Chapter 26 - McGraw-Hill Professional

485 

CHAPTER 26 

Heart and Thoracic Vascular Injuries 

Matthew J. Wall, Jr., Peter Tsai, and Kenneth L. Mattox 

INTRODUCTION 

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. 

HEART INJURY 

■ 

Incidence 

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. 

■ 

Mechanism 

Penetrating Cardiac Injury 

Penetrating trauma is a common mechanism for cardiac injury, 

with the predominant etiology being from firearms and knives 4 

( 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

486 Management of Specific Injuries 

SECTION 3 X 

TABLE 26-1 Etiology of Traumatic Heart Diseases 

I. Penetrating 

(A) Low entry 

1. Stab wounds—knives, swords, ice picks, 

fence posts, wire, sports 

(B) High entry 

2. Gunshot wounds—handguns, rifles, nail guns, 

lawnmower projectiles 

3. Shotgun wounds—close range versus distant 

4. Blast—fragments 

II. Nonpenetrating (blunt) 

(A) Motor vehicle accident 

(B) Vehicular–pedestrian accident 

(C) Falls from height 

(D) Crush—industrial accident 

(E) Blast—explosives, fragments, improvised 

explosive devices 

(F) Assault 

(G) Sternal or rib fractures 

(H) Recreational—sporting events, rodeo, baseball 

III. Iatrogenic 

(A) Catheter induced 

(B) Pericardiocentesis induced 

(C) Percutaneous interventions 

IV. Others 

(A) Electrical 

(B) Embolic—missiles 

(C) Factitious—needles, foreign bodies 

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. 

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. 

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 

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,


487 

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 

Electrical Injury 

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 

■ 

Clinical Presentation 

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. 


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 

Pericardial Injury 

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. 

■ 

Evaluation 

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 

CHAPTER 26 X


SECTION 3 X 

protocol are evaluated and established. 14 Two large-bore intravenous 

catheters are inserted, and blood is typed and crossmatched. 

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 

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. 

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. 

Electrocardiography 

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 seconddegree 

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. 

Cardiac Enzymes 

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 

Echocardiography 

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


489 

■ 

Treatment 

FIGURE 26-1 Transdiaphragmatic exploration of the pericardium 

during laparotomy. ( Copyright © Baylor College of Medicine. ) 

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 ). 

Penetrating Injury 

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. 

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 

CHAPTER 26 X 

FIGURE 26-2 Left anterior thoracotomy (extension across the sternum if required). ( Copyright © Baylor College of Medicine, 2005. )


SECTION 3 X 

A 

B 

C 

D 

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. ) 

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 

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. 


Much debate and discussion has occurred about the clinical 

relevance of “cardiac contusion.” Most trauma surgeons suggest


491 

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. ) 

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 

■ 

Results 

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 

Penetrating cardiac injury 

Sinus/supraventricular tachycardia 

ST segment changes associated with ischemia 

Supraventricular tachycardia 

Ventricular tachycardia/fibrillation 

Blunt cardiac injury 

Sinus tachycardia 

ST segment, T wave abnormalities 

Atrioventricular conduction defects, bradycardia 

Ventricular tachycardia/fibrillation 

Electrical injury 

Sinus tachycardia 

ST segment, T wave abnormalities 

Conduction/bundle branch delay 

Axis deviation 

Prolonged QT intervals 

Paroxysmal supraventricular tachycardia 

Atrial fibrillation 

Ventricular tachycardia, fibrillation 

Asystole (lightning strike) 



SECTION 3 X 

■ 

Follow-Up 

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 

19 , 21 

some. 

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 

Common origin of innominate and left carotid arteries 

(“bovine arch”) 

Ductus diverticulum 

Persistent left ductus arteriosus 

Aberrant takeoff of the right subclavian artery from the 

descending thoracic aorta 

Dextroposition of the thoracic aorta 

Coarctation of the thoracic aorta 

Origin of left vertebral artery off the aortic arch 

Pseudocoarction of the thoracic aorta (“kinked aorta”) 

Double aortic arch 

Right ductus arteriosus 

Persistent truncus arteriosus 

Cervical aortic arch (persistent complete third aortic 

arch) 

Absence of the internal carotid artery 

Cardio-aortic fistula 

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 

(d P /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


493 

TABLE 26-4 Groups of Patients with Thoracic Aortic Injury 

Group Description Time to Diagnosis Location of Death Mortality (%) Cause of Death 

1 

2 

3 

Dead/dying at scene 

Unstable during 

transport 

Stable 

60 min 

1–6 h 

4–18 h 

Scene/EMS 

EMS/EC 

ICU 

100 

96 

5–30 

Bleeding 

Multisystem trauma 

CNS injury 


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. 

PATIENT CLASSIFICATION 

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. 

INITIAL EVALUATION 

■ 

Prehospital Management 

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 

History 

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. 

Physical Examination 

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: 

1. Hypotension 

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


SECTION 3 X 

Chest Radiography 

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 

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. 

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. 

Tube Thoracostomy 

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. 

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. 

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


495 


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. 

TABLE 26-5 Radiographic Clues that should Prompt 

Suspicion of a Thoracic Great Vessel Injury 

Fractures 

• Sternum 

• Scapula 

• Multiple left ribs 

• Clavicle in multisystem injured patients 

• (?) First ribs 

Mediastinal clues 

• Obliteration/double shadow of aortic knob contour 

• Widening of the mediastinum 8 cm 

• Depression of the left mainstem bronchus 140° 

from trachea 

• Loss of perivertebral pleural stripe 

• Calcium layering at aortic knob 

• “Funny-looking” mediastinum 

• Deviation of nasogastric tube in the esophagus 

• Lateral displacement of the trachea 

Lateral chest x-ray 

• Anterior displacement of the trachea 

• Loss of the aortic/pulmonary window 

Other findings 

• Apical pleural hematoma 

• Massive left hemothorax 

• Obvious blunt injury to the diaphragm 

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. 

Impulse Therapy/Beta-Blockade 

The pharmacological reduction of d P /d T 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 d P /d T 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 betablockade 

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. 

SECTION 3 X 

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, 

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. 

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 

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.


497 


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. 

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. 

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


A 

Major Thoracic Injury 

Potential Thoracic Vascular Injury 

SECTION 3 X 

Screening Techniques 

(History, Physical Examination, Chest X-Ray, FAST, Chest CT) 

Patient in 

Extremis 

Hypotensive 

(Unstable) 

Normotensive 

(Stable) 

Diagnostic Techniques 

(Tube thoracostomy, FAST, Arteriogram) 

Hemopericardium 

Immediate 

Thoracotomy 

Massive 

Hemothorax 

Plan Therapy 

Vascular 

Injury 

Endovascular 

Plan position, access, 

imaging, control and devices 

Open 

Procedure 

Plan Position 

& Incision 

Reconstruct 

B 

Blunt Chest Injury 

Potential for Thoracic Aortic Injury 

Suggestive History or Physical Examination 

Afterload reduction 

(unless low BP or patient “unstable”) 

SCREENING Chest X-Ray/CT 

with appropriate protocol 

Strongly Suggestive/Equivocal 

“Normal” 

Treat Other Injuries 

AORTOGRAPHY 

Positive Negative Trivial 

Treatment 

Treat 

Other 

Injuries 

Timely 

Repeated 

Studies 

Immediate 

Delayed 

Open 

Endovascular 

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.


499 

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. 

■ 

Diagnostic Studies 

Catheter Arteriography 

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 ). 


E 

A 

C 

B 

D 

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. )


SECTION 3 X 

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 normalappearing 

mediastinum on admission chest radiography. 

TREATMENT OPTIONS 

■ 

Nonoperative Management 

Nonoperative management of blunt aortic injuries should be 

considered in patients who are unlikely to benefit from an 

immediate repair: 

FIGURE 26-12 Plain chest x-ray of a patient with a penetrating 

wound of the ascending aorta. 

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 

1. Severe head injury 

2. Risk factors for infection: 

• Major burns 

• Sepsis 

• 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. 

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). 

■ 

Endograft Repair 

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


501 

endografting for acute transections of the proximal descending 

thoracic aorta were reported. These were often custom devices 

using aortic or iliac artery extenders. 36 Not 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 ). 37 Many 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 

TABLE 26-6 Comparison of Open Versus Endovascular 

Treatment of Blunt Thoracic Aortic Injury 

Mortality (%) 

Average 

mortality 

(%) 

Paraplegia (%) 

Average 

paraplegia 

Complications 

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 

reported 41 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. 

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 

32 , 34 , 39 

needed. 

■ 

Surgical Repair 

Open 

Operations 

0–55 

13 

0–20 

10% 

ARDS 

CNS problems 

Neurologic 

Endograft 

Repair 

0–12 

3.8 

1 

1 out of 239 cases 

LSCA occlusion 

Graft compression 

Entry site problems 

ARDS, adult respiratory distress syndrome; CNS, central 

nervous system; LSCA, left subclavian artery. 

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 ). 

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 



SECTION 3 X 

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. 

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. 

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. 

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 

Damage Control 

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 

TABLE 26-7 Recommended Incisions for Thoracic Great Vessel Injuries 

Injured Vessel 

Uncertain injury (hemodynamically unstable) 

Ascending aorta 

Transverse aortic arch 

Descending thoracic aorta 

Innominate artery 

Right subclavian artery or vein 

Left common carotid artery 

Left subclavian artery or vein 

Pulmonary artery 

Main/intrapericardial 

Right or left hilar 

Pulmonary vein 

Innominate vein 

Intrathoracic vena cava 

Incision 

Left anterolateral thoracotomy 

Transverse sternotomy 

Right anterolateral thoracotomy (clamshell) 

Median sternotomy 


Neck extension 

Left posterolateral thoracotomy (fourth intercostal space) 

Median sternotomy with right cervical extension 

Median sternotomy with right cervical extension 

Median sternotomy with left cervical extension 

Left anterolateral thoracotomy (third or fourth intercostal space) 

with separate left supraclavicular incision connecting vertical 

sternotomy (“book” thoracotomy) 


Ipsilateral posterolateral thoracotomy 

Ipsilateral posterolateral thoracotomy 


Median sternotomy


503 

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. 

ARTERIAL INJURIES 

Ascending Aorta 

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 

Innominate Artery 

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. 26-15 and 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. 

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 

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. 

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 

FIGURE 26-16 Aortogram of the patient in Fig. 26-12 

demonstrating the tear involving the proximal innominate artery.


SECTION 3 X 

A 

C 

FIGURE 26-17 (A–C) Drawing depicting the bypass exclusion 

technique employed in patients with innominate artery injuries. 

( Copyright © Baylor College of Medicine, 1981. ) 

B 

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. 

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) pumpassisted 

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. 

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 

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. 

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 

FIGURE 26-18 Aortogram demonstrating the classic intimal tear 

and traumatic pseudoaneurysm of the descending thoracic aorta.


505 

FIGURE 26-19 Aortogram in a patient with blunt chest trauma 

demonstrating an intimal tear of the descending thoracic aorta at 

the diaphragm. 

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. 

TABLE 26-8 Current Therapeutic Approaches to the 

Management of Thoracic Aortic Injuries 

1. Surgical (clamp and direct reconstruction with or 

without an interposition graft) 

(a) Pharmacological control of proximal hypertension 

(b) Passive bypass shunts 

(c) Pump-assisted bypass 

• Traditional cardiopulmonary bypass (with 

total-body heparinization) 

• Atriofemoral bypass using centrifugal pump 

(with/without heparinization) 

2. Nonoperative and/or purposeful delay of operation 

(with pharmacological treatment and close radiologic 

surveillance) 

3. Endograft repair 

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 fullthickness 

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 



TABLE 26-9 Possible Contributing Factors Related to the Multifactorial Development of Paraplegia Following 

Operations for Thoracic Great Vessel Injury 

SECTION 3 X 

Injury factors Direct segmental artery injury 

Direct radicular artery injury 

Direct spinal artery injury 

Spinal cord contusion/concussion 

Spinal canal compartment syndrome 

Severity of aortic injury 

Specific anatomic location of aortic injury 

Patient factors Location of arteri radicularis magna(?) 

Continuity of anterior spinal artery 

Caliber of individual segmental radicular arteries 

Congenital narrowing of spinal canal 

(?) Increased blood alcohol levels 

Total perispinal collateral blood supply 

Operative factors Required occlusion of segmental arteries 

Pharmacological agents required 

(?) Declamping hypotension 

(?) Required cross-clamp times (in combination with anatomic and injury factors 

cited in this table); length of required interposition grafting or required exclusion 

(?) Level of systolic (or mean) proximal aortic blood pressure 

(?) Level of distal aortic mean blood pressure 

(?) “Flow” in the aorta distal to clamp 

Postoperative factors Progressive swelling of the spinal cord 

Spinal canal compartment syndrome 

Delayed or secondary occlusion of injured or contused segmental, radicular, or 

spinal arteries 

Pharmacological induced spasm of spinal cord nutrient arteries 

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. 

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 Artery 

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


507 

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 leftsided 

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. 

Pulmonary Artery 

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. 

Intercostal Arteries 

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. 

■ 

Venous Injuries 

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. 

Pulmonary Veins 

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. 



SECTION 3 X 

Subclavian Veins 

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. 

Azygos Vein 

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 

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). 

■ 

Special Problems 

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 

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 

©2005 Baylor College of Medicine 

FIGURE 26-20 Injury to the azygos vein with control with lateral repair, ligation, division, and oversewing. ( Copyright © Baylor College 

of Medicine, 2005. )


509 


Venule 

Bronchiole 

©Baylor College of Medicine 1979 

100 mm 

Hg 

Alveolus 

FIGURE 26-21 Drawing depicting the mechanism of systemic air embolism following a penetrating lung injury. ( Copyright © Baylor 

College of Medicine, 1979. ) 

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. 

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. 

■ 

Postoperative Management 

A significant portion of the in-hospital mortality asso ciated 

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 dis tress 

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


SECTION 3 X 

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. 

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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 

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8. Baumgartner FJ, Rayhanabad J, Bongard FS, et al. Central venous injuries 

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9. Medizinische Klinik IV. Perforation und Ruptur Koronaryarterien. Herz. 

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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. 

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16. Bertinchant JP, Polge A, Mohty D, et al. Evaluation of incidence, clinical 

significance and prognostic value of circulating cardiac troponin I and T 

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contusion after blunt chest trauma. J Trauma. 2000;48:924. 

17. Rozycki GS, Schmidt JA, Oschner MG, et al. The role of surgeonperformed 

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 selfexpandable 

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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. 

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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 

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31. Wheat MW Jr, Palmer RF, Bartley TD, et al. Treatment of dissecting 

aneurysm of the aorta without surgery. J Thorac Cardiovasc Surg. 

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32. Demetriades D, Velmahos GC, Scalea TM, et al. Blunt traumatic thoracic 

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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. 

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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 thirtyyear 

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.


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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.

Chapter 26 - McGraw-Hill Professional

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