a stretcher.
Iatrogenic Cardiac Injury
Iatrogenic cardiac injury can occur with central venous catheter insertion, cardiac catheterization procedures, endovascular interventions, and pericardiocentesis. Cardiac injuries caused by central venous catheter placement usually occur with insertion from either the left subclavian or the left internal jugular vein.8 Perforation causing tamponade has also been reported with a right internal jugular introducer sheath for transjugular intrahepatic portocaval shunts. Insertion of left-sided central lines, especially during dilation of the line tract, can lead to SVC and atrial perforations. Even optimal technique carries a discrete rate of iatrogenic injury secondary to central venous catheterization. Common sites of injury include the superior vena caval–atrial junction and the superior vena cava–innominate vein junction. These small perforations sometimes lead to a compensated cardiac tamponade. Drainage by pericardiocentesis is often unsuccessful, and evacuation via subxiphoid pericardial window or full median sternotomy is sometimes required. At operation, when the pericardium is opened, the site of injury has sometimes sealed and may be difficult to find.
Complications from coronary catheterization including perforation of the coronary arteries, cardiac perforation, and aortic dissection can be catastrophic and require emergency surgical intervention.9
Other iatrogenic potential causes of cardiac injury include external and internal cardiac massage, and right ventricular injury during pericardiocentesis, endovascular interventions, transthoracic percutaneous interventions, and intracardiac injections.10
Cardiac complications after electrical injury include immediate cardiac arrest; acute myocardial necrosis with or without ventricular failure; myocardial ischemia; dysrhythmias; conduction abnormalities; acute hypertension with peripheral vasospasm; and asymptomatic, nonspecific abnormalities evident on an electrocardiogram (ECG). Damage from electrical injury is due to direct effects on the excitable tissues, heat generated from the electrical current, and accompanying associated injuries (e.g., falls, explosions, fires).11
Penetrating Cardiac Injury
Wounds involving the epigastrium and precordium can raise clinical suspicion for cardiac injury. Patients with cardiac injury can present with a clinical spectrum from full cardiac arrest to asymptomatic with normal vital signs. Up to 80% of stab wounds that injure the heart eventually manifest tamponade. Rapid bleeding into the pericardium favors clotting rather than defibrination.1 As pericardial fluid accumulates, a decrease in ventricular filling occurs, leading to a decrease in stroke volume. A compensatory rise in catecholamines leads to tachycardia and increased right heart filling pressures. The limits of right-sided distensibility are reached as the pericardium fills with blood, and the septum shifts toward the left side, further compromising left ventricular function. As little as 60–100 mL of blood in the pericardial sac can produce the clinical picture of tamponade.1
The rate of accumulation depends on the location of the wound. Because it has a thicker wall, wounds to the ventricle seal themselves more readily than wounds to the atrium. Patients with freely bleeding injuries to the coronary arteries present with rapid onset of tamponade combined with cardiac ischemia.
The classic findings of Beck’s triad (muffled heart sounds, hypotension, and distended neck veins) are seen in a minority of acute trauma patients. Pulsus paradoxus (a substantial fall in systolic blood pressure during inspiration) and Kussmaul’s sign (increase in jugular venous distention on inspiration) may be present but are also not reliable signs. A more valuable and reproducible sign of pericardial tamponade is narrowing of the pulse pressure. An elevation of the central venous pressure often accompanies overaggressive cyclic hyperresuscitation with crystalloid solutions, but in such instances a widening of the pulse pressure occurs.
Gunshot wounds to the heart are more frequently associated with hemorrhage than with tamponade. The kinetic energy is greater with firearms, and the wounds to the heart and pericardium are usually more extensive. Thus, these patients present with exsanguination into a pleural cavity more often.
Blunt Cardiac Injury
Clinically significant blunt cardiac injuries include cardiac rupture (ventricular or atrial), septal rupture, valvular dysfunction, coronary thrombosis, and caval avulsion. These injuries manifest as tamponade, hemorrhage, or severe cardiac dysfunction. Septal rupture and valvular dysfunction (leaflet tear, papillary muscle, or chordal rupture) can initially appear without symptoms but later demonstrate the delayed sequela of heart failure.1
Blunt cardiac injury can also present as a dysrhythmia, most commonly premature ventricular contractions, the precise mechanism of which is unknown. Ventricular tachycardia, ventricular fibrillation, and supraventricular tachyarrhythmias can also occur. These symptoms usually occur within the first 24–48 hours after injury.
A major difficulty in managing blunt cardiac injury relates to definitions. “Cardiac contusion” is a nonspecific term, which should likely be abandoned. It is best to describe these injuries as “blunt cardiac trauma with”—followed by the clinical manifestation such as dysrhythmia or heart failure.12
Traumatic pericardial rupture is rare. Most patients with pericardial rupture do not survive transport to the hospital due to other associated injuries. The overall mortality of those who are treated at trauma centers with such injury remains as high as 64%.13 An overwhelming majority of these cases are diagnosed either intraoperatively or on autopsy.7 The clinical presentation of pericardial rupture, with cardiac herniation, can mimic that of pericardial tamponade with low cardiac output due to impaired venous return. When the heart returns to its normal position in the pericardium, venous return resumes. Positional hypotension is the hallmark of cardiac herniation due to pericardial rupture,7 whereas pericardial tamponade is associated with persistent hypotension until the pericardium is decompressed. Therefore, a high index of suspicion is helpful when evaluating polytrauma patients with unexplained positional hypotension.
The diagnosis of heart injury requires a high index of suspicion. On initial presentation to the emergency center, airway, breathing, and circulation under the Advanced Trauma Life Support protocol are evaluated and established.14Two large-bore intravenous catheters are inserted, and blood is typed and cross-matched. The patient can be examined for Beck’s triad of muffled heart sounds, hypotension, and distended neck veins, as well as for pulsus paradoxus and Kussmaul’s sign. These findings suggest cardiac injury but are present in only 10% of patients with cardiac tamponade. The patient undergoes focused assessment with sonography for trauma (FAST). If the FAST demonstrates pericardial fluid in an unstable patient (systemic blood pressure <90 mm Hg), transfer to the operating room can then occur.
Patients in extremis can require emergency department thoracotomy for resuscitation. The clear indications for emergency department thoracotomy by surgical personnel include the following:15
1. Salvageable postinjury cardiac arrest (e.g., patients who have witnessed cardiac arrest with high likelihood of intrathoracic injury, particularly penetrating cardiac wounds)
2. Severe postinjury hypotension (i.e., systolic blood pressure <60 mm Hg) due to cardiac tamponade, air embolism, or thoracic hemorrhage
If, after resuscitative thoracotomy, vital signs are regained, the patient is transferred to the operating room for definitive repair.
Chest radiography is nonspecific, but can identify hemothorax or pneumothorax. Other potentially indicated examinations include computed tomography (CT) scan for trajectory and laparoscopy for diaphragm injury.
In cases of blunt cardiac injury, conduction disturbances can occur. Sinus tachycardia is the most common rhythm disturbance seen. Other common disturbances include T wave and ST segment changes, sinus bradycardia, first- and second-degree atrioventricular block, right bundle branch block, right bundle branch block with hemiblock, third-degree block, atrial fibrillation, premature ventricular contractions, ventricular tachycardia, and ventricular fibrillation. Thus, a screening 12-lead ECG can be helpful for evaluation.
Much has been written about the use of cardiac enzyme determinations in evaluating blunt cardiac injury. However, no relationship among serum assays and identification and prognosis of injury has been demonstrated with blunt cardiac injury.16 Therefore, cardiac enzyme assays are unhelpful unless one is evaluating concomitant coronary artery disease.16
Focused Assessment with Sonography for Trauma (FAST)
Surgeons are increasingly performing ultrasonography for thoracic trauma. The FAST examination evaluates four anatomic windows for the presence of intra-abdominal or pericardial fluid.17 Ultrasonography in this setting is not intended to reach the precision of studies performed in the radiology or cardiology suite but is merely intended to determine the presence of abnormal fluid collections, which aids in surgical decision making.18 Ultrasonography is safe, portable, and expeditious and can be repeated as indicated. If performed by a trained surgeon, the FAST examination has a sensitivity of nearly 100% and a specificity of 97.3%.17 As the use of FAST evolves, and highspeed abdominal CT scans are readily available, the most universally agreed-upon indication for its use is evaluation for pericardial blood.
To evaluate more subtle findings of blunt cardiac injury, such as wall motion, valvular, or septal abnormalities in the stable patient, formal transthoracic echocardiography (TTE) or transesophageal echocardiography (TEE) can be obtained.
TTE can have a limited use in evaluating blunt cardiac trauma because most patients also have significant chest wall injury, thus rendering the test technically difficult to perform. Its major use is in diagnosing intrapericardial blood and tamponade physiology. In stable patients, TEE can be used to evaluate blunt cardiac injury. Cardiac septal defects and valvular insufficiency are readily diagnosed with TEE. Ventricular dysfunction can often mimic cardiac tamponade in its clinical presentation. Echocardiography is particularly useful in older patients with preexisting ventricular dysfunction. However, most blunt cardiac injuries identified by echocardiography rarely require acute treatment.
Subxiphoid Pericardial Window
Subxiphoid pericardial window has been performed both in the emergency department and in the operating room with the patient under either general or local anesthesia. In a prospective study, Meyer et al.19compared the subxiphoid pericardial window with echocardiography in cases of penetrating heart injury and reported that the sensitivity and specificity of subxiphoid pericardial window were 100% and 92%, respectively, compared with 56% and 93% with echocardiography. They suggested that the difference in sensitivity may have been due to the presence of hemothorax, which can be confused with pericardial blood, or due to the fact that the blood had drained into the pleura.19 Although there has been significant controversy in the past with regard to the indication for subxiphoid pericardial window, recent enthusiasm for ultrasonographic evaluation has almost eliminated the role of subxiphoid pericardial window in the evaluation of cardiac trauma. It is almost never needed in the ED.
Pericardiocentesis has had significant historical support, especially when the majority of penetrating cardiac wounds were produced by ice picks and the (surviving) patients arrived several hours and/or days after injury. In such instances there was a natural triage of the more severe cardiac injuries and the intrapericardial blood had become defibrinated and was easy to remove. Currently, many trauma surgeons discourage pericardiocentesis for acute trauma.10
There are probably more injuries from pericardiocentesis than diagnoses acutely.
Indications for use of pericardiocentesis may apply in the case of iatrogenic injury caused by cardiac catheterization, at which time immediate decompression of the tamponade may be lifesaving, or in the trauma setting when a surgeon is not available. For the most part, as a diagnostic tool it has been replaced by the FAST examination. Pericardial exploration is sometimes used via a transdiaphragmatic route during laparotomy to evaluate the pericardium (Fig. 26-1).
FIGURE 26-1 Transdiaphragmatic exploration of the pericardium during laparotomy. (Copyright © Baylor College of Medicine.)
Only a small subset of patients with significant cardiac injury reaches the emergency department, and expeditious transport to an appropriate facility is important to survival. Transport times of less than 5 minutes and successful endotracheal intubation are positive factors for survival when the patient suffers a pulseless cardiac injury.20
Definitive treatment involves surgical exposure through an anterior thoracotomy (Fig. 26-2) or median sternotomy. The mainstays of treatment are relief of tamponade and hemorrhage control. Then reestablishment of effective coronary perfusion is pursued by appropriate resuscitation.
FIGURE 26-2 Left anterior thoracotomy (extension across the sternum if required). (Copyright © Baylor College of Medicine, 2005.)
Exposure of the heart is accomplished via a left anterolateral thoracotomy, which allows access to the pericardium and heart and exposure for aortic cross-clamping if necessary. This incision can be extended across the sternum to gain access to the right side of the chest and for better exposure of the right atrium. Manual access to the right hemithorax from the left side of the chest can be achieved via the anterior mediastinum by blunt dissection. This allows rapid evaluation of the right side of the chest for major injuries without transecting the sternum or placing a separate chest tube. Once the left pleural space is entered, the lung can be retracted to allow clamping of the descending thoracic aorta. The amount of blood present in the left chest suggests whether hemorrhage or tamponade is the primary issue. The pericardium anterior to the phrenic nerve is opened, injuries are identified, and repair is performed.
In selected cases, particularly for small stab wounds to the precordium, median sternotomy can be used. This allows exposure of the anterior structures of the heart, but limits access to the posterior mediastinal structures and descending thoracic aorta for cross-clamping.
Cardiorrhaphy should be carefully performed. Poor technique can result in enlargement of the lacerations or injury to the coronary arteries. If the initial treating physician is uncomfortable with the suturing technique, digital pressure can be applied until an experienced surgeon arrives. Other techniques that have been described include the use of a Foley balloon catheter or a skin stapler (Fig. 26-3). Injuries adjacent to coronary arteries can be managed by placing the sutures deep to the artery (Fig. 26-4). Mechanical support or cardiopulmonary bypass is very uncommonly required in the acute setting.4
FIGURE 26-3 Temporary techniques to control bleeding. (A) Finger occlusion; (B) partial occluding clamp; (C) Foley balloon catheter; (D) skin staples. (Copyright © Baylor College of Medicine, 2005.)
FIGURE 26-4 Injuries adjacent to coronary arteries can be addressed by placing sutures deep, avoiding injury to the artery. (Copyright © Baylor College of Medicine, 2005.)
For multiple fragments in stable patients, diagnosis in the past was pursued with radiographs in two projections, fluoroscopy, angiography, or echocardiography. Recently, the multidetector CT scan can be used to diagnose and locate these fragments. The full-body topogram scan can identify all missiles, and then the cross-sectional images can be directed to precisely locate them. Trajectories can be ascertained. Treatment of retained missiles is individualized. Removal is recommended for intracardiac missiles that are left sided, larger than 1–2 cm, rough in shape, or that produce symptoms. Although a direct approach, either with or without cardiopulmonary bypass, has been advocated, a large percentage of right-sided foreign bodies can now be removed by endovascular techniques.
Blunt Cardiac Injury
Much debate and discussion has occurred about the clinical relevance of “cardiac contusion.” Most trauma surgeons suggest that this diagnosis should be eliminated because it does not affect treatment strategies. The majority of these patients seen are normotensive patients with normal initial ECG and suspected blunt cardiac injury. These cases are managed in observation units, with no expected clinical significance. Patients with an abnormal ECG are admitted for monitoring and treated accordingly. Patients who present in cardiogenic shock are evaluated for a structural injury, which is then addressed.12
Many factors determine survival in patients with traumatic cardiac injury including mechanism of injury, location of injury, associated injuries, coronary artery and valvular involvement, presence of tamponade, length of prehospital transport, requirement for resuscitative thoracotomy, and experience of the trauma team. The overall hospital survival rate for patients with penetrating heart injuries ranges from 30% to 90%. The survival rate for patients with stab wounds is 70–80%, whereas survival after gunshot wounds ranges between 30% and 40%. Cardiac rupture has a worse prognosis than penetrating injuries to the heart, with a survival rate of approximately 20%.
Complex Cardiac Injuries
Complex cardiac injuries include coronary artery injury, valvular apparatus injury (annulus, papillary muscles, and chordae tendineae), intracardiac fistulas, and delayed tamponade. These delayed sequelae have been reported to have a broad incidence (4–56%), depending on the definition. Coronary artery injury is a rare injury, occurring in 5–9% of patients with cardiac injuries, with a 69% mortality rate.4 A coronary artery injury is most often controlled by simple ligation, but bypass grafting using a saphenous vein may be required for proximal left anterior descending or right coronary artery injuries (with cardiopulmonary bypass).4 Off-pump bypass can theoretically be used for cases of these injuries in the highly unlikely event that the patient is hemodynamically stable.
Valvular apparatus injury is rare (0.2–9%) and can occur with both blunt and penetrating trauma.4,5 The aortic valve is most frequently injured, followed by the mitral and tricuspid valves, though most victims of aortic valve injuries likely die at the scene. These injuries are usually identified postoperatively after the initial cardiorrhaphy and resuscitation have been performed. Timing of repair depends on the patient’s condition. If severe cardiac dysfunction exists at the time of the initial operation, and valvular injury is identified, immediate valve repair or replacement may be required; otherwise, delayed repair is more commonly advised.8
Intracardiac fistulas include ventricular septal defects, atrial septal defects, and atrioventricular fistulas, with an incidence of 1.9% among cardiac injuries. The management depends on symptoms and degree of cardiac dysfunction, with only a minority of these patients requiring repair.4 These injuries are also usually identified after primary repair is accomplished, and they can be repaired after the patient has recovered from the original and associated injuries. Echocardiography should be obtained before repair so that specific anatomic sites of injury and incision planning can be accomplished.
Dysrhythmias can occur as a result of blunt injury, ischemia, or electrolyte abnormalities and are addressed according to the injury (Table 26-2). Delayed pericardial tamponade is rare. It can occur as early as 1 hour after initial operation and to days after the injury.
TABLE 26-2 Dysrhythmias Associated with Cardiac Injury
As discussed above, secondary sequelae in survivors of cardiac trauma include valvular abnormalities and intracardiac fistulas.4,19,21 Early postoperative clinical examination and ECG findings are unreliable.4,21 Thus, echocardiography is recommended during the initial hospitalization in all patients to identify occult injury and establish a baseline study. Because the incidence of late sequelae can be as high as 56%, follow-up echocardiography 3–4 weeks after injury has been recommended by some.19,21
THORACIC GREAT VESSEL INJURY
Injuries to the thoracic great vessels—the aorta and its brachiocephalic branches, the pulmonary arteries and veins, the superior and intrathoracic inferior vena cava, and the innominate and azygos veins—occur following both blunt and penetrating trauma. Exsanguinating hemorrhage, the primary acute manifestation, also occurs in the chronic setting when the injured great vessel forms a fistula involving an adjacent structure or when a post-traumatic pseudoaneurysm ruptures.
Current knowledge regarding the treatment of injured thoracic great vessels has been derived primarily from experience with civilian injuries. Great vessel injuries have been repaired with increasing frequency, a phenomenon that has paralleled the development of techniques for elective surgery of the thoracic aorta and its major branches.
A detailed understanding of normal and variant anatomy and structural relationships is important for the surgeon and any one who is a consultant to the surgeon in the evaluation of imaging studies. Venous anomalies are infrequent with the most common being absence of the left innominate vein and persistent left superior vena cava. Thoracic aortic arch anomalies are relatively common (Table 26-3). Knowledge of such anomalies is essential for both open and catheter-based therapies.
TABLE 26-3 Thoracic Aortic Anomalies
ETIOLOGY AND PATHOPHYSIOLOGY
More than 90% of thoracic great vessel injuries are due to penetrating trauma: gunshot, fragments, and stab wounds or therapeutic misadventures.22 Iatrogenic lacerations of various thoracic great vessels, including the arch of the aorta, are reported complications of percutaneous central venous catheter placement. The percutaneous placement of “trocar” chest tubes has caused injuries to the intercostal arteries and major pulmonary and mediastinal vessels. Intra-aortic cardiac assist balloons can produce injury to the thoracic aorta. During emergency center resuscitative thoracotomy, the aorta may be injured during clamping if a crushing (nonvascular) clamp is used. Overinflation or migration of the Swan–Ganz balloon has produced iatrogenic injuries to pulmonary artery branches with resultant fatal hemoptysis; therefore, once a linear relationship has been established between the pulmonary artery diastolic pressure and the pulmonary capillary wedge pressure, further “wedging” may be unnecessary. Self-expanding metal stents have recently produced perforations of the aorta and innominate artery following placement into the esophagus and trachea, respectively.23
The great vessels particularly susceptible to injury from blunt trauma include the innominate artery origin, pulmonary veins, vena cava, and, most commonly, the descending thoracic aorta.24 Aortic injuries have caused or contributed to 10–15% of deaths following motor vehicle accidents for nearly 50 years. These injuries usually involve the proximal descending aorta (54–65% of cases), but often involve other segments—that is, the ascending aorta or transverse aortic arch (10–14%), the mid- or distal descending thoracic aorta (12%), or multiple sites (13–18%). The postulated mechanisms of blunt great vessel injury include (1) shear forces caused by relative mobility of a portion of the vessel adjacent to a fixed portion, (2) compression of the vessel between bony structures, and (3) profound intraluminal hypertension during the traumatic event. The atrial attachments of the pulmonary veins and vena cava and the fixation of the descending thoracic aorta at the ligamentum arteriosum and diaphragm enhance their susceptibility to blunt rupture by the first mechanism. At its origin, the innominate artery may be “pinched” between the sternum and the vertebrae during sternal impact.
Blunt aortic injuries may be partial thickness—histologically similar to the intimal tear in aortic dissection—but most commonly are full thickness and therefore equivalent to a ruptured aortic aneurysm that is contained by surrounding tissues. The histopathological similarities between aortic injuries and nontraumatic aortic catastrophes suggest that similar therapeutic approaches be employed. Therefore, in hemodynamically stable patients with blunt aortic injuries, the concepts of permissive hypovolemia and minimization of arterial pressure impulse (dP/dT)—which are widely accepted in the treatment of aortic dissection and aneurysm rupture—should be considered. In opposition to patients with aortic intimal disease where the adventitia is the restraining barrier, with blunt injury to the descending thoracic aorta, it is the intact parietal pleura (not the adventitia) that contains the hematoma and prevents a massive hemothorax.
True traumatic aortic dissection, with a longitudinal separation of the media extending along the length of the aorta, is extremely rare.25 The use of the term “dissection” in the setting of aortic trauma should be equally rare, being used only in a few appropriate cases. Similarly, the terms “aortic transection” and “blunt aortic rupture” should be used only when describing specific injuries, that is, full-thickness lacerations involving either the entire or partial circumference, respectively.
Increasingly, patients with thoracic great vessel injury have associated head, abdominal, and extremity injury. Often preexisting medical conditions are present, such as diabetes, hypertension, coronary artery disease, or cirrhosis. These patients are also on a large variety of medications, often aspirin, warfarin, or other platelet inhibitors. These interfere with the clotting mechanism and adaptations in treatment must be made.
Three distinctly different groups of patients with thoracic aortic trauma exist (Table 26-4). The epidemiology of aortic injury is changing, due to rapid accident notification and emergency medical system (EMS) transport. The mortality statistics reveal that those whose cause of death is exsanguinating hemorrhage almost all die within the first 0–2 hours of injury. Those who die in the emergency department, operating room, or intensive care unit (ICU) within 2–4 hours of injury often have extensive multisystem injury with hemorrhage often being from sites other than the thoracic aorta. Hemodynamically stable patients who are subsequently found to have aortic injury but who die most often have central nervous system injury as the cause of their injury. It is this later group in whom the diagnosis is made by the trauma team, and therefore amenable to appropriate screening, diagnostic, and therapeutic considerations.
TABLE 26-4 Groups of Patients with Thoracic Aortic Injury
Interventions often performed by paramedics during transport include judicious intravenous fluid administration and endotracheal intubation when indicated.26 Though seldom seen, pneumatic anti-shock garment (PAST) application in patients with thoracic great vessel injuries statistically increases the chance of death in both adult and pediatric populations.27 The PAST elevate blood pressure by increasing afterload and are equivalent to placing a cross-clamp distal to the potential injury—a clearly counterproductive maneuver. Similarly, in patients with acute thoracic great vessel injuries, excessive fluid resuscitation with the goal of increasing blood pressure to normal or supernormal levels increases the incidence of mortality, ARDS, and other postoperative complications.28
Emergency Center Evaluation
In cases of penetrating thoracic trauma, information regarding the length of a knife, the firearm type and number of rounds fired, and the patient’s distance from the firearm is sought from the patient or accompanying persons. Unfortunately, this is frequently unavailable and unreliable.
Although the head-on motor vehicle collision is often considered the typical mechanism for blunt aortic injury, recent epidemiological data reveal that up to 50% of cases occur following side-impact collisions. Blunt aortic injuries have also been reported following equestrian accidents, blast injuries, auto-pedestrian accidents, crush injuries, and falls from heights of 30 ft or more.29
In addition to information involving the mechanism of injury, the emergency transport personnel can provide medical information important in evaluating the potential for a thoracic great vessel injury, such as the amount of hemorrhage at the scene, the extent and location of damage to the vehicle, any history of intermittent paralysis following the accident, and hemodynamic instability during transport.
On arrival to the emergency center, each patient is given a rapid, thorough examination. External signs of penetrating or blunt trauma are noted. With an intrapericardial vascular injury, the classic signs of pericardial tamponade (distended neck veins, pulsus paradoxus, muffled heart sounds, elevated central venous pressure) may be present but not uniformly. Clinical findings associated with thoracic great vessel injury include:
2. Upper extremity hypertension
3. Unequal blood pressures or pulses in the extremities (upper extremity from innominate or subclavian injury, or lower extremity from pseudocoarctation syndrome)
4. External evidence of major chest trauma (e.g., steering wheel imprint on chest)
5. Expanding hematoma at the thoracic outlet
6. Intrascapular murmur
7. Palpable fracture of the sternum
8. Palpable fracture of the thoracic spine
9. Left flail chest
On arrival, a supine anteroposterior 36-in chest radiograph should be performed, ideally in the emergency center and not in a distant radiologic suite. Emergency physicians, radiologists, and surgeons should develop diagnostic experience viewing supine portable chest x-rays as many trauma patients are hemodynamically unstable or have suspected spinal injuries, making an “upright” 72-in posterior–anterior chest radiograph unsafe to obtain. In many cases of great vessel injury, the radiologic findings are sufficient to warrant immediate arteriography or direct transport to the operating room.
For penetrating injuries, it is helpful to place radiopaque markers to identify the entrance and exit sites. Radiographic findings that suggest penetrating thoracic great vessel injury include:
1. Large hemothorax
2. Foreign bodies (bullets or shrapnel) or their trajectories in proximity to the great vessels
3. A foreign body out of focus with respect to the remaining radiograph, which may indicate its intracardiac location (Fig. 26-5)
4. A trajectory with a confusing course, which may indicate a migrating intravascular bullet (Fig. 26-6)
5. “A missing” missile in a patient with a gunshot wound to the chest, suggesting distal embolization in the arterial tree
FIGURE 26-5 Lateral chest x-ray demonstrating an “out of focus” bullet over the cardiac silhouette. The bullet was lodged in the wall of the right ventricle.
FIGURE 26-6 Series of x-rays demonstrating the entrance site of a bullet in the left groin. The bullet embolized to the right pulmonary artery, as confirmed by arteriography.
Several radiographic findings have been associated with blunt injuries of the descending thoracic aorta (Table 26-5). The most reliable of these signs is the loss or “double shadowing” of the aortic knob contour, creating a “funny-looking mediastinum.” Mediastinal widening at the thoracic outlet and leftward tracheal deviation are suggestive of innominate artery injury. These signs are secondary to a mediastinal hematoma, which is an indirect sign of thoracic great vessel injury. The presence of any of these signs is a positive screening test and not a diagnosis.
TABLE 26-5 Radiographic Clues that should Prompt Suspicion of a Thoracic Great Vessel Injury
Missile wounds that appear to traverse the mediastinum create concern regarding injury to the heart, esophagus, trachea, spinal cord, or major vasculature. Should cardiac or vascular injury occur, tamponade or major hemorrhage is usually obvious. The newer multidetector CT is often used to demonstrate missile trajectory and aid the surgeon in a decision regarding directed thoracotomy or endoscopy.
Initial Treatment and Screening
Emergency Center Thoracotomy
Emergency center thoracotomy in patients presenting with signs of life and hemodynamic collapse may reveal injuries to major thoracic vessels. These injuries require temporizing maneuvers that gain rapid control of bleeding, allowing resuscitation, and subsequent transfer to the operating room for definitive repair.30 Subclavian vessel injuries, for example, can be controlled by packing, clamping at the thoracic apex, or inserting intravascular balloon catheters. Major hemorrhage from the pulmonary hilum can be temporally managed by cross-clamping the entire hilum proximally or twisting the lung 180° after releasing the inferior pulmonary ligament.
When the chest radiograph indicates a significant hemothorax, the chest tube can be connected to a repository for autotransfusion. An initial “rush” of a large volume of blood (>1,500 mL) or significant ongoing hemorrhage (>200–250 mL/h) may indicate great vessel injury, and is considered an indication for urgent thoracotomy.
Intravenous Access and Fluid Administration
Currently, unless a patient is in extremis, large-bore intravenous portals are obtained but high-volume resuscitation avoided, until the time of an operation. If a subclavian venous catheter is required in a patient with a suspected subclavian vascular injury, the contralateral side should be used for cannulation.
The treatment of severe shock should include blood transfusion. However, rapid infusions of excessive volumes of either blood or crystalloid solutions prior to operation may increase the blood pressure to a point that a protective soft perivascular clot is “blown out” and fatal exsanguinating hemorrhage ensues. The principles of permitting moderate hypotension (systolic blood pressure of 60–90 mm Hg) and limiting fluid administration until achieving operative control of bleeding are cornerstones in the management of rupturing abdominal aortic aneurysms and equally apply to acute thoracic great vessel injury. Aggressive preoperative fluid resuscitation increases postoperative respiratory complications and may contribute to an increased mortality when compared to fluid restriction.28 With both penetrating and blunt chest trauma, associated pulmonary contusions are common and provide an additional rationale for limiting the infusion of preoperative crystalloid solutions.
The pharmacological reduction of dP/dT has remained a critical component of the treatment of aortic dissection since its original description by Wheat et al. in 1965.31 Based on the similarity between aortic dissection and blunt aortic injury, this principle was first applied to dP/dT reduction to patients with blunt aortic injury in 1970. Subsequent reports have described using beta-blockers in hemodynamically stable patients who had proven blunt aortic injuries but required a delay in definitive operative treatment.32 Some centers routinely begin beta-blockade therapy as soon as an aortic injury is suspected—prior to obtaining diagnostic studies as an attempt to reduce the risk of fatal rupture during the interval between presentation and confirmation of the diagnosis. While retrospective studies suggest that it is safe, no prospective studies have demonstrated either the safety or efficacy of such treatment.
Screening/Planning CT Scan for Thoracic Vascular Injury
Multidetector CT scan of the chest is recommended by many radiologists as a screening test for mediastinal hematoma usually associated with aortic injury.33 In addition, various other aortic wall and intraluminal findings suggest aortic injury on the CT scan. Very often, the initial chest x-ray has already demonstrated findings suggestive of mediastinal hematoma. Some clinicians require the additional screening CT scan to substantiate a request for a diagnostic arteriogram. Although an increasing number of surgeons and radiologists have developed a “skill” and comfort level in performing an operation based on the CT findings alone, many surgeons use the arteriographic roadmap to determine the specific injury and any unexpected vascular anomalies. This also occurs when a confirmatory aortogram is obtained prior to thoracic endograft deployment. It is interesting to thus note in a 2008 report by Demetriades et al. of a multicenter study on blunt aorta injuries that CT was used as the primary “diagnostic” modality in 93% of patients, but as the majority of patients underwent endograft repair an aortogram was usually obtained.34 As resolution and experience in using CT to plan operations increases, it is important to assure that the same information regarding extent of injury, anatomy, and aberrant branches, as well as location of injury, is obtainable. Even when radiologists and surgeons have utilized CT scans as a diagnostic test, this test has primarily been used for injuries of the proximal descending thoracic aorta. Motion artifact in the proximal ascending aorta can be difficult to interpret on CT. CT scan gated to cardiac motion may better delineate the ascending aorta and provide increased resolution.35
The diagnostic controversy regarding CT for thoracic injuries may lie in the technology. CT scan technology has evolved at a very rapid rate. It is important to understand that a 4-channel 16-detector machine has different capabilities than a 64-channel/detector machine. With increasing technical complexity, the protocols for obtaining the CT examination such as number and spacing of detectors, channels, pitch, slice thickness, contrast injection, and timing can significantly alter the information obtained.
The raw CT data are then manipulated in a “postprocessing” function to deliver the final images. The previous static CT film images are now read on digital displays where a knowledgeable observer can further manipulate the image. Three-dimensional reconstructions, while impressive to view, take a lot of processing resources and have not added a lot to the evaluation of blunt aortic injuries (Fig. 26-7). Multiplanar reformatting is a postprocessing mode where the CT slice can be angled and positioned to best display the pathology. This is most useful for the evaluation of blunt aortic injury when the CT slice/virtual gantry is aligned with the curvature of the ascending/arch/descending thoracic aorta and the slices can traverse through the aorta (Fig. 26-8). This is very helpful not only for diagnosis but also for planning, selecting device, and evaluating landing/seal zones for the device. Centerline flow analysis displays the aorta as a straight line along its center allowing precise measurements of diameter and accurate measurements of seal zones/landing zones for planning (Fig. 26-9). It is our observation and a local postulate that as the technology progresses, if the clinician directly caring for the patient cannot manipulate and interpret the images himself or herself, much useful information as well as artifacts may not be appreciated. This may explain a lot of the confusion regarding multiple conflicting reports and opinions on the utility of CT for screening or diagnosis. With appropriate scanners, protocols, processing, display, and experience, CT potentially could yield more information than catheter angiography.
FIGURE 26-7 A three-dimensional reconstruction of the CT in a patient with an injury to the aortic isthmus showing the thoracic endograft deployed.
FIGURE 26-8 Multiplanar reformatting display of a typical injury through the descending thoracic aorta distal to the left subclavian artery. This allows the viewer to align the slice along the axis of the aorta. The small cube in the lower right corner represents the orientation.
FIGURE 26-9 Centerline flow analysis of a patient with injury at the aortic isthmus. This view electronically straightens the aorta along the centerline axis of flow allowing accurate measurements regarding landing zones/seal areas and the device length to the determined. This analysis shows that by covering the left subclavian artery, a 15- to 16-mm proximal seal area is available and a 35-mm area will need to be covered. This display also shows the average aortic diameter to be 19 mm. This can be useful to plan difficult cases for which the landing zones/seal areas are difficult to precisely determine.
If a mediastinal hematoma is visualized on CT, formal aortography is usually obtained to specifically determine the site(s) of the injury(s) and to identify any vascular anomalies that require modifications in the operative approach. This is also uniformly done as part of the process immediately prior to placing an aortic endograft. Decision trees can be constructed to aid the surgeon in reaching a diagnosis and treating a patient with aortic injury (Fig. 26-10). As experience is developed with catheter-based methods, however, the CT scan is also helpful for preoperative planning for stent graft repair and evaluation for access. TEE has added little in the screening or diagnosis of thoracic aortic injury. Magnetic resonance angiography (MRI) can generate similarly detailed information; however, its application in these potentially unstable trauma patients is not currently practical.
FIGURE 26-10 (A) Algorithm for an approach to patients with suspected thoracic vascular injury. (B) Algorithm for the evaluation and treatment of a patient suspected of having a blunt injury to the thoracic aorta.
In penetrating thoracic trauma, catheter angiography is indicated for suspected aortic, innominate, carotid, or subclavian arterial injuries. Different thoracic incisions are required for proximal and distal control of each of these vessels. Arteriography, therefore, is essential for localizing the injury and planning the appropriate incision. Proximity of a missile trajectory to the brachiocephalic vessels, even without any physical findings of vascular injury, can be an indication for arteriography. Although aortography may also be useful in hemodynamically stable patients with suspected penetrating aortic injuries, its limitations in this setting must be recognized. A “negative” aortogram may convey a false sense of security if the laceration has temporarily “sealed off” or if the column of aortic contrast overlies a small area of extravasation (Fig. 26-11). Therefore, an effort must be made to obtain views tangential to possible injuries (Figs. 26-12 and 26-13).
FIGURE 26-11 Misdiagnosis by aortography. (A) Chest radiograph of a patient with a tiny puncture wound from a Philips screwdriver at the left sternal border in the second intercostal space. The patient arrived in the emergency room 30 minutes after being wounded and had stable vital signs for the following 48 hours. (B) Anteroposterior projection of the aortogram was interpreted as showing no injury. (C) Left anterior oblique projection of the aortogram was also interpreted as showing no injury. (D) Near-lateral projection of the aortogram was also read as normal by staff radiologist. (E) Subtraction aortography in the lateral projection demonstrates tiny outpouching of the thoracic aorta anteriorly at the base of the innominate artery and posteriorly on the undersurface of the transverse aortic arch (arrows). Penetrating injury of the transverse aortic arch was confirmed intraoperatively. (Reproduced with permission from Mattox KL. Approaches to trauma involving the major vessels of the thorax. Surg Clin North Am. 1989;69:83. © Elsevier.)
FIGURE 26-12 Plain chest x-ray of a patient with a penetrating wound of the ascending aorta.
FIGURE 26-13 Aortogram of the patient in Fig. 26-9 demonstrating no apparent injury in the anteroposterior projection, but revealing a defect in the anterior aortic wall on the left anterior oblique projection (arrows).
Following blunt trauma, the potential for thoracic great vessel injury—and, therefore, the need to proceed with aortography—is determined based on (1) the mechanism of injury, (2) physical examination, (3) the standard chest radiograph, or (4) a screening CT scan.
As each of these factors has inherent limitations, all must be considered in concert. Traumatic aortic ruptures following seemingly innocuous mechanisms—including low-speed automobile crashes (<10 mph) with airbag deployment and intrascapular back blows used to dislodge an esophageal foreign body—have been reported. Additionally, 50% of patients with thoracic vascular injuries from blunt trauma present without any external physical signs of injury, and 7% of patients with blunt injury to the aorta and brachiocephalic arteries have a normal-appearing mediastinum on admission chest radiography.
Nonoperative management of blunt aortic injuries should be considered in patients who are unlikely to benefit from an immediate repair:
1. Severe head injury
2. Risk factors for infection:
• Major burns
• Heavily contaminated wounds
3. Severe multisystem trauma with hemodynamic instability and/or poor physiologic reserve
In such instances, nonoperative management is actually a purposeful delay in operation that attempts to achieve physiologic optimization and improve the outcome of repair. Nonoperative management has also been used successfully in cases of “nonthreatening” aortic lesions, for example, minor intimal defects and small pseudoaneurysms. Close observation without operation is similarly reasonable for small intimal flaps involving the brachiocephalic arteries in asymptomatic patients, as many such lesions will heal spontaneously.
With the increased use of endograft repair, as well as patients with increasing number of associated injuries, blunt aortic injuries are often definitively repaired greater than 24 hours after presentation when the patient is optimized. In a report by Demetriades et al. of a multicenter study, delayed repair (>24 hours) of stable blunt thoracic aortic injury was associated with improved survival, but also a longer length of ICU stay and a higher complication rate.32
Although apparent minor vascular injuries may resolve or stabilize, their long-term natural history remains uncertain. Life-threatening complications of great vessel injuries—including rupture and fistulization with severe hemorrhage—occurring more than 20 years after injury are not uncommon.29 Therefore, careful follow-up, including serial imaging studies, is a critical component of nonoperative management. Avoiding hypertension and the use of impulse control agents are also recommended when patients with aortic injuries are treated nonoperatively.
From a technical standpoint, a chronic post-traumatic false aneurysm of the descending thoracic aorta should be a logical indication for placement of an aortic endograft. Beginning in the late 1990s, single case reports and small series of thoracic endografting for acute transections of the proximal descending thoracic aorta were reported. These were often custom devices using aortic or iliac artery extenders.36Not infrequently the left subclavian artery was occluded by the endograft, with subsequent left carotid–subclavian bypass in some cases. Iatrogenic injury to the access site of the femoral or iliac artery was occasionally reported. No reports exist for repair of thoracic ascending/arch/aortic injury and have focused on the proximal descending thoracic aorta.
In the United States three commercial devices have been approved by the Food and Drug Administration for thoracic aortic aneurysms by the end of 2008. These devices are FDA approved for the treatment of thoracic aneurysms and are used off-label in patients with traumatic injuries to the descending thoracic aorta. The average diameter of the thoracic aorta among patients with aortic tears is 19.3 cm. The manufacturers recommend 15–20% oversizing. Thus, these thoracic devices need an aorta diameter of greater than 18 mm. Smaller aortas treated with endografts require custom or off-label abdominal devices. With greater oversizing, compression and infolding have been reported and infolding has resulted in a devastating thrombosis of the aorta. Over 85% of descending thoracic aortic tears are less than 1 cm from the orifice of the subclavian artery. A sealing distance on either side of the pathology of 2 cm is recommended. Additionally a young patient’s aorta has significant angulation in the potential proximal seal zone that can cause leading edge “beaking” and infolding. Thus, consideration for covering the left subclavian orifice occurs and can be influenced by the intracerebral and spinal circulation. Engineering challenges still exist regarding the existing approved thoracic aortic endografts when used in young trauma patients.
Preoperative planning involves a carefully protocolized CT angiogram of chest/abdomen and pelvis, and delineating the size, tortuosity, and angulation of arterial vessels for determination of appropriateness or feasibility of introducer sheaths and devices capable of covering the aortic injury.
Access can often be a problem in young patients, especially females, with small iliac/femoral arteries that prohibit safe introducer sheath placement due to small size mismatch. Currently the smallest commercially available thoracic endografts require a 7- to 8-mm external iliac artery. Direct introduction or sewing of an extra-anatomic graft to the common iliac artery or aorta to allow deployment of endovascular stent grafts may be necessary in such difficult cases. It should be noted that the majority of morbidity/mortality from thoracic endograft repair is from disruption of iliac vessels during endograft placement.
In a composite report using a variety of approved and customized endografts, 239 patients have been reported to have been treated for blunt injury to the proximal descending thoracic aorta (Table 26-6).37Many other small series or single case reports exist. Among the 239 cases there were 9 deaths (3.8%), and 1 paraplegia (<0.5%). Even with potential selection bias, the lower mortality and almost nonexistent paraplegia rate make consideration for endovascular repair very compelling.38 The current trend in trauma is to favor delayed repair of stable patients.32,34,39 Yet to be answered are the engineering challenges of graft compression and infolding as well as available smaller sizes, conformation of the endograft to the curvature of the arch, tailored/branched grafts, and improved delivery systems. The short-term and midterm follow-up have seemed favorable for endovascular stenting.40 However, the long-term fate of the endograft as the aorta dilates with age is yet unanswered. With massive changes in the presenting patient population, technology related to diagnosis and imaging, and engineering improvements in endograft technology, the timing, diagnosis, and management of blunt aortic injuries have been dynamic. The report of Demetriades et al. of the AAST multicenter study with its two follow-up manuscripts documented a shift in original diagnostic modality to CT and a shift to endovascular repair with a decrease in mortality and paraplegia but an increase in device-related and access complications and concern for long-term sequelae.32,34,39 These reports have been the most comprehensive to date, and are a template to track results as the technology evolves. Studies documenting the rate of aortic dilation after endograft repair are being reported41 and will be important for assessing the long-term durability of endograft repair. The technology continues to evolve and improve on addressing the above-mentioned anatomic size challenges and capabilities of endografts available to treat acute injuries to the thoracic aorta.
TABLE 26-6 Comparison of Open Versus Endovascular Treatment of Blunt Thoracic Aortic Injury
It is clear that the treatment for a specific patient will continue to be individualized, and multiple approaches (nonoperative/delayed/open/endograft) will continue to be needed.32,34,39
Indications for urgent transfer to the operating room for thoracotomy include hemodynamic instability, significant hemorrhage from chest tubes, and radiographic evidence of a rapidly expanding mediastinal hematoma (Fig. 26-14).
FIGURE 26-14 Plain chest x-ray in a patient with a blunt injury to the descending thoracic aorta. Note the rightward deviation of both the trachea and nasogastric tube in the esophagus.
In the preoperative phase, whenever possible, patients and their families should be made aware of the potential for neurologic complications—paraplegia, stroke, and brachial plexus injuries—following surgical reconstruction of thoracic great vessels. Careful documentation of preoperative neurologic status is important. With any suspicion of vascular injury, prophylactic antibiotics are administered preoperatively. In hemodynamically stable patients, fluid administration is limited until vascular control is achieved in the operating room. An autotransfusion device should be available. During the induction of anesthesia, wide swings in blood pressure should be avoided; while profound hypotension is clearly undesirable, hypertensive episodes can have equally catastrophic consequences.
The operative approach to great vessel injury depends on both the overall patient assessment and the specific injury. The initial steps of patient positioning and incision selection (Table 26-7) are particularly important in surgery for great vessel injuries, as adequate exposure is important for proximal and distal control. Prepping and draping of the patient should provide access from the neck to the knees to allow management of all contingencies. For the hypotensive patient with an undiagnosed injury, the mainstay of thoracic trauma surgery is the left anterolateral thoracotomy with the patient in the supine position. In stable patients, preoperative arteriography may dictate an operative approach by another incision.
TABLE 26-7 Recommended Incisions for Thoracic Great Vessel Injuries
Appropriate graft materials should be available. While the failure mode of an infected prosthetic graft is a pseudoaneurysm, a saphenous vein graft is a devitalized collagen tube susceptible to bacterial collagenase, which may cause graft dissolution with acute rupture and uncontrolled hemorrhage. Therefore, for vessels larger than 5 mm, a prosthetic graft is the conduit of choice, especially in potentially contaminated wounds. However, due to patency considerations, a saphenous vein graft may need to be used when smaller grafts are required. For fragile vessels, such as the subclavian artery and the aorta in young people, a soft knitted Dacron graft is useful.
Patients with severely compromised physiologic reserve often require damage control injury management to achieve survival. The two approaches to thoracic damage control are (1) definitive repair of injuries using quick and simple techniques that restore survivable physiology during a single operation and less commonly (2) abbreviated thoracotomy that restores survivable physiology and requires a planned reoperation for definitive repairs.30 Severe hilar vascular injuries can be quickly controlled by performing a pneumonectomy using stapling devices. Temporary vessel ligation or placement of intravascular shunts can control bleeding until the subsequent correction of acidosis, hypothermia, and coagulopathy allows the patient to be returned to the operating room. En masse closure of a thoracotomy is more hemostatic than towel-clip closure. A “Bogotá bag” closure or “Vac Pack closure” can be used as a temporary closure of a median sternotomy in cases with associated cardiac dysfunction.
Patients with blunt ascending aortic injuries rarely survive transportation to the hospital. Operative repair usually requires use of total cardiopulmonary bypass and insertion of a Dacron graft. If the sinuses or valves are involved, aortic root replacement with reimplantation of the coronary ostia may be required.35
Penetrating injuries involving the ascending aorta are uncommon (Figs. 26-12 and 26-13). Survival rates approach 50% for patients having stable vital signs on arrival at a trauma center.42 Although primary repair of anterior lacerations can be accomplished without adjuncts, cardiopulmonary bypass may be required if there is an additional posterior injury. The possibility of a peripheral bullet embolus must be considered in these patients.
Transverse Aortic Arch
When approaching an injury to the transverse aortic arch, extension of the median sternotomy to the neck is necessary to obtain exposure of the arch and brachiocephalic branches. If necessary, exposure can be further enhanced by division of the innominate vein. When hemorrhage limits exposure, the use of balloon tamponade is useful as a temporary measure. Simple lacerations may be repaired by lateral aortorrhaphy. With difficult lesions, such as posterior lacerations or those with concomitant pulmonary artery injuries, cardiopulmonary bypass can be used. As with injuries to the ascending thoracic aorta, survival rates approaching 50% are possible.42
Median sternotomy is employed for access to innominate artery injuries. A right cervical extension can be used when necessary. Blunt injuries typically involve the proximal innominate artery (Figs. 26-15and 26-16) and therefore actually represent aortic injuries and require obtaining proximal control at the transverse aortic arch. In contrast, penetrating injuries of the innominate artery may occur throughout its course. Exposure is enhanced by division of the innominate vein.
FIGURE 26-15 Plain chest x-ray of a patient with a blunt injury of the innominate artery. Note that the hematoma is at the thoracic outlet rather than the aortic isthmus.
FIGURE 26-16 Aortogram of the patient in Fig. 26-12 demonstrating the tear involving the proximal innominate artery.
In selected patients with penetrating injuries, a running lateral arteriorrhaphy using 4-0 polypropylene suture is occasionally possible. More often, injuries to the innominate artery require repair via the bypass exclusion technique (Fig. 26-17).43 Bypass grafting is performed from the ascending aorta to the distal innominate artery (immediately proximal to the bifurcation of the subclavian and right carotid arteries) using a Dacron tube graft. The area of injury is avoided until the areas for bypass insertion are exposed. A vascular clamp is placed proximal to the bifurcation of the innominate artery to allow collateral flow to the brain via the right subclavian and carotid arteries. Hypothermia, systemic anticoagulation, or shunting is not required. After the bypass is completed, the area of hematoma is entered, and the injury controlled with a partial occluding clamp (usually at the origin of the innominate artery) and oversewn. If concomitantly injured or previously divided, the innominate vein may be ligated with impunity. If the vein remains intact, a pedicled pericardial flap can be positioned between the vein and overlying graft to prevent erosion.
FIGURE 26-17 (A–C) Drawing depicting the bypass exclusion technique employed in patients with innominate artery injuries. (Copyright © Baylor College of Medicine, 1981.)
The treatment of an iatrogenic tracheal-innominate artery fistula deserves special consideration. These fistulae are usually caused by the concave surface of a low riding tracheostomy tube eroding into the innominate artery. Sentinel bleeding through or around the tracheostomy tube should not be misinterpreted as “tracheitis.” Arteriography during a “stable interval” is generally not helpful in making a precise diagnosis; instead, the possibility of a tracheal-innominate fistula should be evaluated via bronchoscopy in the operating room. With massive bleeding, control is achieved by performing orotracheal intubation, removing the tracheostomy tube, and directly tamponading the bleeding digitally through the tracheotomy during transport to the operating room. Through a median sternotomy with a right neck extension, the innominate artery is ligated at its origin from the aorta and distally just before the division into the carotid and subclavian arteries. Despite a greater than 25% chance of neurologic complications, no attempt should be made at revascularization, since delayed graft infection with its dreaded complications inevitably occurs.
Descending Thoracic Aorta
Prehospital mortality is 85% for patients with blunt injury to the descending thoracic aorta.44 In patients who arrive at the hospital alive, the majority of blunt aortic injuries are located at the isthmus (Fig. 26-18). Patients presenting with an injury in the mid-descending thoracic aorta or distally, near the diaphragm, are far less common (Fig. 26-19). Multiple blunt aortic injuries are rare, but may occur.
FIGURE 26-18 Aortogram demonstrating the classic intimal tear and traumatic pseudoaneurysm of the descending thoracic aorta.
FIGURE 26-19 Aortogram in a patient with blunt chest trauma demonstrating an intimal tear of the descending thoracic aorta at the diaphragm.
Injury to the descending thoracic aorta is often accompanied by other organ injuries. If the patient has a stable thoracic hematoma and concomitant abdominal injury, laparotomy should be the initial procedure. For the patient with a rapidly expanding hematoma, however, repair of the thoracic injury should be the primary therapeutic goal. Sequencing is driven by the lesion that is most likely to cause exsanguination.
The current standard technique of repair involves clamping and direct reconstruction (Table 26-8). Three commonly employed adjuncts to this approach are (1) pharmacological agents, (2) temporary, passive bypass shunts, and (3) pump-assisted atriofemoral bypass or cardiopulmonary bypass. In the latter approach, two options exist: traditional pump bypass, which requires heparin, and use of centrifugal (heparinless) pump circuits. All three of these adjunctive approaches to the clamp and repair principle should be in the armamentarium of the surgeon, who must choose the approach most appropriate to the specific clinical situation.
TABLE 26-8 Current Therapeutic Approaches to the Management of Thoracic Aortic Injuries
Injury to the descending thoracic aorta is approached via a posterolateral thoracotomy through the fourth intercostal space. The injury usually originates at the medial aspect of the aorta at the level of the ligamentum arteriosum; however, one must take care to avoid missing a second injury (usually at the level of the diaphragm).
The initial objective is proximal control; therefore, the transverse aortic arch is exposed, and umbilical tapes are passed around the arch between the left carotid and subclavian arteries. Similarly, the subclavian artery is encircled with umbilical tape. Care should be taken to avoid injuring the left recurrent laryngeal nerve though this is often difficult to visualize in the hematoma. If it is suspected that the tear extends to the aortic arch or ascending aorta, cardiopulmonary bypass should be available in the operating room. If the patient has had previous coronary artery bypass surgery with use of the left internal mammary artery as a conduit, repair may require cardiopulmonary bypass perhaps with profound hypothermic circulatory arrest to eliminate the need to clamp the left subclavian artery.
Vascular clamps are applied to three locations: proximal aorta, distal aorta, and left subclavian artery. Close communication between anesthesiologist and surgeon is essential to maintain stability of hemodynamic parameters before, during, and after clamping. The use of vasodilators prevents cardiac strain during clamping. The hematoma is entered and back-bleeding from intercostal arteries is controlled. Care is taken to avoid indiscriminate ligation of intercostal vessels; only those required for adequate repair of the aorta should be ligated. The proximal and distal ends of the aorta are completely transected and dissected away from the esophagus; this maneuver allows full-thickness suturing while minimizing the risk of a secondary aortoesophageal fistula. The injury is then repaired by either end-to-end anastomosis or graft interposition. Graft interposition is utilized in more than 85% of reported cases. Prior to clamp removal, volumes of fluid (blood and crystalloid) may need to be administered to avoid clamp release hypotension.
For patients undergoing repair of blunt descending thoracic aortic injury, the reported mortality ranges from 0% to 55% (average 13%).37,45 As expected in these victims of major blunt trauma, the mortality is primarily associated with multisystem trauma, and is ultimately due to head injury, infection, respiratory insufficiency, and renal insufficiency.
The most feared complication of great vessel injury is paraplegia. Utilization of protective adjuncts when repairing descending thoracic aortic injuries remains a topic of considerable debate. There have been proponents of the use of passive shunts and cardiopulmonary bypass, with and without heparinization. The mortality rate with the use of routine cardiopulmonary bypass is probably secondary to the massive cerebral, abdominal, or fracture site hemorrhage that occurs in these victims of multisystem trauma. Recent experience using centrifugal pumps for left heart bypass without heparinization has provided an attractive alternative for those who wish to use controlled flow bypass without systemic anticoagulation. This also allows unloading of the left heart during clamping, which can be helpful in patients with cardiac disease. The use of bypass systems, however, is not without complications. In the trauma patient, difficulty inserting cannulae may occur due to patient position, the presence of periaortic hematoma, and time constraints imposed by an expanding, pulsatile, uncontrolled hematoma. Intraoperative and postoperative complications include bleeding at the cannulation sites and false aneurysm formation.
Use of simple clamp and repair for injuries to the descending thoracic aorta (without the use of systemic anticoagulation or shunts) is a technique that continues to be used with excellent results. Sweeney in 1992 reported using simple clamp and repair in 75 patients, only 1 of whom developed postoperative paraplegia.
Ultimately, the determinants of postoperative paraplegia are multifactorial (Table 26-9); therefore, the precise causes cannot be precisely identified in an individual patient. Paraplegia has been associated with perioperative hypotension, injury or ligation of the intercostal arteries, and duration of clamp occlusion during repair.46 However, there are reports of patients surviving surgery without paraplegia despite having long segments of aorta replaced and ligation of multiple intercostal arteries. The length of cross-clamp time does not directly correlate with occurrence of paraplegia. A cross-clamp time under 30 minutes has been argued to provide a safe margin against paraplegia, and shunting techniques have been recommended when longer cross-clamp times are necessary.46 The use of a shunt, however, does not offer protection for the area of the spinal cord supplied by the arteries between the clamps. Furthermore, patients requiring longer clamp time or interposition grafts have more extensive injuries than those requiring shorter clamp times or end-to-end anastomoses. Thus, it is likely that an increased incidence of paraplegia associated with longer clamp times is secondary to more extensive disruption of intercostal arteries and other flow to the anterior spinal artery caused by the original injury.
TABLE 26-9 Possible Contributing Factors Related to the Multifactorial Development of Paraplegia Following Operations for Thoracic Great Vessel Injury
Various monitoring techniques are available to assess the effect of aortic occlusion on the spinal cord, including the measurement of somatosensory- and motor-evoked potentials. Although correlation appears to exist between loss of somatosensory-evoked potentials, duration of loss of conduction, and postoperative paraplegia, the use of this modality is not common to all trauma centers, the interpretation of results is still being debated, and actual positive applicability requires further delineation.
Regardless of the technique used, paraplegia occurs in approximately 10% of these patients (range 0–22%).37,45 No prospective, randomized trial has identified the superiority of any single method. Therefore, the choice of operative technique does not infer legal liability when paraplegia occurs.
Even with potential selection bias in favor of endografts, the low mortality and almost nonexistent paraplegia rate make the use of endografting very compelling. The reported complications of graft migration, enfolding, compression, occlusion of the subclavian artery, and problems at the entry site are all technical and engineering challenges that may potentially be solved by new commercial devices.
Subclavian vascular injuries can involve any combination of the following regions: intrathoracic, thoracic outlet, cervical (zone 1), and upper extremity. Preoperative arteriography allows for planning appropriate incision(s) to obtain adequate exposure and control.
A cervical extension of the median sternotomy is employed for exposure of right-sided subclavian injuries. For left subclavian artery injuries, proximal control is obtained through an anterolateral thoracotomy (above the nipple, second or third intercostal space), while a separate supraclavicular incision provides distal control. Although these incisions can be connected to create a formal “book” thoracotomy, this results in a high incidence of postoperative “causalgia”-type neurologic complications and its use should be limited to highly selected left-sided subclavian artery injuries.
In obtaining exposure, it is important to avoid injuring the phrenic nerve (anterior to the scalenus anticus muscle). In subclavian vascular trauma, a high associated rate of brachial plexus injury is seen; thus, documentation of preoperative neurologic status is important. Intraoperative iatrogenic injury to the brachial plexus should also be avoided.
In most instances, repair requires either lateral arteriorrhaphy or graft interposition. It is unusual that an end-to-end anastomosis can be employed. Associated injuries to the lung should be managed with stapled wedge resection or pulmonary tractotomy.47 One pitfall in subclavian injuries is failure to anticipate the exposure necessary for proximal control. When approaching the subclavian artery via the deltopectoral groove without proximal control, exsanguination may occur. Resection of the clavicle may aid in proximal control. A combination of supraclavicular and infraclavicular incisions may be used to avoid the morbidity of clavicular resection. A mortality rate of 4.7% for patients with subclavian artery injuries has been reported, but death is often due to associated injuries.
With the density of vascular structures in the thoracic outlet, and the morbidity of the thoracic incisions needed for proximal control, it would seem that endovascular techniques to address subclavian artery injuries would be advantageous. There are increasing reports of endovascular approaches to the subclavian artery in both stable and unstable patients.48 If diagnostic arteriography is performed in the OR, a balloon catheter can be left in the proximal left subclavian artery for proximal control.
This is most applicable in centers where acute vascular imaging for trauma is available in the operating room and arteriography/covered stent placement can be performed by the trauma/cardiovascular surgeon. With a vascular imaging capable bed, a C-arm with vascular capability, and a simplified set of endovascular tools, even an unstable trauma patient can be brought to the operating room where he or she can be resuscitated, imaged/diagnosed, and bleeding controlled with both open and endovascular techniques.
Left Carotid Artery
The operative approach for injuries of the left carotid artery mirrors that used for an innominate artery injury: a median sternotomy with a left cervical extension added when necessary. As with other great vessel injuries, neither shunts nor pumps are employed. With transection at the left carotid origin, bypass graft repair is preferred over end-to-end anastomosis. Intraoperatively, a carotid shunt can be used to temporize these until resources/assistants can be gathered in the OR.
The intrapericardial pulmonary arteries are approached via median sternotomy. Minimal dissection is needed to expose the main and proximal left pulmonary arteries.49 Exposure of the intrapericardial right pulmonary artery is achieved by dissecting between the superior vena cava and ascending aorta. Although anterior injuries can be repaired primarily without adjuncts, repair of a posterior injury usually requires cardiopulmonary bypass. Mortality rates for injury to the central pulmonary arteries or veins are greater than 70%.22
Distal pulmonary artery injuries present with massive hemothorax and are repaired through an ipsilateral posterolateral thoracotomy. When there is a major hilar injury, rapid pneumonectomy may be a lifesaving maneuver. The use of a large tamponading balloon catheter may control exsanguinating hemorrhage.
Internal Mammary Artery
The internal mammary artery in a young patient is capable of flows in excess of 300 mL/min. Injuries to this artery can produce extensive hemothorax or even pericardial tamponade, simulating a cardiac injury. Such injuries are usually serendipitously discovered at the time of thoracotomy for suspected great vessel or heart injury.
Persistent hemothorax can be caused by simple lacerations of the intercostal arteries. Because of difficulty in exposure, precise ligature can be difficult. At times, control must be achieved by circumferential ligatures around the rib on either side of the intercostal vessel injury.
Thoracic Vena Cava
Isolated injury to the suprahepatic inferior or superior vena cava is infrequently reported. Injury at either location has a high incidence of associated organ trauma and carries a mortality rate greater than 60%. Intrathoracic inferior vena cava injury produces hemopericardium and cardiac tamponade. Exposure of the thoracic inferior vena cava is extremely difficult unless the patient is placed on total cardiopulmonary bypass with the inferior cannula inserted via the groin in the abdominal inferior vena cava. Repair is exposed by a right atriotomy and intracaval balloon occlusion to prevent air entering the cannula and massive blood return to the heart except via the hepatic veins. Repair is achieved from inside the cava via the right atrium. Superior vena cava injuries are repaired by lateral venorrhaphy. At times, an intracaval shunt is necessary.50 For complex injuries a PTFE patch or Dacron interposition tube graft can be used and is more expedient than the time-consuming construction of saphenous vein panel grafts.
Injury to the pulmonary veins is difficult to manage through an anterior incision. With major hemorrhage, temporary occlusion of the entire hilum may be necessary. If a pulmonary vein must be ligated, the appropriate lobe needs to be resected. Pulmonary vein injuries are often associated with concomitant injuries to the heart, pulmonary artery, aorta, and esophagus.
The operative exposure of the subclavian veins parallels that described for subclavian artery injuries: median sternotomy with cervical extension for right-sided injuries and left anterolateral thoracotomy with a separate supraclavicular incision for left-sided injuries. In most instances, repair requires either lateral venorrhaphy or ligation.
The azygos vein is not usually classified as a thoracic great vessel, but because of its size and high flow, azygos vein injuries must be considered potentially fatal. Penetrating wounds of the thoracic outlet can produce combinations of injuries involving the azygos vein, innominate artery, trachea or bronchus, and superior vena cava. These complex injuries have a very high mortality rate, and are particularly difficult to control if approached through a median sternotomy. Combined incisions and approaches are frequently needed for successful repair. When injured, the azygous vein is best managed by suture ligature of both sides of the injury (Fig. 26-20). Concomitant injury to the esophagus and bronchus should be considered and ruled out.51
FIGURE 26-20 Injury to the azygos vein with control with lateral repair, ligation, division, and oversewing. (Copyright © Baylor College of Medicine, 2005.)
Mediastinal Traverse Injuries
Because injuries from both stab and gunshot wounds that traverse the mediastinum are classically felt to have a high probability of injury to the thoracic great vessels and other critical structures, mandatory exploration has been advocated in the past. The evaluation of stable patients using less invasive means—combined aortography, bronchoscopy, echocardiography, and esophagoscopy—has been described. A thoracic CT scan will often show the bullet trajectory and guide a need for surgery or additional diagnostic tests.
Thoracic Duct Injury
Injuries to the thoracic great vessels may be complicated by concomitant thoracic duct injury, which, if unrecognized, may produce devastating morbidity due to marked nutritional depletion.52 Diagnosed by chylous material draining from the chest tube, this condition is usually treated medically. Continued chest tube drainage, coupled with a diet devoid of long-chain fatty acids, usually results in spontaneous closure in less than 1 month. Prolonged hyperalimentation beyond 3 weeks has not consistently resulted in spontaneous closure of thoracic duct fistula. If thoracotomy is required, a fatty meal or heavy cream to increase the chylous flow and facilitate identification of the fistula is given to the patient a few hours before surgery. The fistula is simply ligated with fine monofilament suture (6-0).
Systemic Air Embolism
A fistula between a pulmonary vein and bronchiole due to a penetrating lung injury results in systemic air embolism. The fistula allows air bubbles to enter the left heart and embolize to the systemic circulation, including the coronary and cerebral arteries (Fig. 26-21). Intrabronchial pressure above 60 torr increases the incidence of this complication.53 Manifestations include seizures and cardiac arrest. Resuscitation requires thoracotomy, clamping of the pulmonary hilum to prevent further air embolization, and aspiration of air from the left ventricle and ascending aorta. Cardiopulmonary bypass can be considered; however, very few survivors have been reported.
FIGURE 26-21 Drawing depicting the mechanism of systemic air embolism following a penetrating lung injury. (Copyright © Baylor College of Medicine, 1979.)
Foreign Body Embolism
Because of their central location, the thoracic great vessels may serve as both an entry site and final resting place for intravascular bullet emboli.54 These migratory foreign bodies present a diagnostic and therapeutic dilemma. As the result of intravascular embolization, bullets may produce infection, ischemia, or injury to organs distant from the site of trauma.
Bullets and catheters can embolize to the pulmonary vasculature; 25% of migratory bullets finally lodge in the pulmonary arteries (Fig. 26-6).54 Although small fragments, such as those the size of a BB, can probably be left in place without causing problems, catheter emboli and larger bullet emboli should be removed to prevent pulmonary thrombosis, sepsis, or other complications. Percutaneous retrieval of the foreign body using transvenous catheters and fluoroscopic guidance may obviate the need for thoracotomy.
A significant portion of the in-hospital mortality associated with great vessel injury is secondary to the nature of the multisystem trauma in this group of patients. The operating surgeon is best qualified to direct the patient’s postoperative management. Careful hemodynamic monitoring, with avoidance of both hypertension and hypotension, is critical. While urinary output is a generally a good indicator of cardiac function, for the patient with massive injuries, Swan–Ganz monitoring is often necessary to optimize hemodynamic parameters and manage fluids, pressors, and vasodilators.
Various pulmonary problems—including atelectasis, respiratory insufficiency, pneumonia, and adult respiratory distress syndrome—represent the primary postoperative complications in this group of patients. The presence of pulmonary contusions and the potential for development of adult respiratory distress syndrome mandate that fluid administration be carefully monitored. Ventilatory strategies to address potential complications of these lung injuries can be used. Patient mobility is important, and adequate medication for pain relief results in fewer pulmonary complications. For the management of pain related to a thoracotomy or multiple rib fractures, postoperative thoracic epidural anesthesia can be considered in stable patients without spinal injuries; alternatively, intercostal nerve blocks can be performed intraoperatively and repeated in the ICU.
Postoperative hemorrhage may be due to a technical problem, but is often the result of coagulopathy related to hypothermia, acidosis, and massive blood transfusion. Coagulation studies can be carefully monitored and corrected with administration of appropriate blood products. Blood draining via chest tubes can be collected and autotransfused.
The presence of a prosthetic vascular graft requires special attention aimed at avoiding bacteremia. During the initial resuscitation of these critically injured patients, various intravascular lines are often rapidly placed at the expense of strict sterile technique; all such lines should be replaced after the patient has stabilized in the ICU. Antibiotic therapy should be continued into the postoperative period until potential sources of infection are eliminated. Patients are counseled regarding the necessity of antibiotic prophylaxis during invasive procedures, including dental manipulations.
Most late complications are related to infections or sequelae from other injuries. Long-term complications specifically related to the vascular repair—including stenosis, thrombosis, arteriovenous fistula, graft infection, and pseudoaneurysm formation—are uncommon.
1. Ivatury RR. Injury to the heart. In: Moore EE, Feliciano DV, Mattox KL, eds. Trauma. 5th ed. New York: McGraw-Hill; 2004.
2. Campbell NC, Thomsen SR, Murkart DJ, et al. Review of 1198 cases of penetrating cardiac trauma. Br J Surg. 1997;84:1737.
3. Thourani VH, Feliciano DV, Cooper WA, et al. Penetrating cardiac trauma at an urban trauma center: a 22 year perspective. Am Surg. 1999; 65:811.
4. Wall MJ Jr, Mattox KL, Chen CD, Baldwin JC. Acute management of complex cardiac injuries. J Trauma. 1997;42:905.
5. LeMaire SA, Wall MJ Jr, Mattox KL. Needle embolus causing cardiac puncture and chronic constrictive pericarditis. Ann Thorac Surg. 1998; 65:1786.
6. Maron BJ, Link MS, Wang PJ, et al. Clinical profile of commotio cordis: an underappreciated cause of sudden death in young during sports and other activities. J Cardiovasc Electrophysiol. 1999;10:114.
7. Wall MJ Jr, Mattox KL, Wolf DA. The cardiac pendulum—blunt rupture of the pericardium with strangulation of the heart. J Trauma. 2005; 59:136.
8. Baumgartner FJ, Rayhanabad J, Bongard FS, et al. Central venous injuries of the subclavian–jugular and innominate–caval confluences. Tex Heart Inst J. 1999;26:177.
9. Medizinische Klinik IV. Perforation und Ruptur Koronaryarterien. Herz. 1998;23:311.
10. Ivatury RR, Simon RJ, Rohman M. Cardiac complications. In: Mattox KL, ed. Complications of Trauma. New York: Churchill Livingstone; 1994:409–428.
11. Lee RC. Injury by electrical forces: pathophysiology, manifestations, and therapy. Curr Probl Surg. 1997;34:677.
12. Mattox KL, Flint LM, Carrico CJ, et al. Blunt cardiac injury (formerly termed “myocardial contusion”) [editorial]. J Trauma. 1992;31:653.
13. Galindo Gallego M, Lopez-Cambra MJ, Fernandez-Acenero MJ, et al. Traumatic rupture of the pericardium. Case report and literature review. J Cardiovasc Surg (Torino). 1996;37:187.
14. American College of Surgeons, Committee on Trauma. Advanced Trauma Life Support. Chicago: American College of Surgeons; 2008.
15. Biffl WD, Moore EE, Johnson JL. Emergency department thoracotomy. In: Moore EE, Feliciano DV, Mattox KL, eds. Trauma. 5th ed. New York: McGraw-Hill; 2004.
16. Bertinchant JP, Polge A, Mohty D, et al. Evaluation of incidence, clinical significance and prognostic value of circulating cardiac troponin I and T elevation in hemodynamically stable patients with suspected myocardial contusion after blunt chest trauma. J Trauma. 2000;48:924.
17. Rozycki GS, Schmidt JA, Oschner MG, et al. The role of surgeon-performed ultrasound in patients with possible penetrating wounds: a prospective multicenter study. J Trauma. 1998;45:190.
18. Mattox KL, Wall MJ Jr. Newer diagnostic measures and emergency management. Chest Surg Clin N Am. 1997;7:214.
19. Meyer DM, Jessen ME, Grayburn PA. Use of echocardiography to detect occult cardiac injury after penetrating thoracic trauma: a prospective study. J Trauma. 1995; 39:902.
20. Durham LA, Richardson R, Wall MJ, et al. Emergency center thoracotomy: impact of prehospital resuscitation. J Trauma. 1992;32:779.
21. Mattox KL, Limacher MC, Feliciano DV, et al. Cardiac evaluation following heart injury. J Trauma. 1985;25:758.
22. Matttox KL, Feliciano DV, Beall AC Jr, et al. Five thousand seven hundred sixty cardiovascular injuries in 4459 patients. Epidemiologic evolution 1958–1988. Ann Surg. 1989;209:698.
23. Alfaro J, Varela G, De-Miguel E, de Nicilas M. Successful management of a tracheo-innominate artery fistula following placement of a wire self-expandable tracheal Gianturco stent. Eur J Cardiothorac Surg. 1993; 7:615.
24. Horton TG, Cohn SM, Heid MP, et al. Identification of trauma patients at risk of thoracic aortic tear by mechanism of injury. J Trauma. 2000;48:1008.
25. Rogers FB, Osler TM, Shackford SR. Aortic dissection after trauma: case report and review of the literature. J Trauma. 1996;41:906.
26. Mattox KL. Prehospital management of thoracic injury. Surg Clin North Am. 1989;69:21.
27. Mattox KL, Bickell W, Pepe P, et al. Prospective MAST study in 911 patients. J Trauma. 1989;29:1104.
28. Bickell WH, Wall MJ, Pepe PE, et al. Immediate versus delayed fluid resuscitation for hypotensive patients with penetrating torso injuries. N Engl J Med. 1994;331:1105.
29. McCollum CH, Graham JM, Noon GP, et al. Chronic traumatic aneurysms of the thoracic aorta: an analysis of 50 patients. J Trauma. 1979;19:248.
30. Wall MJ Jr, Soltero E. Damage control for thoracic injuries. Surg Clin North Am. 1997;77:863.
31. Wheat MW Jr, Palmer RF, Bartley TD, et al. Treatment of dissecting aneurysm of the aorta without surgery. J Thorac Cardiovasc Surg. 1965;50:364.
32. Demetriades D, Velmahos GC, Scalea TM, et al. Blunt traumatic thoracic aorta injuries: early or delayed repair—results of an American Association for the Surgery of Trauma prospective study. J Trauma. 2009;66:967–973.
33. Dyer DS, Moore EE, Ilke DN, et al. Thoracic aortic injury: how predictive is mechanism and is chest computed tomography a reliable screening tool? A prospective study in 1561 patients. J Trauma. 2000; 48:673.
34. Demetriades D, Velmahos GC, Scalea TM, et al. Diagnosis and treatment of blunt thoracic blunt thoracic aortic injuries: changing perspectives. J Trauma. 2008;64:1415–1419.
35. Wall MJ Jr, Tsai PI, Gilani R, et al. Challenges in the diagnosis of unusual presentations of blunt injury to the ascending aorta and aortic sinuses. J Surg Res. 2010;163:176–178 [Epub ahead of print].
36. Tehrani HY, Peterson BG, Katariya K, et al. Endovascular repair of thoracic aortic tears. Ann Thorac Surg. 2006;82:873.
37. Mattox KL, Whigham C, Fisher RG, et al. Blunt trauma to the thoracic aorta: current challenges. In: Lumsden AB, Lin PH, Chen C, Parodi JC, eds. Advanced Endovascular Therapy of Aortic Disease. London: Blackwell Publishing; 2007.
38. Patel HJ, Williams DM, Upchruch GR, et al. A comparative analysis of open and endovascular repair for the ruptured descending thoracic aorta. J Vasc Surg. 2009;50:1265–1270.
39. Demetriades D, Velmahos GC, Scalea TM, et al. Operative repair or endovascular stent graft in blunt traumatic thoracic aortic injuries: results of an American Association for the Surgery of Trauma multicenter study. J Trauma. 2008;64:561–571.
40. Fernandez V, Mestres G, Maeso J, et al. Endovascular treatment of traumatic thoracic aortic injuries: short- and medium-term follow-up. Ann Vasc Surg. 2010;24:160–166.
41. Forbes TL, Harris JR, Lawlor K, et al. Aortic dilation after endovascular repair of blunt traumatic thoracic aortic injuries. J Vasc Surg. 2010;52: 45–48.
42. Pate JW, Cole FH, Walker WA, et al. Penetrating injuries of the aortic arch and its branches. Ann Thorac Surg. 1993;55:586.
43. Johnston RH Jr, Wall MJ, Mattox KL. Innominate artery trauma: a thirty-year experience. J Vasc Surg. 1993;17:134.
44. Parmley LF, Mattingly TW, Marian WC, et al. Nonpenetrating traumatic injury of the aorta. Circulation. 1958;17:1086.
45. von Oppell UO, Dunne TT, De Groot MK, et al. Traumatic aortic rupture: twenty-year metaanalysis of mortality and risk of paraplegia. Ann Thorac Surg. 1994;58:585.
46. Mattox KL. Fact and fiction about management of aortic transection [editorial]. Ann Thorac Surg. 1989;48:1.
47. Wall MJ, Hirshberg A, Mattox KL. Pulmonary tractotomy with selective vascular ligation for penetrating injuries to the lung. Am J Surg. 1994;168:1.
48. Gilani R, Tsai P, Wall JR, Mattox KL, Lin P. Endovascular management of complex subclavian artery injuries. J Trauma. 2012 (in press).
49. Clements RH, Wagmeister LS, Carraway RP. Blunt intrapericardial rupture of the pulmonary artery in a surviving patient. Ann Thorac Surg. 1997;64:258.
50. DeBakey ME, Simeone FA. Battle injuries of arteries in World War II: an analysis of 2,471 cases. Ann Surg. 1946;123:534.
51. Wall MJ Jr, Mattox KL, DeBakey ME. Injuries to the azygous venous system. J Trauma. 2006;60:357.
52. Dulchavsky SA, Ledgerwood AM, Lucas CE. Management of chylothorax after blunt chest trauma. J Trauma. 1988;28:1400.
53. Graham JM, Beall AC Jr, Mattox KL, et al. Systemic air embolism following penetrating trauma to the lung. Chest. 1977;72:449.
54. Mattox KL, Beall AC Jr, Ennix CL, et al. Intravascular migratory bullets. Am J Surg. 1979;137:192.