Heart and Thoracic Vascular Injuries
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.
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.14 Two 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.19 compared 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
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.
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.
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