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Blunt Chest Trauma

Introduction
Reports of chest trauma from ancient, medieval, Renaissance, and
even the modern eras reect both an appreciation for and a therapeutic
frustration in caring for patients with chest injuries. Blunt injuries with
ail chest and hemoptysis were described in the Smith Papyrus
(written in Egypt in approximately 1600 BC and thought to probably
represent a copy of an earlier missive written circa 3000 BC), in the
Iliad circa 850 BC, and by Hippocrates in the fth century BC.
1
However, these early writings did not describe effective treatment
strategies for patients with chest injuries. Effective treatment of chest
injuries was made possible by the development of general anesthesia
and positive-pressure ventilation. By the early 1900s, thoracoscopy
and thoracotomy were both being performed, and the advent of
antibiotics allowed the treatment of infection, thereby reducing a
major postoperative risk. Throughout the 20th century, advances in
thoracic, trauma, and critical care surgery attempted to keep pace with
the increasing volume and complexity of cases.
The most signicant advances in the treatment of blunt chest trauma
from the later part of the 20th century involve a better understanding
of acute respiratory failure, creative and exible ventilator treatment
strategies, directed pneumonia and empyema treatments, the diagnosis
and treatment of aortic and great- vessel injury, remarkable advances
in imaging techniques, and operative strategies that have become more
conservative in scope and intervention. Although only perhaps 10% of
blunt chest trauma cases require an operation, these patients typically
present a challenging treatment dilemma, demanding rapid yet
thoughtful decision-making, comprehensive anatomic understanding,
and often prompt operative intervention. In this monograph, we hope
to provide a broad and contemporary summary of the treatment of
patients with blunt chest trauma, an important and changing compo-
nent of trauma care.
Curr Probl Surg 2004;41:223-380.
0011-3840/2004/$30.00 0
doi:10.1016/j.cpsurg.2003.12.004
Curr Probl Surg, March 2004 223
Incidence, Biomechanics, and Prevention
Incidence
Calhoon and Trinkle
2
have noted that in the United States alone, trauma
is responsible for 100,000 deaths and more than 9,000,000 disabling
injuries annually and that 25% of blunt traumatic fatalities are a direct
consequence of chest injury, whereas in as many as another 50%, chest
injury plays a major contributing role. Blunt thoracic injuries are
responsible for approximately 8% of all trauma admissions, with motor
vehicle crashes (MVCs) the dominant injury mechanism.
3
A 4-year
review of patients who required thoracotomy for persistent hemorrhage
after blunt injury identied the mechanism to be MVC in 52%, motor
cycle crash in 10%, pedestrian struck in 9%, and falls in 7% of cases.
4
In
pediatric patients, there is an increased incidence of pedestrian struck
events.
3,5
Disturbingly, child abuse remains a signicant problem, ac-
counting for nearly two thirds of chest wall injuries in children under the
age of 3 years.
6
Biomechanics
Mechanisms of injury with reference to specic organ injuries will be
discussed in subsequent sections. Although traditional research has
focused on deceleration forces (with the resulting shearing and tearing of
organs), crush injury, and intrusion mechanisms, more recent attention
has shifted to viscous response, a concept studied by Viano and
colleagues.
7,8
Their work is nicely summarized by Calhoon and Trinkle in
their 1997 article, and we have taken advantage of their work for this
review.
2
In essence, viscous response is a time function determined by
measuring the velocity of deformation and compressive response of the
body wall to a weighted, pneumatic pendulum. When compared with
compression, injury correlates better with the peak viscous response,
which occurs before maximum compression. Therefore, major intratho-
racic injuries can (and commonly do) occur without rib fractures.
2,7,8
Viano and colleagues also have described the probability of chest injury
with an abbreviated injury score (AIS) of 4 or greater, based on the
viscous response, and have noted that the chest appears to be more
susceptible to viscous trauma than the abdomen.
8
It is important to
remember that signicant intrathoracic injury can exist without signicant
chest wall trauma.
9
The National Automotive Sampling System, composed of the Crash-
worthiness Data System and the General Estimates System, gathers data
from police accident reports.
10
Based on the data collected (including the
224 Curr Probl Surg, March 2004
type of impact, the change in velocity, and the degree of intrusion), it is
possible to predict the likelihood of specic injuries (eg, rupture of the
thoracic aorta) and to modify predictions based on age.
11
Although this
database is still being developed and investigated, it is hoped that this will
ultimately be linked to preventive strategies as well as alerting trauma
response systems to the location of an incident and the likelihood of
signicant injuries. The Crash Injury Research and Engineering Network
has developed a computer database to combine the National Automotive
Sampling System with medical/trauma-related variables in a relational/
object database system that can be shared among participating cen-
ters.
12,13
Preventive Strategies
Attempts to reduce MVC- related injury have included restriction of the
speed limit, the use of active and passive restraints (seatbelts and air
bags), and the use of helmets for motorcycle and bicycle riders. Each has
had a variable impact on the incidence of chest injury.
Decreasing the national speed limit to 55 miles per hour appeared to
reduce the overall incidence of fatal trafc crashes.
2
Similarly, increasing
the speed limit on rural highways in Washington State was associated
with a doubling of trafc fatalities.
14
It is not clear what impact these
changes have had on chest injury specically, since there also has been an
increased awareness of the importance of proper seat-restraint use and air
bags. Newman and Jones
15,16
noted that the use of seatbelts resulted in a
reduction in major chest injuries but an increased incidence of minor
chest injuries. These ndings have been supported by autopsy data that
demonstrated a higher incidence of ascending aortic rupture in unbelted
drivers compared with those who were belted.
17,18
The issue of proper use is critically important, particularly in the
pediatric population. Valent and colleagues
19
reviewed the National
Automotive Sampling System data sets between 1995 and 1999 and
reviewed those incidents involving children 0 to 11 years of age. These
investigators controlled for sex, age, seating position, vehicle weight,
model year, change in velocity, crush, degree of intrusion, and principal
direction of force. They found that compared with children with no
restraints, children with properly tted and applied restraints had a
signicant reduction in the risk of thoracic injury (relative risk of 0.35;
95% condence interval of 0.13 to 0.93).
19
There was no risk reduction
if the restraint system was applied improperly.
Air bags, particularly when used in conjunction with 3-point restraints,
do reduce the risk of chest injury.
2,20
Nevertheless, the deployment of air
Curr Probl Surg, March 2004 225
bags can result in signicant chest injuries. Air bags inate at a rate of 6
L/ms, with the ination being completed within 50 ms.
20
If the individual
is not restrained, if late deployment occurs when the passenger or driver
has been propelled into the area of deployment, and/or if the space
between the air bag and the victim is too close, then there is the likelihood
that the force of deployment (punch-out) will be applied against the
chest or other areas of the body. This in turn can result in severe
intrathoracic injuries, including cardiac rupture.
20
This scenario again
emphasizes the importance of proper use, including the benet of using
3-point restraints in addition to air bags.
The use of helmets has resulted in a reduction in fatal head injury after
motorcycle crashes, but in exchange for an increased incidence of severe
chest and abdominal injuries.
21
Kraus and colleagues
21
described the
incidence of thoracic injuries in fatal and nonfatal motorcycle crash
incidents since the introduction of helmet laws in California. In the year
after the helmet law was implemented, there was a decrease in the
incidence of head injury being the primary cause of death (or most
severely injured body region) from 61% to 43%, whereas there was a
corresponding increase in fatal trunk injuries from 34% to 46%, predom-
inantly in the chest. These investigators noted that of 548 fatalities, 75%
of victims had chest injuries, of whom 86% had an AIS of 3 or greater.
In addition, of 4,214 nonfatal motorcycle crashes, 20.6% of victims had
chest injuries, nearly 42% of whom had an AIS of 3 or greater.
It appears obvious that at the current time the best method of preventing
chest injuries in North America is to stress the appropriate use of seatbelts
in conjunction with air bag systems, including side air bags. In addition,
efforts to control the mayhem on our roads, including controlling speed
and alcohol-related events as well as educating children and their parents
about road safety, need to continue, as frustrating and lacking in
immediate gratication as it is. Further work on dening the biome-
chanics of crashes offers hope for both improving vehicle design and
alerting trauma response systems about the likelihood of specic injuries.
Initial Treatment
Prehospital Care
Treatment of many thoracic injuries can begin in the prehospital setting.
The basic principles of prehospital care, including maintaining a patent
airway, supplying supplemental oxygen and breathing support, establish-
ing intravenous access, and pressure control of obvious hemorrhage, are
likewise essential components of chest trauma treatment. Tracheal intu-
226 Curr Probl Surg, March 2004
bation and chest needle decompression are part of the armamentarium of
many prehospital care providers, and some programs even allow para-
medics to perform eld tracheostomy. Bulger and colleagues
22
reviewed
eld intubations for a period of almost 2 years. They found that intubation
was required in 2,700 cases (5.4%), 18% of whom had sustained
traumatic injuries. A surgical airway was required in only 1.1% of cases,
which these authors attributed to the use of succinylcholine. Although this
report represents a mixed collection of patients and it is difcult to
extrapolate the ndings to blunt- injured patients, for whom there may be
a concern regarding cervical spine injuries, these data nevertheless
suggest that local trauma response systems consider guidelines for adding
the administration of prehospital paralytics to airway treatment in the
eld. Despite being more difcult than in medical resuscitations and
possibly associated with an increased incidence of pneumonia, eld
intubation is often the critical difference that provides a chance for
survival.
23
Sucking chest wounds can be dressed with a 3-way dressing to prevent
the development of tension pneumothorax. This technique can be difcult
to perform under eld conditions, so it is preferable to completely occlude
the wound and perform a needle decompression to avoid the development
of tension pneumothorax.
24
This decompression is performed in the
second intercostal space, in the midclavicular line. Localizing this site can
be difcult in patients with a large body habitus, soft tissue swelling, or
emphysema, and a simple technique is to place the catheter 2 to 3 nger
breadths below the clavicle or at or just below the manubrial-sternal
junction.
The development of progressive respiratory distress in any patient
should prompt decompression because the typical ndings are unreli-
able.
25
Decompression should be performed in any patient suspected of
having a pneumothorax before air transport or in any patient during
transport who develops subcutaneous emphysema, respiratory distress, or
other signs of air under tension.
26
If available, a Heimlich valve can be
used to allow egress of air; if a Heimlich valve is not available, the nger
of a glove with the tip cut off will sufce. Complications can occur but
usually are related to the dislodgment or obstruction of the catheter,
failure to achieve true intrapleural placement, and only rarely to vessel
injury.
27
Unstable chest wall wounds (eg, ail chest) can be stabilized tempo-
rarily with sandbags, but supplemental oxygen and pain medications in
stable patients are the mainstays of treatment. If there is a suggestion of
pulmonary contusion but no hemorrhage, uid should be restricted.
Curr Probl Surg, March 2004 227
The Prehospital Trauma Life Support manual provides an excellent
source of information on the training goals and capabilities of emergency
medical technicians and paramedics and closely follows the Advanced
Trauma Life Support (ATLS) course of the American College of
Surgeons Committee on Trauma.
28
Initial Emergency Room Treatment
The basic ABCs of trauma should be followed. The primary survey
should recognize the cause of and treat impending airway loss, hypoxia,
ventilation compromise, and shock. The principles outlined in the ATLS
course provide excellent guidance in the acute treatment of blunt thoracic
injury, based on the detection of immediately life-threatening injuries
during the primary survey and critical injuries that may manifest in a
delayed fashion during the secondary survey (Table 1).
29
Tube Thoracostomy
Tube thoracostomy is usually regarded as a minor procedure, and yet
the consequences of placing a thoracostomy tube for the wrong indica-
tions or using an incorrect technique can be devastating. The indications
are to drain the uid and/or air from the chest. In patients at risk of
developing tension pneumothorax (eg, those with chest injuries during air
transport or those who require positive-pressure ventilation and can not be
monitored), prophylactic tubes are also indicated. It is critical to
TABLE 1. Categorization of injuries that should be detected during initial assessment
Immediately life-threatening injuries: Should be identied during the primary survey
Airway obstruction
Tension pneumothorax
Open pneumothorax
Flail chest
Massive hemothorax
Cardiac tamponade
Critical injuries: Most commonly identied during the secondary survey
Simple pneumothorax
Hemothorax
Pulmonary contusion
Tracheobronchial disruption
Blunt cardiac injury
Traumatic aortic disruption
Traumatic diaphragmatic disruption
Mediastinal traversing wounds
Adapted from ATLS guidelines
29
Adapted from Advanced Trauma Life Support for Doctors.
29
6th ed. Chicago, Ill: American College of Surgeons; 1997. Used with permission.
228 Curr Probl Surg, March 2004
recognize that in 20% of cases the physical examination will be
misleading.
30
Unstable patients with chest injuries or those with de-
creased breath sounds and increased tympany should have tubes placed
without delay. Stable patients without distress can be allowed the benet
of a chest radiograph (CXR) to conrm the suspected indications for tube
placement. Computed tomography (CT) scans are much more sensitive
for detecting occult pneumothorax. In ventilated patients with a CT-
detected pneumothorax and who do not have a tube, 1 should be placed,
because the risk of developing tension is signicant. If ventilator support
is minimal and extubation is anticipated shortly, careful observation and
repeated radiographs can be employed.
Technique. In stable patients, attention to anesthesia (including local
and, if appropriate, conscious sedation) and sterile technique are impor-
tant. The procedure that most traumatizes patients is chest tube placement
in the emergency department (ED). The usual landmark is the mid- to
anterior axillary line just at the inframammary crease. If there is a
thoracotomy scar, the tube should be placed superior to this scar, because
the diaphragm usually is adhered to the previous incision. There are 2
basic methods: the blunt Kelly clamp and the sharp scissors ap-
proach. We generally prefer the use of curved scissors after a full-
thickness skin incision has been made with a scalpel, nding the sharp
technique quicker, less painful, and safer. Tunneling over 1 or 2 ribs
higher than the skin incision should be done in most circumstances to
provide a sealing tunnel that will afford better closure when the tube is
removed.
30
Complications. Pain is the most common complication of tube thora-
costomy and can lead to splinting, atelectasis, and pneumonia. Laceration
of underlying structures can occur due to high airway pressure and/or
prior adhesions (present in 15% to 20% of patients de novo). Careful
determination of intrapleural placement and controlling the dissection
device carefully can help to avoid this complication. Tubes can become
displaced (1.7% to 5.2% incidence), usually because they are not pushed
in far enough, and when the patient sits up and/or lowers his/her arm, the
tubes are pulled out 1 to 3 cm on average.
31
Of course, if they are not
secured well with heavy sutures (0 silk), the tubes can be pulled out
during transport, etc. Tube misplacement at the time of insertion into the
extrathoracic space can occur in patients with a larger body habitus or a
thick, parietal pleura (eg, empyema) and/or if there is signicant soft
tissue edema. The CXR may not be denitive, but the persistence of
pneumothorax with a lack of respiratory variation can suggest the
diagnosis. The tube should be removed and a new 1 placed through a new
Curr Probl Surg, March 2004 229
incision. Empyema occurs in 2% to 10% of patients who undergo ED tube
thoracostomy. Risk factors include retained hemothorax, poor technique,
shock, extrathoracic infectious sites, pain, pneumonia, etc.
32
Empyema is
discussed more fully later, but it should be briey noted that after injury,
empyema is most commonly due to Gram-positive organisms, and some
centers advocate prophylactic antibiotic treatment (cephalosporin) for 24
hours for all cases in which chest tubes have been placed in an emergency
setting.
33,34
Prospective, randomized studies have not evaluated the
efcacy of this use of antibiotics.
Diagnostic Techniques
Although diagnostic imaging can be a critical component in establishing
a treatment plan for patients with chest trauma, radiologic studies should
complement and never interfere with resuscitation. The unstable trauma
patient with diminished breath sounds and evidence of a thoracic injury
should undergo immediate tube thoracostomy. Waiting for radiographic
conrmation of a tension pneumothorax or a massive hemothorax is
unwarranted. In addition, although the initial CXR usually detects the
immediately life-threatening problems of pneumothorax, hemothorax,
contusion, and the widened mediastinum of aortic or great-vessel injury,
these ndings may manifest late and/or be subtle. Therefore, constant
reevaluation is required. Despite these caveats, the portable supine CXR
remains a standard of care in the early assessment of patients with
thoracic trauma. Although an upright anteroposterior and a lateral CXR
are preferred, patients with signicant blunt torso trauma are rarely so
hemodynamically normal and stable as to allow these radiographs in the
acute phase of treatment, nor is the risk of cervical or thoracic spine injury
excluded early.
More elaborate thoracic imaging techniques include CT, CT angiogra-
phy (CTA), and standard angiography. CT has little or no role in the acute
assessment of lung injury, but it can provide a more detailed description
of lung lacerations and the extent of contusions, as well as clarify the
presence of intrapleural versus extrapleural uid versus lung consolida-
tion.
35
CTA, in which a carefully timed bolus of contrast medium is
administered and small sections (usually 1 mm) are performed rapidly,
has proven to be a useful tool in diagnosing aortic injury in many
circumstances, but it does require careful technique and an experienced
interpreter. In many centers, CTA is considered the equivalent of standard
angiography as a diagnostic screening tool for aortic injury. Usually,
chest CT is performed acutely to evaluate the thoracic aorta and is more
commonly used in the postresuscitation phase.
230 Curr Probl Surg, March 2004
Angiography remains an important technique to evaluate the other great
vessels of the chest (eg, subclavian, innominate, carotid, and vertebral)
and is discussed in later sections. Angiography also has a controversial
therapeutic role in controlling chest bleeding in stable patients.
36
In
patients with signicant or ongoing thoracic hemorrhage, we are more
inclined to use operative rather than angiographic exploration, because
our experience suggests that operative intervention is more successful,
and there is a tendency to delay a needed exploration if embolization is
attempted rst.
4
Trauma ultrasound, or focused abdominal sonography for trauma
(FAST), has become an accepted method of assessing the abdomen and
of detecting pericardial effusion.
37
FAST is also being investigated as a
method of detecting hemothorax and pneumothorax.
38
Although we nd
the FAST examination useful as a screening tool for signicant pericar-
dial effusion, we have not utilized FAST to detect hemothorax or
pneumothorax.
Resuscitative Thoracotomy
The term emergency room resuscitative thoracotomy (ERRT) should
be restricted to a thoracotomy that is performed on a patient in extremis
(impending death) outside the operating room. Many reports include
patients who have undergone urgent thoracotomy and thoracotomy
performed in an operating room after signicant interventions (eg,
intubation, central access, etc). This situation has led to a signicant
variance in the reported survival rates.
A review of 24 published series, with data extracted for 4,620 patients
who met the criteria for ERRT, was performed by Rhee and colleagues
39
and has conrmed the importance of the mechanism injury and the
presenting physiologic features in predicting the outcome (Table 2). The
overall survival rate was 7.4%, with normal neurologic function being
described in 92.4% of those who survived to discharge. These investiga-
tions dened signs of life as 1 of the following: cardiac electrical activity,
respiratory effort, or pupillary response.
An important factor inuencing the outcome is whether or not patients
in cardiopulmonary arrest have been intubated in the eld. Field intuba-
tion protects the airway, enhances oxygenation and ventilation, and has
been demonstrated to provide a survival benet. Durham and colleagues
40
noted that prehospital intubation prolonged tolerable cardiopulmonary
resuscitation to 9.4 minutes compared with 4.2 minutes in nonintubated
patients.
Currently, the indications for ERRT are accepted generally to be
Curr Probl Surg, March 2004 231
dependent on the mechanism of injury, time, and the presence of signs of
life. In general, ERRT has some benet in those patients who have
detectable vital signs before arrival; who have sustained an isolated,
penetrating chest injury; or who experience cardiopulmonary arrest after
arrival or within 5 minutes of arrival.
40,42
Goals of ERRT
Thoracotomy performed for profound shock or arrest in the ED offers
6 potential interventions: 1) control of intrathoracic bleeding; 2) release of
a pericardial tamponade; 3) effective internal cardiac compressions; 4)
pulmonary hilar control for massive air leak; 5) cross-clamping the
descending thoracic aorta; and 6) control of air embolism. Although not
an intervention, thoracotomy also does allow the conrmation of appro-
priate endotracheal tube placement and subsequent lung expansion.
Closed compressions are ineffective in traumatic arrest, either because
there is no effective volume to pump or because tamponade prevents
effective cardiac lling. Cross-clamping the aorta has been advocated as
a means of increasing coronary and cerebral perfusion, but there are
experimental data suggesting that there is increased ventricular strain and
end-organ ischemia with a worse outcome.
43
The primary purpose of
aortic cross-clamping in ERRT is to limit blood loss from wounds below
the diaphragm. Aortic cross-clamping can be challenging in the emergent
setting, and lacerations of the aorta or only partial occlusions have
occurred. To directly visualize and incise the overlying pleura usually
requires an assistant to retract the lung medially. This action impedes
cardiac compressions and may distract the team from controlling intratho-
TABLE 2. Factors associated with survival after emergency room resuscitative thoracotomy
Factor Survival (%)
Mechanism Blunt injury, 1.4%
Gunshot wound, 4.3%
Stab wound, 16.8%
Location of major injury Multiple injuries, 0.7%
Abdominal, 4.5%
Thoracic, 10.7%
Cardiac, 19.4%
Signs of life Absent in eld, 1.2%
Present during transport, 8.9%
Absent on arrival, 2.6%
Present on arrival, 11.5%
Adapted from Rhee PM, Acosta J, Bridgeman A, Wang D, Jordan M, Rich N. Survival after
emergency department thoracotomy: review of published data from the past 25 years. J Am
Coll Surg 2000;190:28898.
39
used with permission.
232 Curr Probl Surg, March 2004
racic injuries. An alternative is to occlude the aorta transiently by blind
compression against the spine, but this action does require occupying 1
persons attention.
Clamping the pulmonary hilum to control massive bleeding or when air
embolism is suspected can be performed by a clamp or a TA stapler
placed from the superior aspect of the hilum.
44
If the inferior pulmonary
ligament is incised on its inferior border, it can easily be divided bluntly,
which will permit either pulmonary torsion or clamping from the inferior
aspect. If air embolism is suspected or documented, attempts can be made
to increase coronary perfusion pressure temporarily by occluding the
descending aorta and administering epinephrine, while performing open
massage and, rarely, venting the left ventricle with a needle.
Urgent Thoracotomy for Hemorrhage
The indications for operative exploration in stable patients who have
ongoing blood loss through chest tubes have undergone reappraisal. In
1970, McNamara and colleagues
45
described a reduction in mortality
rates when thoracotomy was performed early after penetrating trauma.
These investigators commented that
The current report cites criteria for exploration of 1000 to 1500 ml. of
blood in the thoracic cavity on initial insertion of a tube and 500 ml. of
bleeding within the rst hour after insertion. This is somewhat more
aggressive than the criteria suggested by the World War II experience
and is commensurate with the decreased risk of thoracotomy in current
surgical practice.
This and other reports from the early 1970s were the basis for current
ATLS guidelines, according to which initial chest tube output exceeding
1500 milliliters or a continued hourly output of more than 250 milliliters
for three consecutive hours are criteria for surgical exploration after
penetrating chest trauma.
Operative intervention for hemorrhage focuses on 2 goals: 1) stop the
bleeding at the source and 2) allow the lung to fully expand. Evacuating
the hemithorax completely and enabling visceral-parietal pleural apposi-
tion will provide an opportunity for the lung to tamponade bleeding.
Prolonging the interval before this is achieved can result in an insidious
cycle of further blood loss, increasing coagulopathy, and metabolic
derangement. In current civilian practice, there is a low threshold for
operation after penetrating injury, but after blunt trauma there tend to be
signicant delays before operation. The reasons include distraction by
multiple associated injuries, need for complex radiologic tests, and/or
dissatisfaction with operating for multiple chest wall bleeders. This has
Curr Probl Surg, March 2004 233
led to a tendency to watch hourly outputs or to attempt interventional
approaches. The risk with monitoring chest tube output is that the tubes
can be plugged or not properly monitored, or transient decreases in output
can lead to critical delays.
A retrospective, multicenter study of patients who underwent thoracot-
omy within 48 hours of injury because of ongoing bleeding noted that
each 500 mL of tube output was associated with a 60% increase in the
mortality rate, independent of the mechanism of injury.
46
Of the patients
with blunt trauma who underwent operative exploration because of
ongoing hemorrhage alone, the incidence of intrathoracic injuries requir-
ing control was as follows: cardiac, 10%; lung laceration, 28%; great-
vessel injury, 3%, chest wall bleeding, 17%; internal mammary lacera-
tion, 6%; and traumatic aortic rupture, 14%. Diffuse chest wall bleeding
in the setting of coagulopathy is a particularly vexing problem. In our
experience, however, early operation to drain the hemothorax and to
allow the lung to expand greatly aids in the cessation of bleeding,
particularly when coupled with a reversal of coagulopathy and a normal-
ization of body temperature. We advocate thoracotomy for hemorrhage
whenever the total output exceeds 1500 mL in a 24-hour period, with
signs of continued bleeding, regardless of mechanism of injury. In
hemodynamically stable (normal) patients who are not coagulopathic,
mini thoracotomy or thoracoscopic approaches may be feasible. We
evaluated a 6-month experience with this approach compared with our
historical less aggressive indications for thoracotomy after blunt trauma.
The results suggest that this approach allowed patients to reach the
operating room in a more stable condition, with more options for
thoracoscopy and improved outcome (Table 3).
Abbreviated thoracotomy, similar to damage control or abbreviated
laparotomy, is required in up to 5% of patients in civilian practice. The
concept is to focus on stopping the hemorrhage alone and not addressing
TABLE 3. Impact of changing indications for thoracotomy after blunt trauma
SBP on arrival in
ED (mm Hg)
SBP on arrival
in OR (mm Hg)
Thoracoscopy Mortality
Historical control 99 31 88 43 5 (5%) 28 (46%)
N 61
(1/1/9512/31/98)
Period after instituting
1500-mL limit 91 28 111 26 4 (29%) 4 (29%)
(N 14)
(1/1/026/31/02)
SBP, systolic blood pressure; ED, emergency department; OR, operating room.
234 Curr Probl Surg, March 2004
denitive repair or closure.
47,48
The reasons include either not having the
facilities to perform denitive surgery, not being able to spare the
resources or time on a single patient (such as under mass casualty
conditions), and/or recognizing the lethal triad of coagulopathy, hypo-
thermia, and acidosis that reects persistent inadequate resuscitation,
which carries a 60% to 90% mortality rate.
49-51
Under these conditions,
operation must be aborted, the chest closed as quickly as possible, and the
patient transferred to a resuscitation unit. This might be the intensive
care unit (ICU) or a hospital unit farther down the triage line.
The specics of operative damage-control techniques of the lung and
cardiac injuries are discussed later in this chapter. The approach to
packing and chest closure is reviewed here. Unlike the abdominal
compartment, the chest is difcult to pack. The rigid chest wall, in
conjunction with parenchymal consolidation and/or loss, often creates
spaces, as opposed to the more pliable abdominal compartment. In
addition, packing can compromise cardiac function. Areas that can be
packed include the apices, posterior gutters, and lateral wall, while
avoiding the medial sites that might lead to cardiac or vena caval
compression.
47
Closing the chest wall has the advantage of helping the lung act as a
tamponading agent, slowing chest wall bleeding, and helping reduce the
risk of further hypothermia. However, swelling of the heart and lung as a
consequence of ischemia/reperfusion can prevent any closure. Thoracic
compartment syndrome is manifested acutely by cardiac decompensa-
tion when the retractors are removed or subacutely by the inability to
ventilate when the chest wall is closed. Under these circumstances, the
incision may need to be left open. In the most severe cases, the retractor
(either sternal or chest wall) will need to be sutured in place and covered
with a plastic adhesive dressing (Figure 1). Chest tubes must be placed
but do not need to be situated formally. Instead, simply placing them
through the open wound sufces. If the retractor can be removed but
closing the sternum results in cardiac compromise, struts constructed
from large chest tubes or 20- to 60- mL syringes can be secured to hold
the sternal edges apart. This technique is best used if there is enough
laxity in the skin and soft tissues to allow closure over these struts. If the
ribs and/or sternum can be allowed to collapse together without causing
cardiopulmonary decompensation but the patient is physiologically un-
stable and/or if the patient will need packing and operative reexploration,
a simpler method is to place a dressing beneath the sternal edges and
closing the skin (to prevent the raw edges from lacerating the heart).
Suturing the chest wall musculature together decreases bleeding from
Curr Probl Surg, March 2004 235
the wound, but if this is not possible, then simply packing the muscle
and closing the skin are acceptable. A particular concern after blunt
trauma is the possibility that multiple rib fractures will lacerate the
edematous lung. Covering the lung with packs can protect the lung
from further injury.
The timing for operative reexploration and washout depends on the
patients physiologic status. Generally, washout is recommended no later
than 72 hours and preferably within 48 hours after the initial procedure.
Usually, denitive closure is not possible, since patients are still tenuous
and multiple, graduated procedures are required to achieve denitive
closure. Before nal closure, a CXR is advisable, because more often than
not a sponge count has lost its meaning and in fact is relatively
contraindicated at the rst procedure, since it takes valuable seconds away
from the prime goal of getting out. With the use of abbreviated closure
and damage-control techniques, the mortality rate for patients with or who
develop the lethal triad has decreased from the historically quoted 90% to
as low as 30%.
47,51
Fig. 1. Patient with open abdomen and chest after multiple injuries, including those involving the heart,
lung, and liver. Attempts at removing the rib spreader resulted in cardiac arrest. After 48 hours the
chest could be closed, the abdomen was closed on the seventh postoperative day, and the patient
survived neurologically intact. (Color version of gure is available online.)
236 Curr Probl Surg, March 2004
Multiple Traumatic Injuries
Patients sustaining blunt force trauma usually present with multiple
injuries; this situation is in contrast to the more common isolated,
penetrating injury. There are no simple algorithms about how to prioritize
injuries, and it is not uncommon to need to treat head, thoracic,
abdominal, and/or severe orthopedic injuries simultaneously. On occa-
sion, the treatment of 1 injury may have a negative impact on another,
such as the patient with a potential or known aortic rupture and a closed
head injury with evidence of increased intracranial pressure. Many of the
specic problems will be discussed in the ensuing sections, but 2 areas
that deserve special consideration because of their relatively common
occurrence are the treatment of the hemodynamically unstable patient
with blunt chest trauma and the patient with combined pulmonary
contusion and long bone fractures.
The Unstable Patient with Ongoing Thoracic and
Extrathoracic Hemorrhage
Coordinating and prioritizing the initial approach to the patient with
multiple possible causes of hypotension are often difcult. No simple
protocol is foolproof, but some basic principles can be followed. Chest
and pelvic radiographs are a part of the standard assessment and provide
valuable information. Chest tubes must be inserted in the face of any
pneumothorax or even the suspicion of a hemothorax. A blunt trauma
patient who presents in shock with intrathoracic hemorrhage must also be
considered to have intra-abdominal and/or pelvic bleeding. Rapid assess-
ment of the abdominal cavity usually necessitates either a diagnostic
lavage (DPL) or a trauma ultrasound (FAST), bearing in mind that neither
of these techniques is effective for the diagnosis of pelvic bleeding. CT is
not appropriate for the unstable patient. Gross blood on DPL (10 mL free
aspiration) or free uid throughout the abdomen on FAST usually (90%,
in our experience) means that the abdomen is the primary source of
hemorrhagic shock and takes precedence. Such a patient should be taken
immediately to the operating room for laparotomy rst, followed by
thoracotomy if thoracic hemorrhage is massive or persistent. Pelvic
fractures can be stabilized externally to provide some control of venous
bleeding, but angiography and embolization will be required to diagnose
and treat arterial injury. If DPL is not grossly positive or if the FAST is
negative and there is signicant thoracic hemorrhage, then thoracotomy
should be performed without delay. Head trauma that requires operative
evacuation of a mass lesion (eg, epidural or subdural hematoma) usually
Curr Probl Surg, March 2004 237
manifests with lateralizing signs (eg, unilaterally dilated pupil and motor
decit, unilateral posturing), and head CT imaging has a high priority.
These are the principles that provide the best treatment approach to the
majority of patients, However, these principles must be applied individ-
ually to the complex blunt trauma patient.
The most versatile plan is to perform a damage-control laparotomy,
concentrating on stopping the obvious bleeding and then packing the
abdomen. Subsequent thoracotomy is usually performed via the antero-
lateral approach. We acknowledge that this approach has limited expo-
sure, but this can be increased, if needed, by placing a roll behind the side
of interest, by rotating the arm across the table, or by positioning the
patient with both arms extended above the head to allow a more formal
clamshell approach. A formal posterior-lateral thoracotomy does provide
better hemithorax exposure, but it requires more time to reposition and
generally should be reserved for the patient who demonstrates hemody-
namic stability after laparotomy.
The Treatment of Combined Pulmonary Injury and Long
Bone Fractures
Although early fracture xation has become the norm in many centers,
controversy remains regarding the timing of fracture xation in the
patient with blunt chest trauma and a closed head injury.
52,53
A variety of
animal studies have attempted to clarify the effect of fracture, the methods
of xation (intramedullary reamed and unreamed nailing), and the timing
of xation in the setting of pulmonary contusion. There is evidence that
microemboli of bone marrow may be an inciting event, although there is
conicting laboratory evidence whether or not this is greater with reamed
or unreamed xation.
52,54,55
At the same time, there are several potential
advantages to early xation (Table 4).
There has been clinical correlation of experimental results. Pell and
TABLE 4. Potential advantages of early xation
Reduced ARDS
Reduced pneumonia
Reduced deep venous thrombosis
Reduced decubitus ulcers
Improved extremity function through early mobilization
Minimization of muscular atrophy through early mobilization
Reduced analgesic requirements
Reduction of in-hospital costs
Ease in nursing care
ARDS, adult respiratory distress syndrome.
238 Curr Probl Surg, March 2004
colleagues
56
performed transesophageal echocardiography (TEE) on 24
patients undergoing long bone xation (17 tibial and 7 femoral). Copi-
ous showers of small (less than 10 mm) emboli were noted in 6, and
multiple large (greater than 10 mm) emboli were noted in 4. Three of
these patients developed the fat emboli syndrome, and there was 1 death.
The presence of activated leukocytes and their products within the alveoli
and pulmonary interstitium after blunt thoracic trauma may potentate the
subsequent pulmonary endothelial damage. The interaction between
activated leukocytes and fat embolism is underscored by the nding that
microcirculatory disturbances are not observed during simple intravenous
infusion of bone marrow fat alone. Instead, the added insult of fat
embolization to the acutely traumatized, inamed lung rich in activated
leukocytes may be required to induce microcirculatory damage that may
predispose to adult respiratory distress syndrome (ARDS).
52
There is evidence that the process of intramedullary reamed and
unreamed nailing results in the extravasation of marrow elements with
the subsequent embolization of fat, as demonstrated either sonographi-
cally or histologically, and that this process leads to changes in the
permeability of the alveolar-capillary membrane. These ndings in
animal studies have fueled the concern that early xation of long bone
fractures may have detrimental effects in patients with blunt chest
trauma. One study of 106 patients admitted with an injury severity
score (ISS) greater than 18 and femoral fracture found that in patients
with a chest AIS greater than 2, there was an increased incidence of
ARDS (33% versus 8%) and a higher mortality rate (21% versus 4%)
when early xation was performed.
57
In contrast, early fracture
xation in patients with minor chest injuries was associated with a
decrease in ventilator time and ICU stay.
Other reports not only have suggested that early xation is safe but also
that this approach may be associated with an improved outcome. Charash
and colleagues
58
retrospectively evaluated the outcomes of patients with
thoracic injuries and femoral fractures treated by either early or delayed
xation. There was a 48% incidence rate of pneumonia in patients treated
with delayed xation compared with a rate of 14% in those treated with
early xation. Early xation did not result in an increase in the incidence
of ARDS. The overall rate of pulmonary complications was 56% in the
patients with delayed xation compared with 16% in those who under-
went early xation. Furthermore, this analysis considered cases of
bilateral pulmonary contusion separately and found that in this subset,
there was a tendency toward a higher incidence of ARDS in those
undergoing late xation. More recently, in a retrospective review of 328
Curr Probl Surg, March 2004 239
patients from Harborview Medical Center, Brundage and colleagues
59
stratied patients with femur fractures and thoracic trauma on the basis of
the timing of xation. ARDS, pneumonia, hospital length of stay, and
ICU length of stay were lowest in the group undergoing xation within 24
hours. Fixation between 2 and 5 days was associated with a signicantly
increased incidence of ARDS and pneumonia. The severity of chest injury
and the overall injury severity score were not statistically different
between these 2 groups. Other clinical studies of early xation have failed
to demonstrate any detrimental effect on PaO
2
/FiO
2
ratios or the duration
of mechanical ventilation among patients with pulmonary contusions.
60
There have been no prospective, randomized, clinical trials to demon-
strate either a benecial or detrimental effect of early versus late xation
of long bone fractures in patients with blunt thoracic trauma. Outcome
measurements based on retrospective reviews may be biased due to
intangible or unmeasured variables that affect the decision to proceed
with early versus late xation. The results of these studies must therefore
be interpreted with caution.
52
Although experimental and clinical studies demonstrate that emboliza-
tion of marrow elements does occur during fracture xation, clinically
relevant alterations in pulmonary function have not been observed. The
assertion that early xation of long bone fractures in patients with
thoracic trauma leads to increased pulmonary complications or poorer
outcomes has yet to be substantiated by a randomized trial. In the absence
of such studies, the optimal timing of xation of long bone fractures in
patients with blunt thoracic trauma still remains unclear and must be
individualized. However, on the basis of our data, we generally have
advocated fracture xation within 24 hours of injury, even in the presence
of blunt chest trauma. If this cannot be accomplished, we delay fracture
xation until the fth day or later.
Incisions and Positioning
The choice of operative approach is inuenced primarily by the
required exposure but must also take into account likely injuries,
patient stability, available equipment, and experience of the surgeon
(Figure 2). The initial exposure may prove to be inadequate, and
recognizing this and making modications or closing and reposition-
ing are far better than continuing to struggle. At the same time,
particularly in unstable patients, one should not be paralyzed by
indecision in trying to choose the perfect approach.
240 Curr Probl Surg, March 2004
Anterolateral Thoracotomy
The most common urgent incision is the anterolateral thoracotomy.
This incision should be made in the inframammary crease (not the nipple
line), with the incision turning superiorly in the medial aspect after
crossing over the midclavicular line, so that if extension across the
sternum is required, the incision will not be placed too low. The left
anterolateral approach provides good access to the left ventricle and
atrium, distal descending aorta, proximal ascending aorta, left pulmonary
hilum, and the diaphragm. The right atrium and variable portions of the
right ventricle often are not well seen, and persistent bleeding from the
right side (either seen from the operative eld or evidenced by chest tube
output) should prompt extension of the incision across the sternum. In
addition, the clamshell approach will allow better exposure of the
proximal descending aorta, aortic arch, and upper lobes. This incision can
be utilized on either side. Patients presenting in shock with isolated
wounds on the right or with major blood loss through right-sided chest
tubes are better served by a right-sided incision initially than by a left
Fig. 2. Choice of thoracotomy incisions. (From Farber M, Obeid F. Incisions and approaches. In:
Karmy-Jones R, Nathens AB, Stern E, eds. Thoracic Trauma and Critical Care. Kluwer Medical
Publishing; 2002. Used with permission.). (Color version of gure is available online.)
Curr Probl Surg, March 2004 241
anterolateral thoracotomy. If, on entering the chest, high apical bleeding
consistent with great-vessel injury is encountered, packing the apex and
maintaining pressure can arrest bleeding until better exposure (depending
on the injury site) can be performed.
Sternotomy
The heart, pulmonary hilum, and ascending aorta are all best accessible
with a median sternotomy. Sternotomy is most likely to provide the best
exposure for penetrating injuries in the cardiac box (between the
nipples or between the anterior axillary lines) compared with other
approaches.
61
The midline is indicated by a line between the suprasternal
notch and the root of the xiphoid and is marked by the medial
decussations of the pectoralis muscles. There are crossing veins at the
suprasternal notch and just superior to the sternal-xiphoid junction that
often need to be ligated. The aortic arch and great- vessel origins are best
controlled through this approach. Dissection should start within the
pericardium, particularly if there is a superior mediastinal hematoma.
62
The innominate vein can be divided or mobilized to expose the innomi-
nate artery.
Sternotomy in conjunction with a supraclavicular extension offers
excellent exposure to the left subclavian vessels, and we prefer this to the
so-called trap-door approach. On either side, the mid-portion of the
subclavian vessels is best accessed via a supraclavicular incision.
63
This
incision can be further extended across the mid-aspect of the clavicle,
curving down toward the deltopectoral groove for access to the distal
subclavian and axillary artery junction. Sufcient exposure usually
requires division of the sternocleidomastoid muscle attachments to the
clavicle, as well as the attachments of the anterior scalenus muscle onto
the rst rib. Great care must be exercised to avoid injury to the phrenic
nerve and cords of the brachial plexus with this approach. The phrenic
nerve can be injured by incising or cauterizing the mediastinal-pleural
interface too widely beneath the manubrium or when dividing the
scalenus anticus. The brachial plexus is most often injured by too
vigorous retraction with a sternal retractor (more an issue with elective
cases) or by traction or division of the scalenus medius, which overlies the
plexus, mistaking this for the anticus. Resection of the medial portion of
the clavicle potentially can increase exposure of the subclavian artery.
Performing a subperiosteal resection with repair of the periosteum at the
conclusion of the operation provides adequate cosmetic and functional
results without the risk of malunion and persistent pain. Alternatively, if
242 Curr Probl Surg, March 2004
exposure of the midsubclavian vessels is all that is required, a supracla-
vicular approach (ie, splitting the clavicle in the middle) is often adequate.
Clamshell Incision
A dedicated clamshell incision has many of the advantages of
sternotomy, with the additional benet of providing better posterolateral
exposure. Patient positioning is critical. A towel placed longitudinally in
the midline, with the arms raised above the head, will allow the incision
to be made across the sternum at the fourth intercostal space (as opposed
to the usual extension of anterolateral thoracotomy, which is usually
lower, at the fth or sixth space). After the internal mammary arteries
have been divided, the sternum is transected and the intercostal spaces are
opened laterally. Placing bilateral rib spreaders that are sutured in place
and dividing the retrosternal areolar tissue provide access to all central
structures. The carina and right main pulmonary artery can be reached
between the ascending aorta and superior vena cava by incising the
posterior pericardium. This approach is useful in patients who are on
signicant degrees of ventilator support such that a posterolateral thora-
cotomy would not be tolerated and lung expansion would inhibit
exposure; in patients who might need exposure of the arch of the aorta as
well as of descending aorta; and/or in patients who may have multiple and
bilateral injuries, including suspected posterior mediastinal injuries.
Posterolateral Thoracotomy
Posterolateral thoracotomy can be performed using a variety of mus-
cle-sparing techniques. The latissimus dorsi can be mobilized if it is
anticipated that it will be required, but often simply preserving the
serratus anterior, by mobilizing it anteriorly, will provide signicant
support to shoulder function postoperatively. In most cases a fth
intercostal incision provides the best exposure, entering the chest at the
level of the major ssure. The rib spaces can be counted, with the second
rib identied by the insertions of the strap muscles posteriorly near the
spinous ligament. We rarely nd it necessary to resect a rib to provide
adequate exposure, unless there is extensive pleural inammation. This
method may be associated with reduced postoperative pain, since the
pleural edges can be sutured without pericostal sutures that may entrap
nerve bundles of the ribs above and below the incision. Shingling the
rib posteriorly, ie, removing a small portion to decrease tension and
prevent painful friction postoperatively, also helps exposure. Fourth
intercostal space approaches are used for descending aortic injuries (left)
or tracheal injuries (right), and seventh or eighth left intercostal ap-
Curr Probl Surg, March 2004 243
proaches are used for lower esophageal injuries. As a rule of thumb, when
the patient is placed in a exed position, the tip of the scapula will lie over
the sixth rib. Posterolateral thoracotomy provides a dramatically better
exposure than do anterolateral approaches. This is particularly true when
there are associated posterior rib fractures. However, this approach
prevents exploration across the midline, and except for splenectomy from
the left, prevents treatment of intra-abdominal injuries. Therefore, al-
though this incision provides superior exposure, it should not be used if
there is a question of bilateral or combined injuries that may require
simultaneous treatment.
Closure
Closing incisions requires diligence. Sternotomy closure should not
allow movement of the 2 halves. If 1 or both sternal side are thin, suturing
around the bone rather than through is helpful. In extreme cases, a half
S-curve will allow closure. Closing the fascia over the sternal plate is an
important component in obtaining sternal stability and healing. When
closing rib spaces, attention should be given to avoiding excessive
approximation, since this can lead to nerve injury and chronic pain. One
approach in stable patients is to drill holes through the ribs for suture
placement, thereby reducing the risk of nerve entrapment.
Thoracoscopy
Minimally invasive or endoscopic operation has been applied effec-
tively to a variety of diagnostic and therapeutic purposes after penetrating
chest injury. However, in the setting of blunt trauma, thoracoscopy has
been utilized primarily to treat acute hemothorax, evacuate clotted
hemothorax or empyema, diagnose diaphragmatic injury, and occasion-
ally manage persistent air leak (although this is also much more common
in penetrating injury).
64-66
Although thoracoscopy does offer the advan-
tage of smaller incisions and less pain and morbidity, it should be
remembered that thoracotomy can be performed in a variety of manners,
including minimal approaches, nonrib spreading, muscle sparing, etc
(Table 5). These modications are often useful adjuncts to thoracoscopic
approaches. The appeal of thoracoscopic approaches is that they poten-
tially carry only the morbidity of a chest tube, without the pain associated
with chest tube placement, and coupled with the possibility of a specic
intervention. However, thoracoscopy should not be used as an end to
itself but rather simply as an additional approach, with specic indications
and contraindications. The primary contraindication is hemodynamic
instability.
244 Curr Probl Surg, March 2004
Technique of Port Placement
Up to 7% of patients will experience chronic (longer than 6 weeks) pain
along the course of the intercostal nerve. One method to minimize this
postoperative pain is to use the port introducers as little as possible. This
method will reduce the pressure trauma on the neurovascular structures.
Local anesthetic should be injected before incision. This appears to
reduce postoperative pain by inhibiting stimulation of local pain bers
that are not affected by general anesthesia. The rst incision should be
made under direct vision, cutting down directly to the superior aspect
of the rib and identifying the pleura. This technique will help avoid
creating an extrapleural plane, injuring the lung, and/or creating trouble-
some bleeding. Subsequent ports can be placed under thoracoscopic
guidance.
Rigid versus VATS Approaches
Rigid thoracoscopy with a mediastinoscope allows pleural explora-
tion to be performed through a single port without the requirement for
single-lung ventilation. Video-assisted thoracoscopy (VATS) is contrain-
dicated primarily in patients who cannot undergo intubation with a
double-lumen tube, who cannot tolerate single-lung ventilation, and/or
who have a complex pleural space preventing the lung from dropping
away from the chest wall. The limitations of rigid thoracoscopy include
a less panoramic view and an inability to perform lung stapling or more
advanced interventions (eg, pericardial resection, etc). Rigid thoraco-
scopic approaches are particularly useful when the goal of the operation
is to drain the pleural space and when, due to either an inability to place
TABLE 5. Terminology associated with thoracoscopy
Rigid thoracoscopy Using a mediastinoscope, cystocscope, or rigid
bronchoscope
Flexible thoracoscopy Using exible bronchoscope inserted through a
rigid scope
Videothoracoscopy Using a beroptic scope with camera
Mini-thoracotomy Also known as access thoracotomy, an
incision 28 cm long but without rib
spreading
Muscle-sparing thoracotomy Preserving serratus anterior and/or latissimus
dorsi muscles
Video-assisted
thoracoscopic surgery (VATS)
Using video scope to facilitate intrathoracic
procedure so that no thoracotomy or a
minithoracotomy can be utilized
Curr Probl Surg, March 2004 245
a double-lumen endotracheal tube or intolerance of single-lung ventila-
tion, video approaches are not an option.
Specic Indications
Active Bleeding. Thoracoscopy can be performed in patients who have
persistent, but not massive, bleeding. The primary sites and sources that
are amenable to intervention are isolated intercostal or mammary vessels
of the chest wall or limited lung parenchyma. Clips can be applied if
active bleeding is noted. Often, the primary therapeutic role is to simply
evacuate the hemithorax and allow full lung expansion, with resultant
tamponade or cessation of contusion-related oozing. It is worth empha-
sizing that in our opinion, thoracoscopy should not be performed in
patients who have had any evidence of hemodynamic instability.
Retained Hemothorax. Retained hemothorax in trauma patients re-
mains a major risk factor for the development of empyema.. In brief, early
thoracoscopy and clot evacuation appear to decrease morbidity. Meyer
and colleagues
66
randomized patients into a VATS (n 15) or a second
chest tube (n 24) group. The patients treated primarily with VATS had
a shorter length of stay and lower hospital costs. Ten of the 24 second
chest tube patients required subsequent operative intervention.
Diaphragmatic Injury. The diagnosis of diaphragmatic injury remains
problematic. The initial CXR is notoriously unreliable and unrevealing,
CT offers little advantage, and even laparotomy misses up to 15% of
injuries, particularly the very posterior left-sided injuries and those
right-sided injuries that may be obscured by the liver. Thoracoscopy is
effective in excluding diaphragmatic injury, and compared with laparos-
copy, thoracoscopy offers the advantages of greater accuracy, the ability
to wash out the hemithorax, and avoiding the risk of tension pneumotho-
rax. In practice, thoracoscopy is best used for this purpose in patients who
have a chest tube in place and who do not have any evidence of abdominal
injury. If diaphragmatic injury is diagnosed, repair can be performed via
VATS approaches or, if close to the chest wall, by a minimal extension
of a port site and direct suture. We prefer to suture the defects directly
rather than mass stapling, although others have found stapling to be
acceptable.
Thoracoscopic irrigation and washout can be useful in patients who, at
laparotomy, are diagnosed as having a diaphragmatic laceration, partic-
ularly with spillage of gastric or enteric contents. This may reduce the risk
of subsequent empyema. Thoracoscopy is particularly advantageous in
evaluating patients suspected of having a chronic diaphragmatic hernia or
eventration. In symptomatic patients, thoracoscopic plication is effective.
246 Curr Probl Surg, March 2004
Air Leak After Injury. The indications for operation for persistent air
leak (in the absence of suspected tracheobronchial laceration) have been
based primarily on data for spontaneous pneumothorax. Schermer and
colleagues
67
reviewed the course of 39 patients who, except for air leak,
were ready for discharge. This was determined by air leak of greater than
3 days duration. Twenty-ve underwent VATS, with a reduced chest
tube duration (8 versus 12 days) and length of stay (10 versus 17 days).
VATS is required (as opposed to rigid thoracoscopy), since the majority
of patients will require some form of parenchymal stapling. Although not
absolutely required, a CT scan can be helpful in determining the likely
location of injury, as well as in evaluating the underlying pulmonary
characteristics that might modify the approach (eg, in a patient with
emphysema).
Chylothorax. Chylothorax is a rare complication of chest injury. If
diagnosed, esophageal rupture should be excluded. Thoracoscopy can be
used to treat the leak. Techniques include pleural abrasion, pleurectomy,
and pleurodesis in conjunction with clipping or pouring brin glue over
the site of the leak or at the right side of the diaphragmatic hiatus where
the thoracic duct enters the chest. Keeping the patient intubated with
positive-pressure ventilation overnight may assist in obliterating the
pleural space.
Summary. Thoracoscopy is a valuable tool in the treatment of thoracic
injuries. Rigid thoracoscopy is an alternative to VATS approaches.
Thoracoscopy requires that the patient be hemodynamically stable. It is
particularly useful in the early evacuation of hemothorax and the
identication of diaphragmatic injury.
Chest Wall Injuries
Rib Fractures
Rib fractures are common, yet they often appear trivial in the setting of
major multisystem injury. The incidence of chest trauma ranges from 4%
to 10% of all trauma admissions (the higher numbers being seen in
dedicated trauma centers), although the true incidence is probably higher,
since up to 50% of rib fractures may be missed on initial CXRs.
68,69
Chest
wall trauma is also a marker of signicant associated injury, including an
increased risk for intra-abdominal injuries.
69
The incidence of splenic
injury is increased by 1.7-fold and hepatic injury by 1.4-fold in the
presence of rib fractures.
70
In addition, 50% of patients with blunt cardiac
injury have rib fractures.
71
Rib fractures themselves, without associated injuries, cause signicant
Curr Probl Surg, March 2004 247
morbidity due to pain and the subsequent atelectasis, as well as underly-
ing pulmonary contusion.
72
Ziegler and Agarwal
73
noted that of 84
patients admitted with rib fractures, 12% died, 94% had associated
injuries, 32% had hemothorax and/or pneumothorax, 26% had a lung
contusion, and 55% required either an immediate operation and/or ICU
admission. The intermediate- and long-term impact was reected by a
35% incidence of pulmonary complications and a similar incidence of
discharge to an extended- care facility. The documentation of 3 or more
rib fractures has been associated with an increased requirement for ICU
care, abdominal injury, and overall mortality rate and is a useful triage
tool to determine patients who should be transferred to a tertiary care
unit.
70
Interestingly, although rib fractures indicate an overall increased
injury severity, the presence or absence of rib fractures (including rst or
second) does not appear to be a useful tool alone in determining the
likelihood of aortic rupture.
74,75
The impact of rib fractures is magnied at the 2 extremes of age. The
ribs and chest wall of children are much more pliable than those of adults.
As a result, rib fractures in children are less common, but pulmonary
contusion is more common. When rib fractures do occur in pediatric
patients, they are a sign of signicant energy transfer. Pediatric patients
with rib fractures have an increased mortality rate, particularly when
combined with closed head injury.
6
The elderly are also at increased risk of morbidity and mortality from
rib fractures. Bergeron and colleagues
76
found that patients older than 65
years with 3 or more rib fractures had a 5-fold increased mortality rate and
an almost 4-fold increased incidence of pneumonia compared with
younger patients. Bulger and colleagues
77
found that in the elderly,
patients with 3 or 4 rib fractures had a 19% mortality rate and a 31% rate
of pneumonia. For an elderly patient with more than 6 rib fractures, the
mortality rate was 33% and the rate of pneumonia was 51%. For each
additional rib fracture in patients 65 years and older, the risk of
pneumonia increased by 16% and the mortality rate increased by 19%. In
this study, the elderly faired signicantly worse compared with an 18- to
64-year-old cohort by all outcome measures, including the following:
number of ventilator days, length of ICU stay, length of hospital stay, and
mortality. In addition, pneumonia and late pulmonary effusion were
signicantly more likely in the elderly. The incidence of ARDS was also
higher in the elderly group. Compared with younger patients in whom this
risk plateaued after 3 rib fractures, in the elderly the risk increased
linearly with each additional fracture. These and other data suggest that
older patients are more susceptible to pneumonia and respiratory insuf-
248 Curr Probl Surg, March 2004
ciency after simple rib fracture, and these patients warrant closer
in-hospital observation and aggressive efforts at pulmonary toilet and
pain control.
77,78
Flail Chest
Flail chest has been dened as a fracture of more than 3 consecutive ribs
in 2 or more places. As Mayberry and Trunkey
69
note, a better denition
may be an incompetent segment of chest wall large enough to impair the
patients respiration. The important features of a ail segment of the
chest wall is the underlying pulmonary contusion that invariably accom-
panies this high-energy injury, coupled with respiratory failure from
unstable chest wall mechanics and pain. Clark and colleagues
79
found a
16% mortality rate with either isolated pulmonary contusion or ail chest,
but when combined, the mortality rate increased to 42%. It is difcult to
separate how signicant a pulmonary contusion is compared with a ail
chest wall. Clark and colleagues found that 57% of patients with isolated
ail chest required mechanical ventilation as opposed to 31% with an
isolated pulmonary contusion. Freedland and colleagues
80
found that 48%
of patients with a ail chest and a mild contusion required ventilation
compared with 75% of patients with ail chest and a severe pulmonary
contusion. Both studies noted that overall injury severity, age, and
requirement for transfusions were signicant contributing factors in
determining the outcome. Increasing age also is associated with an
increasing risk of death with ail chest, likely because of comorbid
conditions and less ability to tolerate respiratory compromise.
81
Pain Control
The majority of complications resulting from rib fractures are related to
chest wall pain, which limits pulmonary function. The inability of patients
to clear secretions adequately and the development of atelectasis from
chest wall splinting are risk factors for the development of pulmonary
infection. In addition, prolonged mechanical ventilation increases the risk
of pneumonia, and pain from multiple rib fractures may inhibit weaning
from the ventilator.
82
As a result, the care of patients with rib fractures has
focused on adequate pain control and aggressive respiratory care to
optimize pulmonary function.
Although the most common pain relief therapy is carefully titrated
intravenous narcotics, a variety of other techniques have been employed,
including local rib blocks, pleural infusion catheters, and epidural analgesia.
Each of these approaches carries its own set of advantages, disadvantages,
and complications (Table 6).
83,84
Some studies have suggested that epidural
Curr Probl Surg, March 2004 249
anesthesia results in improved functional lung volumes, a reduction in
respiratory failure, and improved outcomes
69,85,86
Although class 1 evidence
supporting the routine use of epidural anesthesia in the treatment of patients
with multiple rib fractures is lacking, most clinicians nd epidural analgesia
valuable in the treatment of these patients.
Bulger and colleagues
77
noted a mortality rate of 16% in patients over
age 65 with rib fractures treated without epidural analgesia compared
with a 10% mortality rate in those treated with an epidural. Wisner and
colleagues,
87
in a retrospective study of elderly chest trauma patients,
reported that epidural analgesia was an independent predictor of both a
decreased mortality rate and a decreased incidence of pulmonary com-
plications in an elderly population. Three studies have examined prospec-
tively the use of epidural analgesia versus intravenous narcotics. The rst,
by Ullman and colleagues,
88
randomized 28 patients to epidural versus
TABLE 6. Strategies for pain management of rib fractures and ail chest
Technique Advantages
Possible
disadvantages/complications
Systemic opioids Simple Cough and/or CNS or respiratory
depression
Oral analgesics and
NSAIDs
Simple, useful as supplement,
lack of CNS and/or CVS
side effects
Peptic ulcer, renal dysfunction,
platelet disorder, insufcient
control of pain
TENS Safe, simple, more effective
than NSAIDs
Limited data and experience,
inadequate pain control
Intercostal LA
(extrapleural
catheter)
No CNS effects Pneumothorax, LA toxicity
Interpleural LA No CNS depression or need
for multiple injections
Reduced efcacy if adhesions
present, must be able to
tolerate chest tube clamping,
potential for LA toxicity
Paravertebral LA Easier to perform technically
compared with epidural,
stable hemodynamics, no
CNS depression
Pneumothorax, potential for LA
toxicity, coverage not as
predictable
Epidural opioids Low dosage, intact sensory
and motor, bilateral pain
control, hemodynamic
stability
Urinary retention, risk of
respiratory depression,
breakthrough pain
Epidural LA No CNS depression, bilateral
and superior pain control
Hypotension, urinary retention
Epidural opiods LA Improved analgesia Epidural LA opioids
NSAIDs, nonsteroidal anti-inammatory drugs; TENS, trancutaneous electrical nerve stimula-
tion; LA, local anesthetics; CNS, central nervous system; CVS, cardiovascular system.
Adapted from Karmakar HK, Ho AM. Acute pain management of patients with multiple
fractured ribs. J Trauma 2003;54:61525.
84
Used with permission.
250 Curr Probl Surg, March 2004
intravenous narcotics and demonstrated improvements in ventilator time
and ICU and hospital length of stay in the epidural group. Mackersie and
colleagues
86
randomized 32 patients to epidural fentanyl infusion com-
pared with an intravenous fentanyl infusion. These investigators demon-
strated a mild improvement in pulmonary mechanics in the epidural group
along with a decreased incidence of respiratory depression. These authors
did not demonstrate any difference in outcome parameters, however.
Finally, a recent study by Moon and colleagues
89
demonstrated improve-
ments in subjective pain control and in some respiratory mechanics with
epidural opioid infusion compared with parenteral opioid analgesia;
however, these investigators failed to evaluate the effects on patient
morbidity and mortality rates.
Epidural approaches are contraindicated or relatively contraindi-
cated in the setting of bleeding disorders, prior back surgery, spine
injury, and/or elevated intracranial pressure. Epidurals with local
anesthetics are contraindicated in the setting of mitral or aortic
stenosis or hypovolemia because of the risk of systemic vasodilation
with xed cardiac output.
84
Elderly patients with even isolated rib
fractures should be considered at high risk of developing pulmonary
complications. These and all patients with multiple rib fractures
should have exquisite pain control. Some individuals can be treated
effectively with oral and parenteral narcotics and nonsteroidal anti-
inammatory agents. However, patients who exhibit splinting and
poor cough or inadequate pain control should have an epidural.
Prophylactic intubation is not indicated. However, if a patient requires
mechanical ventilation because of an underlying contusion or other
injuries, internal stabilization is possible. Every effort should be made
to wean the patient as soon as possible, again by using epidural or
other aggressive pain control techniques if possible. A generalized
protocol is outline in Figure 3.
Operative Repair
Stabilization of multiple rib fractures of ail segments has long held
great attraction as a treatment, yet it has failed to garner wide sup-
port.
69,83,90
This situation is likely due to the effectiveness of long-term
ventilation rather than the risk of operative intervention. The majority of
patients will demonstrate some brosis and stabilization of the ail
segment within 3 weeks, thereby allowing weaning from mechanical
ventilation. The presence of a ail segment itself is not an indication to
continue mechanical ventilation, but pulmonary dysfunction and inability
to ventilate are indications. Occasionally, however, the chest wall
Curr Probl Surg, March 2004 251
instability is so great that rib fracture xation seems to be an attractive
alternative to long-term mechanical ventilation.
The question of whether or not early rib xation can lead to improved
outcomes has been studied in a few small series. Isolated rib fractures do
not require specic operation in the acute setting, although nonunion and
Fig. 3. Algorithm for treating patients with chest wall pain. PCA, patient-controlled analgesia.
252 Curr Probl Surg, March 2004
pain rarely may be indications in the chronic phase. Most authors agree
that stabilization of ail chest is warranted if there is an indication for
thoracotomy other than the ail chest; if instability clearly prevents
weaning; or if pain control is ineffective. Fixation may not provide any
benet if there is an underlying pulmonary contusion. Voggenreiter and
colleagues
91
found that operative xation appeared to offer a benet over
internal pneumatic stabilization (mechanical ventilation) in patients with-
out pulmonary contusion but no benet if pulmonary contusion was
present (Table 7).
Tanaka and colleagues
92
prospectively studied patients with ail chest
who required at least 5 days of mechanical ventilation. All patients
received aggressive pulmonary toilet and epidural anesthesia. Operative
stabilization was then performed in 18 patients by using Judet struts, and
internal pneumatic stabilization was performed in 19. The operative group
had a shorter ventilatory time (10.8 3.4 versus 18.3 7.4 days), a
lower incidence of pneumonia (24% versus 77%), and a higher return-to-
work rate at 6 months (61% versus 5%). Ahmed and Mohyuddin
93
reported on a comparison between operative xation and internal
stabilization approaches that suggested advantages favoring operative
repair (Table 8). Interestingly, all deaths were attributed to ARDS.
A major problem is the lack of consistently reliable tools for xation.
Options include pericostal sutures around or through the ribs, plates,
wires used for orthopedic procedures, and/or the Judet staple, which is a
form of plate that can wrap around the rib.
69
The problems of xation are
as follows: 1) intercostal nerves can be trapped, thereby increasing the
pain; 2) the bone is often too thin to hold hardware; and 3) the ribs
normally move not only up and down but outwards with respiratory
effort, thereby placing a variety of tension forces on any repair site.
Nevertheless, this is an area that continues to be explored. We have rarely
resorted to rib fracture stabilization in the treatment of fractures or ail
segments but do consider this treatment option for the patient who has a
TABLE 7. Comparison of outcomes between open repair and internal stabilization
Treatment
Flail
chest
Pulmonary
contusion
Ventilator
days
Pneumonia
(%)
OR xation (N 10) 6.5 7 1 (10%)
OR xation (N 10) 30.8 34 3 (30%)
Internal stabilization (N 18) 26.7 29 5 (28%)
OR, open repair.
Adapted from Voggenreiter G, Neudeck F, Aufmkolk M, Obertacke U, Schmit-Neuerburg KP.
Operative chest wall stabilization in ail chestoutcomes of patients with or without
pulmonary contusion. J Am Coll Surg 1998;187:1308.
91
Used with permission.
Curr Probl Surg, March 2004 253
severe ail chest with minimal underlying contusion and who clearly is
not responding to pain control or has a grossly unstable chest that
prevents weaning (Figure 4). We tend to favor using pericostal sutures,
often through the ribs rather than around them, with gure-of-8 sutures or
plates at the anterior and posterior margins of the fractures to secure the
free oating ribs to more stable elements, if possible. A more aggressive
use of operative xation may become a more reasonable alternative as the
techniques evolve.
Late Sequelae. Flail chest is associated with signicant late morbidity,
in terms of chronic pain and the sensation of decreased ventilatory
capacity. As many as two thirds of patients with ail chest alone will
suffer long-term disability.
94
Chronic dyspnea can persist in a similar
number; nearly one half have intermittent chronic chest wall pain, and one
fourth complain of chest tightness.
95
Early xation may reduce the late
debility, and this aspect deserves more study.
96
Some patients with a
traumatic thoracoplasty and/or multiple, painful nonunion of rib frac-
tures may benet years after injury from resection and plating of the
painful sites.
97,98
Because of relatively poor vascular supply, cartilagi-
nous injuries are more prone to chronic complications, including aseptic
and septic necrosis, which may require resection. Signicant infections of
the lower aortic arch may require reconstruction with muscle aps.
72
Sternal, Clavicular, and Scapular Fractures
Because of the force implied, sternal fractures have been associated
with an increased incidence of both cardiac and great vessel injury.
Reports of the incidence of cardiac injury associated with sternal fracture
range from 18% to 62%.
99,100
Occasionally, tamponade can occur from
TABLE 8. Outcomes for operative xation of ail chest and internal stabilization
Outcome
Operative
xation
(N 25)
Internal
stabilization
(N 38)
Average days ventilated 3.9 15
Tracheostomy 11% 37%
Complications
Chest infection 15% 50%
Septicemia 4% 24%
Barotrauma 0% 8%
Mortality rate 8% 29%
Adapted from Ahmed Z, Mohyuddin Z. Management of ail chest injury: internal xation vesus
endotracheal intubation and ventilation. J Thorac Cardiovasc Surg 1995; 110:167880.
93
Used with permission.
254 Curr Probl Surg, March 2004
Fig. 4. Patient 2 weeks after blunt trauma with persistent fever, pain, and chest wall instability. A) CT
scan demonstrates persistent atelectasis with signicant volume loss and displaced rib fragments
(arrow). B) CT scan of the same patient demonstrates persistent hemothorax (arrow). At operation the
patient had empyema and a free-oating chest wall in multiple segments.
Curr Probl Surg, March 2004 255
extrapericardial blood collection without intrapericardial hematoma or
injury, and requires operative decompression, preferably by sternotomy
(Figure 5).
101
As with rib fractures, the treatment is primarily supportive.
Most fractures are transverse, involve the sternal-manubrial junction or
upper one third of the sternum, and stabilize with pain control.
102
Unstable fractures, fractures associated with chronic pain, or those
associated with infection (indicated by a new sternal click in the setting
of fever and/or erythema) require operative intervention. Options include
wires in a gure-of-8 fashion, plates, or both. The advantages of plate
xation are that it is easier and can be performed as an outpatient
procedure in some cases. However, in our experience, when attempting to
cross a more acute angle, there is an increased incidence of the screws
loosening. In many instances, however, by the time the patient notices
plate motion and/or radiographs document loss of xation, there has been
sufcient healing to allow plate removal without loss of stability.
Longitudinal fractures may require closure similar to that for a sternot-
omy incision. Sternal fractures complicated by mediastinal abscess
Fig. 5. Patient after MVC. CXR demonstrates a widened mediastinum. Clinical ndings suggesting
tamponade prompted an echocardiogram, which revealed tamponade due to retrosternal hemor-
rhage. The patient responded to drainage via sternotomy.
256 Curr Probl Surg, March 2004
require debridement. Simple approaches include placement of an irriga-
tion system, but recalcitrant or widespread infection requires closure with
muscle and/or omental aps after widespread debridement.
43
Large Chest Wall Defects
Large, complex open wounds require a multidisciplinary approach.
Initially, aggressive wound debridement, drainage of hemothorax, and
simple packing are appropriate.
32
Subsequent treatment depends on
which levels are involved as well as the location (eg, ribs, muscle,
intrathoracic, skin, etc).
103
A dreaded complication is a necrotizing
wound infection, characterized by rapidly progressive sepsis with local
erythema and at times, minimal supercial evidence of the infection.
104
These infectious complications require wide debridement and reconstruc-
tion. If sepsis is not a concern, bony stability can be achieved, depending
on the size of the defect, with a variety of meshes and/or methylmethac-
rylate sandwiches. Probably the most important factor is the use of
vascularized tissue aps (Table 9).
Traumatic lung hernia, characterized by protrusion of the lung paren-
chyma outside the ribs, is uncommon but has been described as a
complication of chest tubes, thoracotomy, or trauma.
105
More often, these
occur in patients who require high-pressure ventilation. As long as there
is no evidence of incarceration or infarction, immediate repair is not
TABLE 9. Options for ap coverage based on location of defect.
SITE of defect FLAP choices
Intrathoracic defect Serratus anterior muscle
Pectoralis major muscle
Latissimus dorsi muscle
Rectus abdominis muscle
Omentum
Sternal defect Pectoralis major muscle
Rectus abdominis muscle
Omentum
Anterior chest wall Pectoralis major muscle
Latissimus dorsi muscle
Rectus abdominis muscle
Omentum
Lateral chest wall Pectoralis major muscle
Latissimus dorsi muscle
Parascapular fasciocutaneous
Posterior chest wall Latissimus dorsi muscle
Trapezius muscle
Reproduced with permission from Karmy-Jones R, Nathens A, Stern E, eds. Thoracic Trauma
and Critical Care. Boston, Mass: Kluwer Academic Publishers; 2002:24751.
103
.
Curr Probl Surg, March 2004 257
needed. If there is evidence of lung necrosis, early repair of the chest wall
defect (using mesh or other techniques) accompanied by resection of the
involved lung will be required (Figure 6).
105
Lungs and Pleura
Hemothorax
The treatment of patients with ongoing hemorrhage has been
described earlier, and the approach to those who are stable and have
a retained hemothorax will be discussed in later, but the acute
treatment of patients who present with hemothorax without immedi-
ately obvious indications for operation deserves consideration. For
simplicity, patients can be considered to be in 1 of 2 extremes. The
rst set includes those patients who are stable, with minimal respira-
Fig. 6. Right parasternal lung hernia (arrow) after blunt trauma
258 Curr Probl Surg, March 2004
tory distress, who do not require any operative intervention (thoracic
or extrathoracic) and who have minimal blunting on the CXR without
pneumothorax. These patients can be treated with pain control as
needed and observation with repeated CXRs in 4 to 6 hours and at 24
hours. Typically, there is a small increase in uid with no symptoms,
and this situation can be monitored. If the patient requires a general
anesthetic or if there is an increase in uid greater than one fourth of
the hemithorax, then tube thoracostomy should be performed. This
situation is relatively uncommon. The more typical scenario is the
other extreme of patients, who present with multiple injuries, often
require orthopedic and/or abdominal procedures, and are ventilated. In
this group, chest tubes should be placed without hesitation. If, on
placing a tube, more than 750 mL of blood (or 10 mL/kg) is drained
within a few minutes, we recommend that a second chest tube be
placed if the patient is not a candidate for immediate thoracotomy.
This second tube ensures adequate pleural drainage and minimizes the
risk of clotted blood occluding the single chest tube and obscuring any
ongoing hemorrhage.
Pneumothorax
Pneumothorax is present in as many as one fourth of patients suffering
from blunt trauma.
106
This injury may be a cause of preventable death in
the eld in up to 16% of cases.
107
Less than 5% of patients with traumatic
pneumothorax have isolated chest injuries, meaning that the presence of
associated injuries makes the diagnosis both more difcult and more
critical.
106
As many as 20% have bilateral pneumothorax.
The clinical diagnosis, if based solely on auscultation, is incorrect in
20% to 30% of cases. As a result, prehospital treatment guidelines for
possible pneumothorax have been adopted by some agencies that allow
for needle or tube chest decompression in the eld or hospital without
waiting for conrmatory tests. The Italian Resuscitation Council, for
example, recommends immediate tube decompression under the follow-
ing circumstances: in the presence of subcutaneous emphysema or
unilateral decreased breath sounds plus either severe dyspnea or arterial
oxygen saturation less than 90% on 100% O
2
or a systolic blood pressure
of less than 90 mm Hg.
106,108
A South African study has demonstrated
that chest tubes placed in the eld by physicians are effective and safe,
with a low nontherapeutic rate (less than 3%) and rare (less than 1%)
dislodgment or malposition rate.
109
Simple decompression with percuta-
neous kits and Heimlich valves has also proven to be effective when
Curr Probl Surg, March 2004 259
performed by nonphysician prehospital caregivers.
110
In 1 series, 55% of
chest drains were placed before arrival in the ED.
106
Even in stable patients, the plain CXR can miss subtle and/or anterior
pneumothoraces (Figure 7).
111
Confounding factors include contusion,
hemothorax, monitoring lines, and/or the presence of backboards. The
widespread use of chest and abdominal CT scans has increased an
awareness of these small pneumothoraces, with a reported incidence
ranging from 5% to 55%.
112,113
Although the clinical signicance of
these missed pneumothoraces is debatable, we perform tube decom-
pression if the patient requires positive-pressure ventilation for any
reason, since up to one third of ventilated patients will proceed to develop
tension pneumothorax.
114
Thoracic ultrasound shows some promise in the
detection of pneumothoraces, both prehospital and in the ICU. Dul-
chavsky and colleagues
38
noted no false-positives among 270 patients
after blunt injury, and 1/11 false-negative. Detecting pleural sliding was
associated with a true-negative rate of 100%. Accuracy is affected by
subcutaneous emphysema.
The majority of pneumothoraces after blunt injury are due to lung
laceration from rib fractures or shear injuries. Full expansion of the lung
will, in the majority of cases, result in eventual healing. Persistent
pneumothorax despite chest tube placement may be due to several causes
(Table 10). One common cause of persistent pneumothorax is pain,
resulting in atelectasis. Effective pain control, incentive spirometry, and,
in many cases, discontinuing the tube to allow more mobilization, can
relieve the residual air collection. Recurrent pneumothorax can occur in
up to 25% of patients once the tube is removed.
115
If this is thought to be
the result of an error in technique during tube pulling, rather than
reinsertion, either catheter aspiration or observation should be employed.
A rare form of persistent pneumothorax despite tube drainage is
pneumothorax ex vacuo.
116,117
Acute endobronchial blockage (eg, by
blood) can lead to a sudden increase in negative pleural pressure, in turn
resulting in gas to be drawn into the pleural space. The pneumothorax is
limited to the space created by the collapsed lobe and will not respond to
tube drainage unless the bronchial obstruction is cleared.
116,117
In up to one third of parenchymal injuries, air can dissect along
perivascular places to the mediastinum, resulting in pneumomediastinum
(the Maklin effect).
118
Pneumomediastinum should prompt an evalua-
tion for aerodigestive injuries. However, this dissection can extend into
the pericardium, resulting in pneumopericardium. Pneumopericardium
may also result from congenital or acquired traumatic pericardial defects
and rarely may originate from extrathoracic sources.
118
There is a risk for
260 Curr Probl Surg, March 2004
Fig. 7. Patient admitted after blunt trauma. A) CXR reveals right parenchymal consolidation. B) CT
scan identies an anterior persistent pneumothorax (arrow).
Curr Probl Surg, March 2004 261
the development of tension pneumopericardium, and this risk is increased
in patients who are receiving positive-pressure ventilation. This diagnosis
is suggested by CXR in conjunction with the clinical signs of tamponade,
auscultatory ndings, and/or unexplained hypotension. Treatment in-
cludes tube thoracostomy and pericardial window.
119
Since 25% of
patients or more have an associated airway injury, bronchoscopy should
be performed, and if the severity of the mechanism warrants it, esopha-
goscopy as well.
118
Pulmonary Contusion
Pulmonary contusion represents a spectrum of lung injury characterized
by the development of parenchymal inltrates and various degrees of
respiratory dysfunction. Dupuytren is credited with coining the term in
the late 19 th century.
1,120
There is a spectrum of injury severity, ranging
from localized consolidation with little clinical impact, to acute lung
injury (ALI) and ARDS; (Table 11).
It has been argued that pulmonary contusion is the most common
potentially life-threatening chest injury. Although the mortality rate is
often dictated by the associated injuries, in particular closed head injury,
most reviews report a mortality rate of 5% to 30%, with contusion being
the direct cause of death in 25% to 50% of fatalities.
121
In essence,
transmission of kinetic energy (with or without overlying rib fractures and
the subsequent laceration) results in bruising of the lung, characterized
by interstitial and alveolar edema, hemorrhage, and subsequent alveolar
collapse (Figure 8).
122
Contrecoup injuries can occur, and the extent of
bony injuries depends on the compliance of the chest wall itself.
TABLE 10. Possible causes of persistent pneumothorax after tube decompression
Presence of air
leak
Possible cause
No air leak Misplaced/extrathoracic chest tube
Plugged tube
Nonfunctional tube as lung expanded
Airway obstruction
Lung collapse
Lung contusion
Compete airway laceration with obstruction
Persistent air leak Airway injury
Tube dislodged or disconnected
Large parenchymal injury
Underlying parenchymal disease (eg, bullae)
High levels of positive airway pressure
262 Curr Probl Surg, March 2004
Clinically, hypoxia and ventilatory embarrassment develop within 24 to
48 hours, although changes can occur in a much shorter time depending
on the extent of injury and the need for volume replacement, which
aggravates the process.
123
Initial CXRs may be normal or at most
demonstrate patchy changes, but as resuscitation continues, a blossom-
ing is noted with opacication and air bronchograms. If there are
signicant changes noted on an initial radiograph taken shortly after
injury, in general the course will be severe. Chest CT can grade the
degree of injury more accurately and may lead to better predictions of the
TABLE 11. Distinctions between acute lung injury (ALI) and adult respiratory distress syndrome
(ARDS)
ALI Acute onset
PaO
2
/FiO
2
300
PCWP 18 or no clinical evidence of increased
left atrial pressure
Inltrates on CXR
ARDS PaO
2
/FiO
2
200 regardless of PEEP
PEEP, positive end-expiratory pressure; CXR, chest radiograph; PCWP, pulmonary capillary
wedge pressure.
Fig. 8. CT scan of chest demonstrates patchy areas of consolidation and edema after blunt injury
Curr Probl Surg, March 2004 263
clinical course, but other than detecting occult changes (eg, pneumotho-
rax not appreciated on the CXR) that can change the treatment strategy in
up to 30% of patients, this approach does not lead to signicant
improvement in the outcome.
124
Treatment is generally supportive.
122
Oxygen (including continuous
positive airway pressure mask, if needed) should be supplied early.
Intravenous volume should be restricted if possible (ie, in a hemodynam-
ically normal patient), since the associated capillary leak will lead to a
worsening of pulmonary edema. Diuresis is indicated in the presence of
volume overload (pulmonary occlusion pressure greater than 18 mm Hg
or an end-diastolic volume index greater than 135 mL/m
2
).
125
Whether or
not colloid solutions are superior in terms of reducing lung injury when
used for resuscitation after pulmonary contusions has not been proven,
although there is ongoing research into such agents that may have
antioxidant properties as well.
122,126
Intubation should be performed for the usual indications and not for
prophylaxis. In 1 study, 12 of 75 patients with ALI or mild contusion
were treated without intubation, stressing the importance of clinical
evaluation.
127
Flail chest per se is not an indication for mechanical
ventilation.
90
Instead, meticulous and effective pain control should be
attempted rst. Once the patient is intubated, lung-protective strategies
should be employed. Steroids have been studied in experimental models,
but there is no evidence that the benets outweigh the risk of immuno-
suppression in patients with contusion.
122
Ventilator Treatment. The treatment of pulmonary contusion requires
prolonged ventilatory support similar to that required in the treatment of
ARDS. Indeed, the risk of developing ARDS is directly related to
contusion size. Miller and colleagues
128
noted that if the contusion
volume (based on the CT scan) is greater than 20%, the risk of developing
ARDS is much greater (82% versus 22%) than with lesser injuries. In the
trauma population, ARDS is reported to be associated with a mortality
rate as high as 50%.
129,130
A complete discussion of the treatment of
ARDS is beyond our scope, but some salient points can be summarized.
In brief, a major focus of treatment and research has been to reduce
barotrauma, prevent shear injury on the alveoli, and limit stimulation of
the systemic inammatory response.
129
Indeed, many investigators be-
lieve that ventilator-induced lung injury may be the primary cause of
ARDS in a substantial number of patients, arguing that the inammatory
effects of ventilator-induced lung injury may lead to both progressive
parenchymal and systemic inammation.
129,131
264 Curr Probl Surg, March 2004
Initial treatment is directed at reducing barotrauma.
125
Aiming for lower
tidal volumes (4 to 8 mL/kg) and peak airway pressures less than 30 to 40
cm H
2
O appear to reduce both barotrauma and secondary inammatory
changes and to improve ventilation to more compliant lung regions.
Positive end-expiratory pressure (PEEP) has a protective effect and
preserves functional reserve capacity. This may require permissive
hypercapnia, by allowing the PaCO
2
to increase to 80 to 100 mm Hg
while maintaining the arterial oxygen saturation at greater than 90%.
131
Buffering agents should be used to keep the arterial pH greater than
7.28.
129
This method requires paralysis and sedation. The ARDS NET, in
a randomized clinical trial of 800 patients, found a 25% reduction in
mortality in patients ventilated at tidal volumes of 6 mL/kg compared
with those ventilated at 12 mL/kg.
132
The benet of this approach is
independent of the primary underlying etiology.
133
High-frequency ventilation has been used for both ALI and ARDS as
well in the treatment of patients with bronchopleural stula (BPF).
134,135
This technique appears to be associated with less cardiovascular impact
than conventional ventilation but has not been shown clearly to provide a
survival benet.
135
Complications include dislodgment, airway necrosis,
and gas trapping, and these considerations, coupled with increased cost,
have limited its use in the adult population.
Pressure-control, inverse-ratio ventilation has been used by some
centers as the primary mode of ventilation in the setting of ALI/ARDS
and as a rescue mode in others when alternative approaches have
failed.
136
This approach also requires medical paralysis. By setting a
pressure limit, barotrauma may be reduced compared with volume-
controlled approaches, and by increasing the expiratory time, it is
hypothesized that alveolar recruitment is enhanced.
136,137
Complications
include the development of excessive auto-PEEP, which can cause
barotrauma and lead to insufcient oxygenation.
Prone ventilation has been shown to improve oxygenation, possibly by
improving ventilation to dorsal areas of the lung that have preferential
perfusion, even in the prone position.
138
Several other factors have been
suggested for this improvement, including better diaphragmatic excursion
and reducing the compressive effect of the heart and mediastinum.
139
Patients who might be considered for prone positioning are those who
require prolonged elevated levels of PEEP. Controversy remains about
safety. When used in unstable patients, turning the patient prone can lead
to catastrophic cardiovascular collapse. This quandary has led to some
centers using this technique early or not at all. In addition, there is
concern regarding suctioning and monitoring and uncertainty about how
Curr Probl Surg, March 2004 265
long patients should remain prone. Most centers that use this approach
have established protocols regarding indications and nursing care. Cur-
rently, prospective studies are under way to determine whether prone
positioning will reduce mortality rates in ventilated patients with
ALI/ARDS.
139
Inhaled nitric oxide has been reported to overcome pulmonary vascular
hypertension and improve oxygenation.
140
Unfortunately, improvements
in oxygenation are not necessarily associated with a reduction in mortality
rates.
141
One possible complication is that overcoming appropriate
hypoxic vasoconstriction may actually worsen a shunt.
142
Extracorporeal cardiopulmonary bypass (ECMO) continues to excite
research and clinical efforts. By offering a method of maintaining both
oxygenation (PaO
2
) and ventilation (PaCO
2
) while reducing ventilator-
induced lung injury to a minimum, ECMO appears to be an ideal
approach.
143
ECMO was rst utilized in a broad way in the treatment of
neonatal respiratory failure.
144
Indications in adults are controversial
because reversible respiratory failure (within 2 to 3 weeks, the limit of
ECMO therapy) is difcult to dene with certainty. A variety of
techniques are available, but in adults the most promising appears to be
venovenous support, including both extracorporeal CO
2
removal and
venovenous ECMO.
143
Venovenous ECMO offers the advantages of
maintaining normal pulmonary perfusion without the need for arterial
cannulation, with its attendant risk of thromboembolism. The primary risk
in the trauma setting is bleeding, a risk that has been partially reduced by
the development of heparin-bonded circuits. Once ECMO is established,
ventilator settings are reduced to the minimum. Repeated bronchoscopy
may be required to help clear secretions. Operative procedures (such as
evacuation of hemothorax) are possible while the patient is on ECMO.
Future trials need to conrm the benet of ECMO against contemporary
rather than historical ventilator strategies, and there is hope that a
practical articial lung can be developed that will permit longer use with
reduced anticoagulation requirements.
145
Occasionally, the contusion is severe but unilateral. In this setting,
placement of a double-lumen endotracheal tube and split-lung ventilation
may be appropriate.
146
The goals are to maintain normal ventilation for
the relatively uninjured lung while providing minimal ventilation at low
pressure to the injured side.
147
Two ventilators are required, but in our
experience there is no need for computer synchronization. Potential
problems include difculty in placing a double-lumen tube, clearing
secretions through the smaller lumens, possible airway necrosis if
prolonged (more than 5 to 7 days), and displacement.
266 Curr Probl Surg, March 2004
Lung Injuries Requiring Operation
It has been estimated that 20% to 30% of patients who undergo
thoracotomy after trauma will require some form of lung resection.
148,149
Considering all patients with chest trauma, as few as 1% to 2% of all blunt
injuries will require resection. A multicenter study found that 0.5% of
blunt-injured patients required urgent thoracotomy (within 24 hours), of
whom 17% (or 0.1% of all blunt-injured patients) required lung resec-
tion.
65
Mortality rates as high as 3% to 50% after lobectomy and of 70%
to 100% after pneumonectomy reect the severity of lung and overall
injury in patients requiring extensive resection.
148,150,151
A majority of parenchymal injury is due to laceration from associated
rib fractures. Various degrees of supercial and deep hemorrhage from
shear injury and contusion can coexist. Severe deceleration can lead to
shear injury at the hilum, resulting in deep central lacerations, or more
peripherally, leading to tearing along the ssures at the branches of the
bronchi.
The use of nonanatomic and stapling techniques has been advocated as
a method of both damage control and rapid, denitive resection under
appropriate circumstances, suggesting the potential for reduced operative
time and blood loss and increased parenchymal salvage.
49,149,152-154
However, although the majority of patients who present with penetrating
injuries have peripheral injuries that are simple to treat, blunt trauma often
results in combinations of diffuse contusion and lung maceration that are
extremely difcult to salvage.
The most common procedures required are simple suture repair or
wedge resection. Tractotomy is used either to dene deep injuries or to
treat peripheral injuries that pass through the parenchyma. Lobectomy
and pneumonectomy are rarely required and can be performed nonana-
tomically by using staplers (the so-called simultaneously stapled lobec-
tomy or pneumonectomy [SSP]) or anatomically. The latter is usually
required in the setting of complete ssures, may take longer, and may be
more difcult if diffuse edema and bleeding are present.
Minimal peripheral injuries often are encountered when operating for
associated injuries.
155
Typically, the patient undergoes operation for
ongoing hemorrhage due to intercostal vessel damage. The intercostal
arteries are perfused at systemic pressures and as a result, can bleed
profusely. Rarely, a fragment of rib has lacerated the lung and is similar
to a deep stab wound. Standard stapling devices may be used safely
without pledgets or oversewing of the edges.
Whereas treatment of the most severe and the most minor injuries is
Curr Probl Surg, March 2004 267
straightforward, the treatment of deep lobar injuries is more controversial.
Simple oversewing of any entry and/or exit site is insufcient, since there
is invariably continued deep parenchymal hemorrhage that results in
aspiration, pneumonia, and unremitting ARDS. In general, pulmonary
tractotomy should be performed. This can be achieved with either a
stapler or between clamps. This method will expose deep bleeding vessels
and may allow denitive control. In those patients with continued
instability or associated injuries that must be addressed, the procedure
may be considered denitive.
153
It is common that after performing
tractotomy, there is such diffuse bleeding that simple suture ligation is
inadequate. Placing large, pledgeted, mattress sutures, similar to liver
stitches, from the depth of the wound to the edge provides excellent
control. After completion of these initial maneuvers, a minority of
patients still will have signicant air leaks or long tracts of devitalized
tissue. If these patients remain stable, they should be considered for
resection up to and including lobectomy. Tractotomy was initially
described as a damage-control technique. It may be associated with
increased postoperative complications compared with lobectomy, but this
is debated. Certainly, if major blood loss continues or if there is obvious
extensive lobar destruction, lobectomy must be performed as soon as
possible. In patients with complete ssures, a stapled lobectomy similar
to the pneumonectomy procedure described later may be possible.
Otherwise, anatomic lobectomy can be performed by skilled surgeons
with almost the same rapidity.
155
Patients with perihilar injuries or extensive lung maceration generally
present with class III or IV hemorrhagic shock and undergo operation
quickly with minimal resuscitation. Survival correlates with the rapidity
of control. On entering the chest, if large central bleeding is encountered,
hilar control should be the rst maneuver performed. The pulmonary
ligament is divided to the level of the inferior pulmonary vein. This
allows torsion of the entire lung as a temporizing method. In addition, if
the ligament is not divided, the distance that a clamp or stapler is required
to cover is tripled. Rarely, very proximal injuries may require intraperi-
cardial control of the pulmonary artery. In cases of small injuries to a
single structure, a noncrushing vascular clamp may be applied proximally
before repair is attempted. When both artery and vein are injured or when
a signicant length of vessel is damaged, the patient will benet from an
early decision to perform a pneumonectomy. A linear stapler is red
across the hilum and an SSP is performed. A TA-90 stapler with 3.5-mm
staples is sufcient, although some centers use 4.5-mm staples. The
stapler approach has the signicant advantage over most vascular clamps
268 Curr Probl Surg, March 2004
in that the latter are often held slightly apart by the bronchial cartilages,
and the thin-walled vessels can slip out of the clamp with fatal results
when the lung is amputated.
44
It must be emphasized that this
represents a damage-control approach for the most extreme emergencies
associated with central major hilar vascular trauma or the even rarer
devastating complete parenchymal disruption.
Trauma pneumonectomy generally is associated with a 50% to 100%
mortality rate, and although it should not be delayed, it should not be
performed without at least quickly assessing whether more conservative
options are possible.
65
One common cause of acute mortality is sudden
right heart failure, a consequence of both the volume of resuscitation and
a sudden halving of the pulmonary circuit. If this occurs immediately on
clamping, there is usually no hope. However, if it occurs hours or days
later, supportive efforts can be tried with diuretics, vasodilators, and
occasionally ECMO. It is preferable in patients with isolated hilar injuries
to stop all uid boluses when the hilum is controlled to avoid aggravating
the right heart strain by excessive uid administration. A second pitfall
related to SSP is the potential for increased bronchial stump leak and/or
empyema. In fact, animal models have shown that SSP stumps have a
similar bursting strength when compared with individual ligation and
oversewing of the artery, vein, and bronchus. Wagner and colleagues
44
noted a reduction in stump leak in SSP survivors compared with
individual stapling. Nevertheless, the bronchus is usually longer (partic-
ularly with right- sided pneumonectomy) than in elective cases, and this,
in conjunction with the increased risk of empyema, has led to the
suggestion that elective reexploration, washout, and stump reinforcement
with viable tissue be performed as soon as the patient is stable enough to
tolerate the procedure.
A multicenter review identied 143 patients who underwent emergent lung
resection after trauma (28 blunt).
65
Simple suture, tractotomy, and wedge
resection were performed predominantly after penetrating injury. Relatively
speaking, lobectomy and pneumonectomy were more often required after
blunt trauma, which tended to be associated with signicant, diffuse paren-
chymal destruction. The overall mortality rate after blunt injury was 68%. Of
the 28 patients who underwent acute lung resection after blunt trauma, the
following mortality rates based on the technique of resection were noted:
simple suture, 1 of 1; tractotomy, 1 of 2; wedge resection, 8 of 15; lobectomy,
7 of 8; and pneumonectomy, 2 of 2.
The choice of resection was determined by the extent of lung injury, and
each increment in resection was associated with an 80% relative risk of
increased mortality, but the mortality rate was encouragingly low for this
Curr Probl Surg, March 2004 269
group of extremely unstable patients. The sole survivor of lobectomy was
the only patient who underwent anatomic as opposed to a stapled
resection. However, this reects the fact that stapled techniques were
performed in more critically injured patients.
Whatever the reason for parenchymal resection, the outcome will be
impacted signicantly by the degree of air leak at the time of closing and
the residual space that is anticipated. In unstable patients, abbreviated
closure must be employed, with plans to reexplore and perform washout.
Patients with extensive contamination and those in whom it is anticipated
that there will be signicant residual clot, reexploration, or placement of
irrigation systems should be considered. The smaller the space, the sooner
the air leak will seal, and the lower the complication risk will be.
Complications
Pneumonia. The most common complication of chest trauma is
pneumonia. This is linked to the need for intubation and mechanical
ventilation, increasing from as low as 6% in nonintubated patients to 44%
in those who require ventilation.
156
There is, however, no role for
prophylactic antibiotics. Of all patients admitted with a diagnosis of
pulmonary contusion, nearly 50% will develop pneumonia, barotrauma,
and/or major atelectasis, and one fourth will go onto full-blown ARDS.
Ventilator-associated pneumonia (VAP, dened as pneumonia arising
more than 48 hours after the initiation of mechanical ventilation) is
difcult to dene and diagnose. In our institution, however, we have an
incidence of VAP of 20% to 30% among patients intubated for longer
than 7 days. Clinical suspicion is often raised by new inltrates, recurring
fever, rising leukocytosis, and/or a change in endotracheal secretions, but
distinguishing between colonization and infection may require special-
ized techniques. Quantitative cultures obtained from a variety of ap-
proaches increases the specicity (although perhaps with reduced sensi-
tivity) of endobronchial cultures, and each institution must dene cut off
values based on whether or not the patient is already receiving antibiotics
(Table 12 and Figure 9).
Retained Hemothorax. Tube thoracostomy fails to evacuate the hemi-
thorax completely in approximately 5% of cases.
157
Complications that
may result from retained or undrained traumatic hemothorax include
empyema and/or brothorax. Predisposing conditions include prolonged
ventilation, development of pneumonia, a break in pleural integrity (eg,
after tube thoracostomy), and other sites of infection.
158
On the other
hand, stable, nonventilated patients with small effusions (less than one
fourth of hemithorax) after blunt trauma with no obvious pleural
270 Curr Probl Surg, March 2004
disruption usually will resolve without sequelae. In these patients the
cornerstone of therapy should be observation (Figure 10).
Evacuation of hemothorax within 7 days has been shown to reduce the
incidence of complications in military personnel.
159
However, recogniz-
ing the extent of hemothorax can be difcult. CXR can underestimate
both the extent of parenchymal consolidation and the volume of retained
blood, particularly in ventilated patients. Chest CT is much more accurate
in this setting, but interpretation requires some individualization.
160
In
brief, nonintubated patients who are ambulating, have no infection risk,
and whose hemothorax results in minor blunting of the costophrenic angle
do not necessarily require further procedures.
4
On the other hand, even
moderate effusions in ventilated patients or in those with other risk factors
should be drained aggressively when detected by CT.
43,158
When recognized acutely after injury, the simplest and most expeditious
treatment is to place a second chest tube. When recognized after 1 to 2
days, this may not be helpful because it may simply increase pain,
splinting, and the risk of pneumonia with subsequent seeding of the
pleural space. Intrapleural streptokinase (250,000 units) or urokinase
(40,000 units) has an efcacy rate of 65% to 90%.
161
Complications
include fever and pain, but the risk of restarting bleeding is negligible.
Disadvantages include longer therapeutic time (several days) versus the
more direct operative drainage, and kinase therapy will not break down
loculations. Therefore, the use of these agents may be more useful after
debridement when it is suspected that the clot is relatively soft.
Thoracoscopy offers the advantage of complete removal of all clot
without the excess morbidity of a formal thoracotomy. Meyer and
TABLE 12. Yields of diagnostic tests for ventilator-associated pneumonia
Threshold
Sensitivity
(%)
Specicity
(%)
Endotracheal aspirate Any pathogen 7095 50
Endotracheal aspirate 10
6
CFU/mL 2570 7085
Bronchoscopy
PSB culture 10
3
CFU/mL 30100 80100
BAL culture 10
4
CFU/mL 5595 70100
BAL cytology 27% CAB 3085 65100
Nonbronchoscopic
PSB 10
3
CFU/mL 60100 75100
BAL 10
4
CFU/mL 70100 6595
PSB, protected specimen brush; CFU/mL, colony-forming units per milliliter; BAL, bron-
choalverolar lavage; CAB, cell-associated bacteria.
Reproduced with permission from Karmy-Jones R, Nathens A, Stern E, eds. Thoracic Trauma
and Critical Care. Boston, Mass: Kluwer Academic Publishers; 2002:397402.
522
Curr Probl Surg, March 2004 271
colleagues
66
compared the placement of a second chest tube versus
thoracoscopy for the treatment of retained traumatic hemothorax. Patients
undergoing thoracoscopy had a shortened length of time requiring chest
tube drainage, a shortened hospital stay (2.7 days less), and a lower total
hospital cost ($6,000 less) compared with those patients treated with a
second chest tube. There were no failures and no complications, and no
patients in the group randomized to early thoracoscopy required conver-
sion to a formal thoracotomy. In contrast, a second chest tube failed to
evacuate the retained hemothorax completely, requiring operative treat-
ment in more than 40% of the patients.
Fig. 9. Approach to the diagnosis of ventilator-associated pneumonia. BAL, bronchoalveolar lavage;
CFU, colony-forming units.
272 Curr Probl Surg, March 2004
Fig. 10. A) Patient 2 days after MVC. Pain was well controlled and she was ambulating. Small
residual hemothorax noted (arrow). B) Three months later with no evidence of pleural complications.
Curr Probl Surg, March 2004 273
Thoracotomy through mini approaches is often sufcient to allow the
removal of soft, gelatinous, visceral and pleural rind, permitting full lung
expansion. Irrigation with warm saline facilitates clot removal. The
denser the adhesions, the greater the exposure must be, and if a formal
decortication of a formed visceral peel is anticipated, a standard approach
is required. This can be facilitated by subperiosteal rib excision to allow
safe identication of the pleura.
In summary, patients with retained hemothorax at risk of empyema
should be treated aggressively, preferably by early thoracoscopic drain-
age.
158
There are occasional patients who present with delayed effusions
days after blunt injury, presumably partially due to a missed small
hemothorax and partially due to a reactive uid accumulation. If these
patients have adequate pain control, have small effusions (less than one
fourth of the hemithorax), and have no signs of infection, tube thoracos-
tomy does not need to be performed, since the risk of brothorax is
negligible. Patients who present late (usually more than 3 months after
injury) with an element of brothorax (but with no infection) should be
treated nonoperatively because at 6 to 9 months in the majority of cases,
there is some remodeling and adaptation, and if operation is required,
there is no increased difculty if it is undertaken at a later date.
Persistent Air Leak Individuals sustaining thoracic trauma may develop
air leaks from the airways or lung into the pleural space from a variety of
causes. Such leaks have been loosely referred to as BPFs, but it is
important to recognize that leaks originating from the central airways
have a pathogenesis, natural history, and treatment that are distinct from
peripheral parenchymal leaks. In addition, the correct treatment is
affected critically by whether or not the patient is ventilated, as well as to
what degree of underlying ALI/ARDS is present.
A true BPF is located centrally and is dened as a direct communi-
cation between the pleural cavity and the lobar or segmental bronchi.
162
The incidence and etiology of BPF after elective lung resection have been
described well and include issues relating to stump length, induction
therapy, the extent of lymph node dissection, etc.
163
In contrast, an air
leak originating from the lung parenchyma located peripherally and,
although commonly referred to as a BPF, is more accurately dened by
the terms parenchymal-pleural stula (PPF) or alveolar-pleural stula.
True BPF is an infrequent nding in patients sustaining thoracic trauma,
and lung resection often is not required. However, of those that do require
resection, approximately 5% will develop BPF from breakdown of the
operative closure.
163
Prolonged mechanical ventilation and reintubation
are risk factors for the development of postresection BPF, suggesting that
274 Curr Probl Surg, March 2004
elevated peak airway pressures contribute to stump breakdown. Further-
more, the incidence of comorbid underlying lung conditions (eg, emphy-
sema) can complicate simple lacerations that would otherwise be ex-
pected to heal. Peripheral leaks may also be a complication of tube
thoracostomy, barotrauma, and/or necrotizing lung infections.
Air leaked through the chest tube can reduce the effective tidal volume,
resulting in respiratory acidosis and an increased ventilation-perfusion
mismatch. Incomplete lung expansion and dissipation of intrathoracic
PEEP contribute to hypoxemia, whereas factitious ventilator cycling
triggered by chest tube suction may cause respiratory alkalosis and
ventilator dyssynchrony. Infection is another major concern, since BPF
and PPF appear to predispose the patient to empyema and pneumonia. In
general, postresectional BPF and ARDS-related PPF are associated with
mortality rates as high as 70% and 80%, respectively.
162
Pierson and colleagues
164
reviewed the course of 39 cases (from a
population of 1,700 mechanically ventilated patients) who presented with
air leak lasting more than 24 hours, 27 of whom were trauma patients.
The risk for mortality was related to the following factors: air leak present
on admission or shortly thereafter (45%, versus 94% if developed later);
air leak greater than 500 mL per breath (57%, versus 100% if greater);
and after chest trauma (56%, versus 92% for nontrauma admissions). The
majority of the trauma patients presented with early air leak.
The diagnosis of a PPF in a ventilated patient is usually obvious,
manifesting with a deterioration in gas exchange or tension pneumotho-
rax. The presence of bubbling in the Pleur-evac during the inspiratory
cycle exclusively (in patients receiving positive-pressure ventilation) or
the expiratory cycle (in the absence of positive-pressure ventilation)
indicates a small leak, whereas larger leaks generate bubbling throughout
the respiratory cycle. In ventilated patients, at least 100 mL per breath
must escape through the BPF or PPF before differences between the
delivered and end tidal volume measured at the endotracheal tube can be
detected after correction for compressible volume. Only in this latter
circumstance do stulas compromise gas exchange potentially. The
precise volume leaked with each breath can be measured by connecting a
pneumotachograph or spirometer to the chest tube, but this is not
necessary for clinical purposes.
162
The Emerson pump is the optimal
choice for evacuating leaks greater than 28 L/min.
The overall approach to patients with a BPF or PPF is fundamentally
different.
162
In general, the goal of treating the patient with a postresec-
tional BPF or a traumatic central airway injury is to repair the tear. In
contrast, a PPF can be viewed primarily as a marker of the severity of the
Curr Probl Surg, March 2004 275
underlying lung disease and, in the majority of cases, the treatment of a
PPF is purely supportive. It is unusual for a peripheral stula to cause
life-threatening respiratory compromise, in part because the leaked gas
participates in gas exchange. A reduction or elimination of the leak
usually does not alter ventilation, and there is no evidence that it affects
outcome. Although it may be disconcerting not to intervene in the face of
large air leaks, the low yield and potentially high risk of operative
attempts to seal the leak must be kept in mind. As the lung recovers from
the acute disease process, peripheral stulas nearly always resolve
without specic therapy and hence, the emphasis belongs on treating the
underlying disorder. In general, attempts are made to minimize airway
pressure and treat pneumothorax.
162
Bronchoscopy may be required to
exclude an occult major bronchus laceration (ie, BPF).
Methods of minimizing transpulmonary pressures should be used. The
end-inspiratory plateau pressure, a gross estimate of alveolar pressure,
optimally should be kept below 30 cm H
2
O. This may require the use of
permissive hypercapnia and higher levels of supplemental oxygen. The
use of lower tidal volumes and high inspiratory ow rates, along with
minimizing the number of positive-pressure breaths, all allow more time
for expiration and minimize the risk of gas trapping. These measures,
along with using the minimum chest tube suction necessary to keep the
lung inated, reduce the ow of gas across the stula, which may be
important in healing. Use of plateau pressures as a surrogate for
transpulmonary pressure is less reliable in patients with elevated pleural
pressures resulting from a chest wall injury or transmission of elevated
intra-abdominal pressure. These patients may require higher airway
pressures to be ventilated adequately. As with central leaks, the use of
pressure support as the stand-alone mode of ventilation should be
avoided.
Although the vast majority of patients with central and peripheral leaks
can be treated successfully with the approach outlined, a few patients
cannot. In these, a variety of creative techniques have been attempted.
Some authorities have reported improving oxygen saturations in hypox-
emic patients by occluding and/or applying PEEP to chest tubes.
162
Presumably, this prevents the dissipation of intrathoracic pressure via
chest tube leakage, but it can also compromise the drainage of air, blood,
or pus from the pleural space. High-frequency jet ventilation (HFJV) and
independent lung ventilation (ILV) have unclear roles in patients who do
nor respond to conservative treatment.
162
Because it consistently pro-
duces lower peak airway pressures, the use of HFJV is theoretically
appealing in patients with central stulas and has been used with success
276 Curr Probl Surg, March 2004
in patients with disrupted proximal airways. However, HFJV does not
reduce mean airway pressures consistently, reduce the amount of ow
across the stula, or improve gas exchange. At this time, HFJV is not
widely available or approved by the US Food and Drug Administration
for the treatment of persistent air leaks, and it should not be used in the
setting of PPF nor routinely used in patients with BPF.
ILV is routinely employed in the operating room and allows the leaking
lung to be kept inated with a minimum of pressure, whereas the
nonleaking lung is ventilated with normal or supranormal pressures that
help to preserve overall gas exchange. Conicting reports of efcacy, a
lack of randomized trials, and the high risk associated with the sustained
use of double-lumen endotracheal tubes argue against the use of ILV,
however.
162
Although it may be impractical in patients with severe gas
exchange abnormalities, selective intubation of the contralateral lung has
also been used to treat persistent leaks, including those in the setting of
prior pneumonectomy and unilateral bronchial injury.
A wide variety of approaches to endobronchial occlusion of a BPF and
PPF are described in the literature.
162
Central leaks usually are localized
by direct visualization with a bronchoscope, whereas the balloon catheter
occlusion technique is the primary means of localizing peripheral air
leaks.
165
This procedure begins with a systematic examination of the
segmental airways of the affected lung, looking for the presence of air
bubbles arising from a bronchus.
166
One of a variety of balloon catheters
is then passed through the suction port of the bronchoscope and the
balloon is inated sequentially in all suspected airways. If ination results
in a marked reduction in air leak, the occluded airway is contiguous with
the stula and efforts to seal the airway are appropriate. A failure to
reduce air leak with all attempts at airway occlusion indicates that the
patient likely has multiple stulas and generally is not a candidate for
endobronchial blockage. A large variety of materials have been described,
including lead shing weights, brin, doxycycline or tetracycline com-
bined with autologous blood, Gelfoam, and various vascular occlusion
coils.
165
The use of these materials and devices can result in a dramatic
reduction of air leak and subcutaneous emphysema, as well as an
improvement in oxygenation.
165
The timing and decision-making regarding operative intervention are
determined by whether or not the patient is ventilated, there is preexisting
underlying lung disease, and/or the degree of respiratory embarrassment
caused by the leak (Figure 11). Of course, airway injury should be
excluded, as should simple technical problems (eg, a displaced chest
tube). The CT scan can provide useful anatomic details that will predict
Curr Probl Surg, March 2004 277
the possibility of thoracoscopic approaches. In general, we prefer to avoid
operation in patients who require PEEP of more than 7.5 cm H
2
O. The
treatment of persistent air leak in the nonventilated patient appears to be
facilitated by early resection, including thoracoscopic approaches, al-
though the ability to accomplish this after blunt lung injury, which tends
to have more diffuse and complex lacerations, may be much less than
after penetrating injury.
65
Operative treatment can vary from simple
suture placement to formal lobectomy, depending on the underlying depth
and complexity, as well as whether or not pneumonia is present. When
attempting to suture or staple inamed or diseased lung, the use of
pledgets or buttressed staple lines can markedly reduce the risk of
failure.
167
On occasion the lung is too dense, and either larger staples (4.8
mm as opposed to 3.5 mm) may be needed or suturing should be used in
place of staples. Biological sealant(s) may help, but if the patient is
requiring signicant positive-pressure ventilation, those materials are
likely to fail.
Empyema. The diagnosis of empyema is based on the documentation of
an exudative effusion, characterized in particular by an elevated pleural/
serum lactate dehydrogenase ratio (greater than 0.6).
168,169
In approxi-
mately 25% to 30% of cases, cultures will be negative due to suppression
but not eradication of bacteria by antibiotics.
43
Many patients will present
with indolent courses, often characterized by an inability to be weaned
Fig. 11. Algorithim for determining when operation should be considered in the presence of persistent
air leak
278 Curr Probl Surg, March 2004
from ventilation, with radiographic evidence of persistent uid after
injury and despite tube drainage.
158
In many instances once these
contaminated hemothoraces are drained, the clinical picture rapidly
improves.
43
A CT scan with intravenous contrast can reveal a rim sign
of enhancing pleura, indicative of ongoing inammation.
Operative intervention for empyema most commonly occurs in 1 of 3
scenarios: parapneumonic empyema; empyema complicating traumatic
hemothorax; and empyema occurring after lung resection and compli-
cated by BPF.
49
In the rst 2 conditions the primary goal of therapy is
directed at draining the pleural space and hopefully, allowing full lung
expansion. In the latter, although the infected pleural space also must be
tackled, the approach must take into account the persistent contamination
via the airway into the empyema cavity and vice versa. Trauma patients
are at risk of Gram-positive multiloculated empyema less amenable to
simple drainage, owing to the presence of hemothorax (Table 13).
49,170
Empyema has been described as having 3 stages. The rst, usually
within 1 to 7 days, is referred to as the acute or serous phase. This
distinction is important, because the thin, exudative uid has a high
likelihood of being drained successfully by tube thoracostomy. There
have been regular attempts to treat this early stage by simple aspiration.
Evidence of vigorous inammation (pH less than 7.0) almost universally
predicts failure of this approach.
169
It is imperative that complete
drainage be achieved, or failing that, that early operative drainage is
performed before progressive pleural obliteration occurs, characteristic of
progression to the second or subacute phase and nally the third or
chronic phase. Palpation at the time of tube thoracostomy placement or
ndings on CT scans or even CXR can alert the surgeon to the presence
of loculations that indicate that simple tube thoracostomy is unlikely to
succeed.
One major reason for earlier intervention is that minimally invasive
approaches are more successful early, whereas later, the combined impact
of pleural space obliteration and lung trapping makes thoracotomy both
mandatory and less effective. In this regard it is critical to note the
TABLE 13. Risk of infection complicating residual hemothorax
Ventilated patient
Splinting due to pain
Onset of pneumonia
Abdominal hollow viscus injury
Chest tube in emergency department
Extrathoracic infection
Curr Probl Surg, March 2004 279
differences between empyema after traumatic injury and parapneumonic
empyema (responsible for more than 85% of all empyema). Empyema
after trauma is much more likely to require operative intervention because
the blood, pleural injury, and inammation create a vigorous inamma-
tory reaction.
32,49
Therefore, aggressive treatment of retained or contam-
inated hemothorax reduces the potential morbidity.
32,171
Patients with
residual or persistent hemothorax after chest tube placement that is
detectable on the CXR (opacication or more than one third of hemitho-
rax) should be considered for drainage. Several other risk factors for
developing empyema are listed. In contrast, asymptomatic patients who
present with late effusions and who have not undergone tube thoracos-
tomy do not necessarily require drainage.
The primary treatment goals for empyema are to drain the pleura and
permit lung expansion. There are several local considerations when
deciding which therapeutic approach is ideal in any given case (Table 14).
Predominant among these are to determine whether or not loculation has
occurred, if there is a peel that might prevent lung expansion, and if
parenchymal inammation/consolidation is so severe as to prevent
expansion. In the acute setting, particularly when patients show signs of
active infection, the primary goal simply is to attain pleural drainage.
Evidence of loculations suggests that simple tube drainage will be
ineffective and that some additional therapy is required to drain the uid
collection fully. These alternatives range from ultrasound or CT-directed
percutaneous drainage catheter placement, thoracoscopic drainage,
minithoracotomy, or formal thoracotomy and decortication. Thrombolytic
therapy has been used as an alternative to operative intervention.
172
Current data suggest that when compared with thoracoscopy as a primary
intervention, thrombolytics are associated with a higher failure rate, an
increased length of stay, and greater cost.
66,173
Thoracoscopic approaches (VATS and direct-vision rigid thoracoscopy)
have been compared with thoracotomy in an unselected manner. VATS
appears to be associated with decreased morbidity rates and length of
TABLE 14. Considerations with treating empyema
Residual space?
Quality of lung parenchyma?
Trapped lung?
Density of loculations?
Patient ventilated?
Air leak?
Lung abscess?
280 Curr Probl Surg, March 2004
stay, although usually it is attempted much earlier in the course, when
loculations are less evident.
66,173
An alternative approach when VATS is
contraindicated is rigid thoracoscopy. The major reason why ICU patients
are not VATS candidates is the inability to use a double-lumen tube, an
inability to tolerate single-lung ventilation, and/or pleural symphysis. One
report documented the results of rigid thoracoscopy combined with
irrigation in the ICU setting.
43
Fourteen procedures were performed
successfully in 13 patients (1 bilateral). Seven patients were ventilated,
and in 11 cases a single-lumen endotracheal tube was required. All were
discharged from the hospital alive. Signs of sepsis abated within 48 hours
of decortication.
The use of an irrigation system can be modied according to circum-
stances (eg, a Jackson-Pratt drain, connected to intravenous tubing via a
3-way stopcock). Postdecortication irrigation appears to be benecial in
the immediate postoperative period, perhaps because the new blood is
washed away. Usually antibiotics are not used, but in the presence of
resistant bacterial or fungal infections they may be helpful. The volume
of irrigation can be exible. Irrigation at 100 mL/h is often sufcient, with
care to make sure that the drainage does not fall behind and allow the
uid to accumulate in the chest. It is important to close the deep tissue at
all chest tube and port sites to avoid leaking. When the irrigant is clear
and cultures negative, irrigation can be discontinued.
43
A potential
disadvantage of irrigation is that it may inhibit postdecortication pleural
symphysis, allowing residual spaces to be left. On the other hand, if a
residual space is anticipated, irrigation appears to be particularly effec-
tive. If the irrigation is left in place for more long-term treatment,
repeated cultures from the chest tube or serial lactate dehydrogenase
evaluations may indicate whether pleural sepsis has been controlled or
not.
The residual pleural space remains a problem and can be approached in
several ways, based on whether or not the lung can expand to ll the space
(Table 15). A 3-year review of our experience with thoracoscopic
drainage of empyema found that all 4 of the 21 early posttraumatic
procedures failed due to trapped, lung whereas of the 15 of 81
nontraumatic procedures that failed, 10 were due to an infected residual
space as a consequence of either lung resection and/or parenchymal
consolidation. This nding emphasizes the point that the primary reason
for failure after decortication for empyema after traumatic injury is a
restrictive peel, debridement of which usually allows adequate lung
expansion.
Curr Probl Surg, March 2004 281
When performing thoracotomy for empyema, there a few technical
points that are helpful. First, avoid counting ribs. This will reduce the
chance of creating an extrathoracic infected space. Second, excising the
rib rather than shingling will provide a safer avenue for entering the
thorax through a very inamed and thick pleura. When attempting
visceral decortication, maintain ventilation in the affected lung if possi-
ble. This will allow both denition of the plane between the visceral peel
and the underlying lung as well as helping to conrm that the lung will
expand after the peel is removed. Signicant peripheral lung leaks can be
tolerated if the lung expands to obliterate the pleural space. If the lung
parenchyma is too consolidated to expand and the pleural peel resection
is proceeding poorly (technically difcult, bloody, large air leaks), it may
be necessary to abandon pleurectomy in favor of a strategy aimed at
managing the persistent space, such as drainage with an irrigation system,
tissue aps, and/or open drainage.
In summary, the principles of treating empyema are as follows: drain
the space; debride the space; maximize lung expansion; if lung expansion
is not possible, consider tissue aps to ll the space; if this is not possible,
consider chronic open drainage approaches; and close signicant BPFs.
Earlier intervention allows less invasive procedures (principally thoracos-
copy) a higher likelihood of success. Thoracoscopy using rigid techniques
still can be considered in ventilated patients. Patients who are malnour-
ished with signicant comorbidity may be better treated by chronic open
drainage.
Lung Abscess. The causes of lung abscess in the operative ICU
population include aspiration, complications of necrotizing pneumonia,
retained foreign body, septic emboli, and/or infected traumatic injury.
Specic causes in the blunt trauma population include aspiration (with or
without bronchial obstruction), infected pneumatocele, infected site of
resection (possibly increased after tractotomy), and late complications of
VAP and/or necrotizing pneumonia (Figure 12).
174
The overall treatment
of lung abscess has remained relatively uniform during the past 20
TABLE 15. Managing the residual space
Irrigation antibiotics
Positive-pressure ventilation expands consolidated lung
Bronchoscopy to rule out/treat obstruction
Decortication to release trapped lung
Open drainage for chronic treatment, particularly in debilitated patients
Tissue aps to ll space and close air leaks
Combination: Clagget procedure
282 Curr Probl Surg, March 2004
years.
175
In the 3 decades preceding this, there were some rapid
advancements based on an understanding of the importance of antibiotics,
recognizing the role of aspiration, and nally stressing the possibility of
surgical intervention.
175
During this period, mortality rates have im-
proved from nearly 50% to remain at approximately 10%.
175
The initial
therapy should be medical, including aggressive drainage, bronchos-
copy, and use of antibiotics.
175
Percutaneous drainage has allowed a
reduction in the need for thoracotomy and can be performed in critically
ill and ventilated patients.
174
Should empyema result, simple chest tube
placement is sufcient in the majority of cases. The resultant BPF is
rarely so signicant as to impair oxygenation.
Several patients do not respond and require operative approaches (Table
16). Usually lobectomy will be the minimal resection possible, since the
parenchymal consolidation can prevent more conservative procedures. In
rare cases, the patient will not tolerate complete resection. Open drainage
and closure with a muscle ap are reasonable alternatives.
174
At operation, there are several technical points that can help avoid
complications: prevent aspiration, preferably with a double-lumen tube;
Fig. 12. Necrotizing pneumonia with lung abscess (arrow). Patient was treated initially by
percutaneous drainage owing to hemodynamic instability and subsequently underwent debridement
and closure with a latissimus dorsi ap.
Curr Probl Surg, March 2004 283
ensure lung separation before placing the patient in a posterolateral
position; expose the proximal pulmonary artery early because of the risk
of bleeding; place a nasogastric or an esophascope tube in the esophagus,
since the anatomy may be obliterated; and refrain from resecting small
(less than 2 cm) abscesses. Air leak is not uncommon, and consideration
should be given to placing an irrigation system for 24 to 48 hours to help
clean the residual cavity.
Pneumatocoele/Lung Cyst/Hematoma. When the lung is lacerated
there is frank disruption of lung tissue, causing a localized internal leak
of air (pneumatocele) and blood (hematoma) in variable quantities. As air
TABLE 16. Classic indications for operative intervention for lung abscess
6 cm and not responding to medical therapy
Persistent fever and signs of sepsis after 2 weeks of therapy
Persistence after 68 weeks without reduction in size
Recurrent or major hemoptysis
Bronchopleural stula
Empyema
Cannot exclude cancer
Fig. 13. Partially uid-lled pneumatocele (arrows).
284 Curr Probl Surg, March 2004
enters into the laceration a spherical or elliptical cavity is formed due to
inherent lung elasticity, and bleeding occurs from the margins of the
laceration. The lesion is best described as a pulmonary laceration. These
are usually single, at times multilobulated, and on occasion multiple
(Figure 13). Pulmonary lacerations typically are not apparent on the initial
radiograph because of a superimposed contusion or pulmonary hemor-
rhage that obscures the laceration. Over time, pulmonary lacerations
appear as thin-walled cavities, often containing an air-uid level, usually
2 to 5 cm in diameter (but as large as 14 cm; Figure 14).
35
The location of the laceration(s) depends on the mechanism of forma-
tion. Four types of lacerations have been described on the basis of CT
scan ndings and the mechanism of injury: 1) compression-rupture, the
most common and usually located centrally within the pulmonary
parenchyma; 2) compression-shear; 3) rib penetration, usually small and
peripheral; and 4) the rare adhesion tears.
35,176
Pulmonary lacerations are
present immediately after injury but often are masked by contusions. On
subsequent examinations, the wall of the pulmonary laceration becomes
thicker because of edema or hemorrhage around the margin of the lesion.
Initially some lacerations are completely lled with blood, and the
Fig. 14. Residual hematoma (arrow) 2 months after injury.
Curr Probl Surg, March 2004 285
air-uid level does not appear for 2 or 3 days after evacuation of a portion
of the blood. The compression-shear type of laceration usually appears
inferiorly in a paramediastinal location as an elongated cavity extending
from the region of the hilus to the diaphragm. Care should be taken not
to confuse these lesions with a loculated posterior medial pneumotho-
rax.
35
An air-lled pulmonary laceration usually disappears in 1 to 3
weeks but occasionally will persist longer than this. Not surprisingly, CT
scanning shows many more pulmonary lacerations than does the CXR.
Uncommonly, pneumatoceles may become infected and should be treated
similarly to lung abscess.
1,176
Pulmonary hematoma manifests as a smooth, round to ovoid mass of
variable size. Initially the hematoma itself may be obscured by the
surrounding patchy inltrates of pulmonary contusion, but as the contu-
sion clears, a solid, more sharply dened, radiodense area appears.
177
It
usually takes 1 of 2 courses: it may remain solid, or an air-uid level may
appear within the lesion as a result of partial evacuation of the blood.
Rarely a brin ball forms within the lesion and is manifested by a crescent
of air on its superior surface.
35
This is similar in appearance to a fungus
ball within a cavity. Lung hematomas gradually shrink over several
months, typically to normal or to very small lung scars. They have been
given the descriptive term vanishing lung tumor and should not be
mistaken for a more sinister pulmonary abnormality if one is aware of the
history of trauma.
177
The shrinking process may take 3 to 6 months or
more.
1,177
Identication of the shrinking process on serial radiographs
indicates resolution of the process and should allay any concern that this
dense area represents a more serious lesion requiring medical investiga-
tion or operative intervention.
Chylothorax. Primary traumatic chylothorax after blunt injury is
uncommon, and although it might be supposed that it is linked to vertebral
injuries, is associated with spine fractures in only 20% of cases.
178
This
condition can manifest in a delayed fashion with recurrent effusions, as a
persistent, milky, chest tube output associated with the diet, or even in 1
case as a tension chylothorax resulting in respiratory distress.
179-181
Chylothorax also can be a complication of operation, particularly repair of
a descending aortic rupture. This diagnosis can be established by
analyzing the content of the effusion and documenting the presence of fat
(triglyceride levels greater than 110 mg/dL) and/or predominant lympho-
cytes in the effusion. The primary complication of chylothorax is
nutritional deprivation and systemic immunocompromise.
182
Parenteral
nutritional support should be instituted, and full lung expansion should be
maintained, possibly assisted (in ventilated patients) by increasing PEEP
286 Curr Probl Surg, March 2004
levels.
183
How long medical therapy should be tried is not clear, but
generally 4 weeks is the maximum time, depending on the nutritional
reserves of the individual patient.
178,181,182,184
Lymphangiography (either
by CT, nuclear studies, or formal lymphangiogram) may be helpful in
identifying the site of leak. If no specic leak is documented and
collaterals are seen to drain superiorly into the venous system, it is much
more likely that conservative treatment will be successful. Although low-
fat diets will reduce the ow of chyle, even the oral intake of water has
been noted to increase chyle ow, and the optimal approach is to support
nutrition parenterally while maintaining complete enteral rest
184,185
An
almost immediate cessation of chyle leak on assuming this approach is a
good prognostic sign. Octreotide also has been used successfully in
conjunction with parenteral nutritional support in a variety of clinical
settings.
186-188
An interventional technique based on identifying the duct
and then embolizing it using microcoils can, on occasion, help control the
rate or occlude the stula.
189
A persistence space such as after pneumo-
nectomy is associated with a marked failure rate and earlier intervention
is recommended. Ultimately, operation should be considered if the leak
persists after 2 and certainly after 4 weeks, if the patient is falling
behind in nutritional or immune status, and/or if there is another
indication for operation.
182,190
If operation is required, both thoraco-
scopic and open approaches have been used in conjunction with biolog-
ical adhesives and decortication.
182
Mass ligation at the level of the
diaphragm on the right side may be required, but if the specic site can
be identied (assisted by feeding cream just before the start of the
operation), this can allow a precise ligation.
In our approach, when chylothorax is diagnosed within 7 days of
thoracotomy and is affecting the operative side (eg, after repair of aortic
rupture), early reoperation is easy and hastens recovery. At operation the
use of brin glue and direct ligation of the site of leak are employed (with
ligation at the diaphragmatic level if right-sided), and pleurectomy is also
performed. If there is any question that the lung will not completely
reexpand, the patient is ventilated overnight. Strict nothing by mouth is
maintained with parenteral nutrition for 7 days. In our limited experience
of 3 cases over the years (after ruptured aorta, blunt esophageal injury,
and combined injury to the spine and right lower lobe), this method
achieved complete success. If patients present later than 7 days or are
thought to be too ill to undergo thoracotomy, then strict nothing by mouth
with parenteral nutrition, octreotide, and pleural drainage is used for 2
weeks, unless there is evidence that despite support the patient is losing
ground nutritionally or the output is greater than 1500 mL/d for 7 days,
Curr Probl Surg, March 2004 287
in which case an attempt at interventional occlusion is made, and if not
successful, operative approaches are taken.
Lobar Torsion. Lobar torsion is exceedingly rare after trauma and has
been reported more often after lung resection when the middle lobe can
swing freely in the residual space.
1
Patients may present with a variety of
signs and symptoms, ranging from persistent atelectasis to frank pulmo-
nary sepsis, but the diagnosis should be suspected when there is persistent
anatomic lobar collapse, particularly if this involves the middle lobe after
right upper lobectomy if the ssure between the middle and the lower
lobes is complete. This diagnosis is conrmed by bronchoscopy, which
documents a sh mouth appearance of the affected bronchus, indicating
torsion, occasionally with purulence or blood draining intermittently from
it.
191
Schamaun
192
reviewed 26 cases of torsion in the literature and noted
that 5 were posttraumatic. Although torsion after blunt trauma remains a
diagnosis based on suspicion, torsion after lobectomy (particularly upper
lobectomy) should be anticipated by noting if the middle lobe in
particular is freely mobile, and if so, should be prevented by stapling the
middle to the lower lobe.
192
When diagnosed, immediate operative
exploration should be performed. If not obviously infarcted, the lobe
should be untwisted to determine if perfusion can be restored, after which
it should be stapled to an adjacent lobe to help secure it. If nonviable,
lobectomy is required.
Cardiac Injuries
History and Mechanism
The rst reported cases of blunt cardiac injury (in which valvular
rupture was noted) may have been in 1676 by Borch
194
and subsequently
by Berard in 1826,
193-196
but it was not until 1955 that the rst successful
repair of a rupture (at the right atrial-superior vena cava junction) was
reported by Desforges and colleagues.
197
Blunt cardiac injury manifests
as a variety of clinical conditions, usually in association with multiple
injuries of other organs and difcult treatment issues. Blunt cardiac injury
also occurs infrequently, often with subtle signs, making recognition and
suspicion of this injury difcult. The terminology of blunt cardiac injuries
is outlined in Table 17. Importantly, the exact injury associated with blunt
cardiac contusion has been enigmatic, and discussions about this entity
have frustrated clinicians, associated with inconsistency regarding its
diagnosis and clinical signicance.
198-200
For discussion purposes, it is
useful to consider contusion, rupture, and complex injuries as distinct
entities, when in reality they usually coexist. Signicant cardiac injury
288 Curr Probl Surg, March 2004
can be present in isolation, although more commonly concomitant chest
wall injuries including rib fractures (53%), ail chest (19%) pulmonary
contusion (44%), hemothorax (30%), and/or pneumothorax (33%) are
present.
201
Depending on the denition as well as whether the series is an
autopsy or a clinical review, the incidence ranges from 16% to 76%.
201
A variety of mechanisms have been proposed. Direct blows or antero-
posterior compression of the sternum against the heart can lead to direct
injury, usually to the underlying right ventricle.
201,202
Acceleration-
deceleration can lead to tearing of the heart at xed positions, commonly
the junctions between the superior and/or inferior vena cava and the right
atrium.
203
The inferior vena cava is additionally at risk of tearing at the
diaphragmatic hiatus, where the sharp edge of the diaphragm can cut
into the vessel, since it moves anteriorly.
204
Acute venous hypertension,
either from chest compression or abdominal injury, can lead to acute
overdistention of the right heart, leading to blow-out of the thin-walled
right atrium or ventricle.
205
This latter mechanism may not manifest with
obvious signs of chest injury, but rather with slowly developing tampon-
ade.
196
Intracardiac pressures of more than 320 mm Hg appear to be
required to cause rupture or valve dehiscence.
206,207
Finally, fragments of
rib and/or sternum can directly lacerate the underlying cardiac structures.
TABLE 17. Organ injury scale (OIS) of the American Association for the Surgery of Trauma
(AAST) with reference to blunt cardiac injury (BCI)
Grade Injury description
I BCI with minor ECG abnormality (nonspecic ST-segment or T-wave changes,
PAC, PVC, or persistent sinus tachycardia)
II BCI with heart block (R or LBBB, LAHB, AV block) or ischemic changes (ST-
segment depression or T-wave inversion) without cardiac failure
III BCI with sustained ( 5 bpm) or multifocal PVCs
BCI with septal rupture, pulmonary/tricuspid insufciency, papillary muscle
dysfunction, or distal coronary occlusion without heart failure
BCI with heart failure
IV BCI with septal rupture, pulmonary/tricuspid insufciency, papillary muscle
dysfunction, or distal coronary occlusion 3 heart failure
BCI with aortic or mitral incompetence
BCI of right atrium, right ventricle, or left atrium
V BCI with proximal coronary occlusion
BCI with left ventricular perforation
VI Blunt avulsion of the heart (lethal)
BCI blunt cardiac injury; ECG, electrocardiogram; PAC, premature atrial contraction; PVC,
premature ventricular contraction; LBBB, left bundle branch block; LAHB, left anterior hemi
block; AV, atrioventricular.
Adapted from Moore EE, Malangoni MA, Cogbill TH, Shackford SR, Champion NR, Jurkovich GJ,
et al. Organ injury scaling, IV: thoracic vascular, lung, cardiac, and diaphragm. J Trauma
1994;36:299300.
199
Used with permission.
Curr Probl Surg, March 2004 289
Contusion
Myocardial contusion represents such a wide spectrum of conditions
that there have been multiple attempts to change the term contusion to
blunt cardiac injury.
208,209
For the purposes of this discussion, contu-
sion will refer to myocardial injury without rupture or associated complex
cardiac injuries. Even within this context, contusion represents a broad
pathologic spectrum. The salient point is that as opposed to infarction,
contusion represents a varying degree of hemorrhage but not invariably
cell death.
201
Supercial areas of minor epicardial bruising may mask
deeper hemorrhagic changes extending varying distances from the ven-
tricular wall into the septum.
205,210
Acute and usually transient maldis-
tribution of coronary ow may play a role in causing transient conduction
abnormalities, without resulting in frank cell death.
211
True posttraumatic
infarction is uncommon and usually requires a coronary artery inju-
ry.
212,213
It has been estimated that the incidence of contusion after blunt chest
trauma is 10% to 20%.
214
The signicance of establishing the diagnosis
in asymptomatic patients is not clear, nor is the best method. It has been
argued that only 1% to 20% of patients will develop complications that
require treatment (life-threatening arrhythmias or pump failure) and that
these are self-evident.
202,214,215
However, these patients may have symp-
toms that are masked by associated injuries. Furthermore, if extensive
operation is required in the setting of occult or frank right and/or left
ventricular dysfunction, the perioperative course may be complicated. In
this circumstance, a pulmonary artery occlusion catheter may be helpful.
The incidence of cardiac contusion is unclear. Macdonald and col-
leagues
216
diagnosed contusion in 29 of 169 (17%) patients admitted to a
trauma ICU, of whom 24 (83%) developed clinically signicant symp-
toms or complications, and 5 (17%) died as a direct result of contusion.
Lindstaedt and colleagues,
214
using echocardiograms and creatine ki-
nase-MB isoenzyme levels (CK-MB), diagnosed contusion in 14 of 118
(12%) blunt chest trauma patients, more than 90% of whom required ICU
admission because of associated injuries, and none of whom developed
signicant complications requiring specic treatment. It is clear that
patient selection plays a role in these reports, but all patients with blunt
force to the chest are at risk of some injury to the heart.
The screening electrocardiogram (ECG) is considered essential in blunt
chest trauma patients, even if asymptomatic. If the ECG is normal at
admission and 4 hours later, the risk of developing life-threatening
arrhythmias is essentially nil. However, nonspecic changes warrant
290 Curr Probl Surg, March 2004
cardiac monitoring for a 24-hour period.
202
This latter recommendation is
nonspecic, and clinicians must judge what constitutes ECG changes or
abnormalities. Patients with atrial or ventricular arrhythmias clearly
warrant careful observation, as do those with ST-segment changes.
Ultimately, the majority of ECG changes appear to be self-limited and by
themselves rarely are associated with adverse clinical outcomes.
200
Cardiac isoenzymes have been used to dene the presence of absence of
contusion. CK-MB isoenzymes have proven to be irrelevant in the
diagnosis since they do not predict the risk of complications, which are
instead related to overall injury severity and ECG changes.
202,217
In a
study by Bif and colleagues,
202
107 of 359 (30%) blunt chest trauma
patients during a 4-year period were diagnosed as having suffered
myocardial contusion, but only 17 patients developed complications
requiring treatment (14 with dysrhythmias, 3 with cardiogenic shock). All
of these complications occurred within 24 hours of injury, 11 being
present at admission. CK-MB levels were not found to be useful in
predicting the likelihood of their occurrence. Both cardiac-specic
troponin I (cTnI) and T (cTnT) also have been studied, and it appears that
cTnI may be more specic than cTnT since cTnI is not expressed in any
degree by skeletal muscle.
218,219
Both forms of cardiac-specic troponins
suffer from the limitation that there is little independent correlation with
the clinically relevant risk for developing complications, or at least
complications that are not self-evident.
219-222
Nevertheless, if cTnI or
cTnT is elevated, this probably warrants 24-hour monitoring and consid-
eration for early transthoracic echocardiography. On the other hand, a
normal admission ECG, cTnI level, and echocardiogram with a repeated
normal cTnI at 8 hours are sufcient evidence to exclude any signicant
myocardial injury.
223
There is ongoing research in the medical literature
to identify markers that reect specic myocardial damage that is
clinically relevant that might be useful in the trauma setting. For example,
brain natriuretic peptide appears to identify patients who are at risk of
developing myocardial failure or of determining whether myocardial
dysfunction is contributing to the symptoms.
224-226
Our routine is to
perform ECG and cardiac troponin enzymes in the ED in patients with a
suspicious mechanism of injury. Cardiac monitoring is performed during
the ED evaluation, and since most patients with this possible diagnosis are
admitted to an ICU, 24 hours of ECG monitoring is performed. Repeated
ECG and troponin measurements are performed on any patient with
abnormalities of enzymes or rhythm. An echocardiogram is obtained if
these repeated studies are also abnormal or on the basis of clinical signs,
symptoms, or suspicion. Table 18, adapted from a study by Bertinchant
Curr Probl Surg, March 2004 291
and colleagues,
219
reviews the sensitivity and specicity of several tests
in the diagnosis of contusion, with ECG and/or echocardiogram ndings
as the reference standard.
Echocardiography has largely replaced nuclear medicine studies be-
cause the former can be performed at the bedside, provides detailed
information regarding overall chamber performance and volume status,
and can detect intracardiac injuries as well as help determine the impact
of therapeutic interventions, such as modifying ventilator settings.
215
In
particular, high levels of PEEP can signicantly affect cardiac perfor-
mance, and the degree of impact may be assessed by echocardiogra-
phy.
227
Echocardiographic ndings usually document right ventricular
contusion or wall motion abnormality but not uncommonly will note left
or biventricular changes, occult pericardial effusion, or rarely, occult
septal defects.
228
Unsuspected contusion (with or without intracardiac
defects) may be a source of hypoxia during operative repair of other
injuries and may be diagnosed by echocardiogram.
229
The treatment of arrhythmias follows standard algorithms. There is no
evidence to support antiarrhythmic prophylaxis, and benign rhythm
disturbances (eg, occasionally unifocal premature ventricular contrac-
tions) do not need to be treated.
215
Although tachyarrhythmias appear to
be the rule, signicant conduction bundle blocks can necessitate place-
ment of a temporary pacemaker.
214,215,230
TABLE 18. Correlation between serum levels of isoenzymes and diagnosis of myocardial
contusion
Assay
Sensitivity
(%)
Specicity
(%)
Positive
predictive
value (%)
Negative
predictive
value (%)
CK 100 IU/L 92 21 31 87.5
CK 1,000 IU/L 15.5 85 28.5 72
CK-MB 15 IU/L 77 49.5 37 84.5
CK-MB 40 IU/L 19 91 45.5 74.5
CK-MB mass 5 g/L 81 35.5 32.5 82.5
CK-MB mass 40 g/L 27 91 54 76.5
CK-MB activity/CK ratio 6% 42.5 64 31.5 74
Myoglobin 90 g/L 96 23.5 32.5 94
Myoglobin 1,000 g/L 19 84 31 73
cTnI 0.1 g/L 23 97 75 76.5
cTnT 0.1 g/L 12 100 100 74
CK, creatine kinase; CK-MB, creatine kinase, myocardial band; cTn, cardiac troponin.
Adapted from Bertinchant JP, Polge A, Mohty D, Nguyen-Ngoc-Lam R, Estorc J, Cohendy R, et
al. Evaluation of incidence, clinical signicance, and prognostic value of circulating cardiac
troponin I and T elevation in hemodynamically stable patients with suspected myocardial
contusion after blunt chest trauma. J Trauma 2000;48:92431. Used with permission.
292 Curr Probl Surg, March 2004
Low cardiac output may require support with an intra-aortic balloon
pump (IABP), especially in patients who require major orthopedic or
general operative procedures.
231
The incidence of clinically signicant
cardiogenic shock has been reported to represent as many as 65% of
cases, although the usual incidence is quoted as 10% to 20%.
201,215,232
Cardiogenic shock can be due to severe right ventricular dysfunction,
dilation of the right ventricle with resultant shift of the septum into the left
ventricle, direct injury to the left ventricle, or a combination of all these
conditions.
215,233
The diagnosis is often self-evident but can be masked
by other injuries requiring invasive or echocardiographic assess-
ment.
215,234
Transthoracic echocardiography or TEE can be critical in
determining the best therapy and its impact. Left ventricular failure can,
as mentioned, be assisted by an IABP. Right ventricular dysfunction may
be assisted by both increasing preload and reducing pulmonary afterload
with dobutamine or similar agents.
215
Echocardiography can also help
determine the impact of ventilatory changes on cardiac function in those
who have coexisting ALI or ARDS.
Left ventricular thrombus is uncommon but not rare after blunt cardiac
injury.
214
Thrombus can form if there is an akinetic segment of the
ventricular wall and presents the risk of embolization.
235,236
Treatment is
primarily anticoagulation for a period of 3 to 6 months.
Operations can be performed in the setting of acute myocardial
contusion, but appropriate monitoring (pulmonary artery occlusion cath-
eter, intraoperative transthoracic echocardiogram) may be needed to help
adjust inotrope medications.
221
An IABP may be required, or very rarely,
femoral-femoral percutaneous bypass.
231,237
Follow-up echocardiography at 3 months is often recommended to
detect occult or developing lesions (eg, septal defects).
238
The majority of
nonspecic changes (wall motion abnormality, mild dilation) noted will
have resolved by 12 months.
239
In 1 series of 17 patients found acutely by
echocardiogram to have wall motion abnormalities, 7 resolved by 3
months and an additional 6 resolved by 12 months.
214
In this same series
1 patient was noted at 3 months to have developed a left ventricular
thrombus. New-onset cardiac failure in the absence of acute echocardio-
graphic changes is also rare.
214
Blunt Cardiac Rupture
Blunt cardiac rupture is almost immediately fatal in more than 90% of
victims and may be directly responsible for as many as 5% of all blunt
trauma deaths and 10% to 30% of all deaths after blunt chest injury
specically.
17,196,240,241
Delayed presentation is possible, as noted by an
Curr Probl Surg, March 2004 293
early case report of cardiac rupture involving a 9-year-old boy who
remained asymptomatic after a crush injury until he suddenly suffered a
cardiac arrest 5 days later.
242,243
The mechanisms are varied and include
laceration from bony fractures, acute right atrial distension due to
compression of the abdomen, deceleration resulting in motion and tension at
the caval-atrial junctions, direct compression, and/or delayed necrosis as a
complication of contusion or coronary artery injury.
208,237,241,244-246
The
right side is affected most commonly (right atrium, 33% to 41%; right
ventricle, 30% to 39%) and is associated with a greater chance of survival
than left-sided ruptures (left atrium, 17% to 25% and ventricle, 6% to 13%
incidence, respectively).
241
Of patients with blunt rupture who survive to reach a trauma center with
some vital signs, survival rates of 20% to 50% have been recorded.
241,247
The trauma group at Portlands Emanuel/Legacy Hospital reported a
remarkably good overall survival rate of 41% in 27 patients for a 9-year
period, including 3 of 9 patients who presented without vital signs or
electrical activity.
42
Interestingly, the operative procedures were per-
formed in a designated operating shock/trauma room immediately adja-
cent to the ED, assisted by dually trained cardiothoracic and trauma
surgeons and operating room nurses. Patients may present with initially
stable vital signs and then progress to develop evidence of tamponade.
215
Survival is reduced in the setting of multichamber rupture. The diagnosis
usually is made by emergency thoracotomy in patients who arrive in
extremis but can be made because of persistent hypotension by a
pericardial window or ultrasound.
240,244
Rarely, a CT scan performed to
evaluate a widened mediastinum will reveal a oating heart suggestive
of a small laceration.
248
Pericardial rupture, present in as many as 33% of
cases, can lead to false-negative FAST or echocardiogram studies since
the pericardial blood can decompress into the chest; therefore, a negative
scan when there is an adjacent hemothorax does not preclude the
possibility of rupture and tamponade.
196,249
Patients with a negative
echocardiogram but who have a mediastinal hematoma and who persis-
tently have unexplained hypotension may require a subxiphoid pericardial
window to exclude occult cardiac laceration in this setting.
249
Pericar-
diocentesis, as a temporizing measure, may allow time to reach the
operating room but should not be performed as a diagnostic maneuver,
nor should it delay rapid transfer to an operating suite if the diagnosis is
suspected.
196,243
Operative treatment requires immediate exploration. Sternotomy offers
the best overall exposure, followed by right anterolateral thoracotomy,
since more than two thirds of injuries are right-sided.
196,250
Simple atrial
294 Curr Probl Surg, March 2004
ruptures or superior vena caval-atrial junction tears can be treated by
clamping and suturing, and in patients who present with vital signs can be
associated with survival rates as high as 70%.
196
The outcome is always
signicantly better in those patients who present with vital signs and in
those with atrial injuries
42,251
In this subset, mortality is dictated by the
associated injuries, especially head injuries.
196
Survival rates based on the
site of injury from representative clinical series are listed in Table 19.
Survival after rupture of more than 1 chamber is very rare but has been
reported.
243,250,252
Complex tears involving the inferior vena caval
junction with the right atrium often require circulatory arrest or at least
cardiopulmonary bypass. Ventricular lacerations cannot be clamped.
Digital control and rapid suture closure are the best methods. Pledgets
may be required for more complex lacerations, particularly those involv-
ing the thinner right ventricle. Bicaval occlusion, as used for proximal
aortic injuries, may allow better visualization and less blood loss, as may
the use of a Foley catheter inserted into a defect.
62,196,250
Inducing
ventricular brillation or using adenosine to achieve transient arrest may
also be useful adjuncts in patients with small injuries to allow better
visualization. Occasionally, in patients who present with vital signs,
formal cardiopulmonary bypass will permit both operative repair and
resuscitation.
251
A variant of cardiac rupture is rupture of the intrapericardial great
vessels. Pulmonary vein laceration represents a form of left atrial rupture,
and embryologically the left atrium is simply a conuence of the veins.
Varghese and colleagues
253
reported a case in which an injury was noted
at right thoracotomy, performed for large hemothorax. Survival was
attributed to the chest tubes becoming plugged with thrombus, thereby
preventing exsanguination, although at the same time the low-pressure
bleed did not result in tension hemothorax. Ambrose and colleagues
254
reviewed 7 cases of pulmonary artery rupture after blunt trauma, 6 of
whom survived. Four cases involved the main pulmonary artery. The
diagnosis was made or suggested by CT scan in 3 cases, with clinical
evidence of hemothorax in the remainder. Intrapericardial pulmonary
artery rupture will tend to manifest with tamponade, and extrapericardial
TABLE 19. Survival after blunt cardiac rupture
Right atrium Left atrium
Right
ventricle
Left
ventricle
Incidence % (range) 43% (3350%) 22% (1633%) 26% (1638%) 10% (813%)
Survival % (range) 41% (3844%) 2% (050%) 58% (033%) 33% (0100%)
Curr Probl Surg, March 2004 295
rupture manifests with hemothorax. Repair can usually be performed
without needing cardiopulmonary bypass or a patch.
254
Tears involving
the right main pulmonary artery proximally (since it passes behind the
aorta) and the pericardial reection can be controlled by incising the
pericardium between the superior vena cava and the aorta.
204
Intraperi-
cardial superior vena caval rupture usually can be repaired primarily.
204
Simple lacerations of the inferior cava can be repaired with sutures, but
complex tears extending onto the heart require shunting, cardiopulmonary
bypass, and/or occasionally circulatory arrest, since acute clamping of the
inferior vena cava or the atriocaval junction is poorly tolerated.
255
Valve Injury
The most common form of complex injury is valve rupture, noted in 5%
of autopsies. The mitral valve is the most common valvar injury noted in
autopsy series, whereas the aortic valve is the most commonly described
valve injured in clinical series.
208
Aortic injuries usually involve rupture
of the annulus at the cusps or cusp detachment.
205
Mitral injuries usually
involve papillary and/or chordal rupture, although the leaets can be
lacerated also.
256
The left-sided valves are presumably at greater risk than
the right-sided valves due to higher pressures.
201
Delayed papillary
rupture affecting the atrioventricular valves may occur because of either
hemorrhagic necrosis or occlusion of the arterial supply.
257
Air bag
deployment has been implicated as the mechanism of injury in occasional
reports of tricuspid and aortic valve rupture.
20,258
Pretre and colleagues
208
in 1994 summarized the clinical experience reported to that date and the
pathophysiologic considerations unique to each valve injury (Table 20).
Zakynthinos and colleagues
206
reviewed the literature regarding mitral
and tricuspid injuries (Table 21). Thirty-eight mitral valve injuries were
found, and in 22 patients, 1 or both papillary muscles were involved.
Injuries involving the papillary muscles tended to be diagnosed earlier,
and patients underwent operative repair within hours or days; if rupture
was limited to chordae tendineae and/or leaets, a more indolent course
was noted, with diagnosis and/or repair commonly performed months or
years after the injury. The diagnosis was made predominantly by clinical
ndings in 8 cases, echocardiography in 28 cases, and cardiac catheter-
ization in 2. Interestingly, transthoracic echocardiography was performed
in 16 cases but in 8 was suboptimal or inaccurate, requiring catheteriza-
tion or TEE.
206
Sixteen patients (42%) had at least 1 associated cardiac
injury or complication. Forty-nine patients with tricuspid valve injuries
were reviewed. The most common site of injury involved the chordae to
the anterior leaet (Table 21). Patients with papillary muscle rupture
296 Curr Probl Surg, March 2004
tended to be identied earlier and/or require operation earlier, but it was
not uncommon for several years to pass before repair was needed.
Twenty-two (45%) patients had at least 1 associated cardiac injury or
complication. The anterior leaet mechanism was also found by Maisano
and colleagues
259
to be the most commonly affected in a review of 74
cases.
The timing of mitral, tricuspid, and the rare pulmonary dehiscence is
often affected by the presence of multiple combined injuries, including
ALI, that preclude immediate repair.
260
Considerations include the
presence of head injury, severe pulmonary contusion, and/or signicant
myocardial contusion that would be anticipated to complicate open
cardiac repair. Deciding to what extent hypoxia is due to tricuspid valve
injury as opposed to other causes (eg, myocardial stunning and/or
pulmonary insufciency) can be difcult, although transthoracic echocar-
diography may help in determining the relative contributions of
each.
229,260
Temporization with medical treatment is often possi-
ble.
261,262
Performing the operation under elective circumstances offers a
greater chance of repair as opposed to replacement.
257
Furthermore,
suture placement is easier when there has been a period of brosis,
particularly involving the valvular and subvalvular apparatus of the
atrioventricular valves.
263,264
Rarely, tricuspid insufciency can be com-
TABLE 20. Physiologic features and incidence of blunt valvar rupture
Pulmonary valve Very uncommon
Short artery with low pulmonary vascular resistance,
therefore not subjected to acute pressure rise
Anatomically protected because it lies midway between
sternum and vertebral column
Tricuspid valve 40 reported cases
More anterior than pulmonary valve, therefore
subjected to sternal compression but protected by
lower right ventricular and pulmonary artery pressures
Mitral valve 34 surviving patients reported by Shammas et al
523
Posterior location protective, and if injured, implies
such severe force that survival unlikely
At risk during early systole with a full ventricle before
aortic valve opens or late diastole in conjunction with
some compression or kinking of aortic outow
Aortic valve 37 operative cases reported by Pretre and Faidutti
274
Commonly associated with other lesions
At risk during early diastole when the aorta is full of
blood, pressure is maximal, and the empty ventricle
does not provide any subvalvular support
Adapted from Pretre R, Bednarkiewicz M, Faidutti B. Blunt cardiac injury: in achieving a
practical diagnostic classication. J Trauma 1994;36:4623.
208
Used with permission.
Curr Probl Surg, March 2004 297
plicated by shunting through a patent foramen ovale, leading to a
recalcitrant right-to-left shunt. This can require earlier repair and closure
of the foramen ovale.
208,265
Mitral valve injury can manifest early or in
a delayed fashion with unexplained pulmonary edema.
206
As is the case
with nontraumatic mitral insufciency, progressive annular dilation and
heart failure are not uncommon, and early repair rather than continued
TABLE 21. Anatomy of blunt atrioventricular valve rupture
Valve
Age
range
(years)
Anatomic features of injury Associated lesions
Mitral 649 APM (12) Contusion (7)
(N 38) PMP (5) VSD(s) (4)
APM PMP (1) Pericardial laceration (4)
Papillary muscle not specied (3) Tricuspid valve (3)
APM chordae tendineae (1) Pericardial effusion (2)
Chordae tendineae (4) Aortic annulus (1)
AL chordae tendineae (2) Pericarditis (1)
AL (1) LV rupture (1)
PL (4) Cardiac hematoma (1)
AL PL (1)
Annulus (1)
Annulus chordae tendineae (1)
Valve PMP (1)
Not specied (1)
Tricuspid 980 Chordae tendineae (1) Mitral valve (1)
(N 49) Anterior chordal rupture (15) Contusion (4)
Posterior chordal rupture (1) Ventricular hematoma (2)
AL (5) PFO (7)
SL (3) VSD (2)
AL SL (5) ASD (3)
APM (6) Pericardial laceration (6)
Post PM (2) Constrictive pericarditis (2)
APM Post PM (2) Right aortic cusp laceration (1)
AL chordal rupture (1) Sinus of Valsalva aneuysm (1)
APM chordal rupture (2) LV-RA stula (1)
APM Septal chordal rupture
(1)
LV aneurysm (1)
Papillary rupture not specied (1) Acute myocardial infarction (1)
Not recorded (4) RCA-RA stula (1)
Pericardial effusion (2)
RCA dissection (1)
APM, anterior papillary muscle; PMP, posteriomedial papillary muscle; VSD, ventricular septal
defect; LV, left ventricle; AL, anterior leaet; PL, posterior leaet; SL, septal leaet; Post PM,
posterior papillary muscle; RA, right atrium; RCA, right coronary artery; PFO, congential patent
foramen ovale; ASD, atrial septal defect;
Adapted from Zakynthinos EG, Vassila Kopoulos T, Routsi C, Roussos C, Zakynthinos S. Early-
and late-onset atrioventricular valve rupture after blunt chest trauma: the usefulness of
transesophageal echocardiography. J Trauma 2002;52:990-6.
206
Used with permission.
298 Curr Probl Surg, March 2004
medical treatment should be considered if there is echocardiographic
evidence of progressive changes.
261
A rare variant is the development of
subvalvular left ventricular saccular aneurysms in conjunction with mitral
insufciency.
266
These aneurysms may be associated, in turn, with
ventricular septal defects, leading to left ventricular-to-right atrial stu-
la.
238
Aortic valve injury usually results in signicant insufciency that
precludes intra-aortic counterpulsation. Urgent repair is usually re-
quired.
258,267
In some cases, usually associated with contusion or partial-
thickness injuries, the aortic valve injury is minor, but these injuries
need to be monitored because saccular aneurysms of the aortic root have
been reported after blunt injury, with subsequent enlargement and
rupture.
268
One variant is the traumatic sinus of Valsalva stula. This
condition has been reported in association with right atrial stulization
from a tear in the right sinus, which can be repaired in the usual fashion
by repairing the cusp and closing the stula with a patch from within the
aortic root.
269,270
The tricuspid valve can be treated by repair rather than replacement
in some cases depending on the degree of damage, right heart failure,
and pulmonary hypertension. Maisiano and colleagues
259
were able to
perform repair in 6 cases. The predominant pathologic nding in their
series was anterior leaet prolapse in conjunction with annular
dilation, which they approached by using a combination of ring
implants (5), articial chordae (4), papillary reinsertion (2), posterior
annuloplasty (1), commisuroplasty (1), and the double-orice tech-
nique. Mitral repair rather than replacement is also often possible.
Combinations of papillary or chordal reattachment, leaet repair,
and/or annuloplasty have been reported. Misfeld and colleagues
271
reported a case in which papillary rupture was repaired thorough an
area of ventricular rupture, allowing both preservation of the valve and
repair of the rupture. Mitral valve repair or replacement may be easier
through a biatrial transseptal approach, since the left atrium is often
small and exposure via a left atrial incision may be difcult. Aortic
lacerations usually require valve replacement, but rarely resuspension
of an isolated prolapsed valve or suture repair of a small lacerations,
limited to 1 cusp, is possible.
268,272,273
Competence should be
assessed by intraoperative TEE.
268
In the majority of cases valve
replacement is required because attempts to repair more complex
injuries have been associated with acute and chronic failure requiring
reoperation.
273-275
In particular, repair in the setting of membranous
septal defects has been associated with poor outcome and in patients
Curr Probl Surg, March 2004 299
near or at adulthood replacement may be the choice even if the injury
seems reparable.
276
Combined Cardiac and Vascular Injuries
Combinations of cardiac injuries and aortic/great-vessel injuries pose
difcult treatment issues of timing of the repair and how to perform the
operation. Zakynthinos and colleagues
206
noted that cardiac injuries were
present in 42% of traumatic mitral and 45% of tricuspid injuries. Pretre
and Faidutti
268
reviewed 33 cases in which operative repair of aortic valve
injury was performed, in 10 of which there were wounds involving the
ascending aorta and in 5 of which involved the left ventricle. Associated
innominate artery rupture also has been described.
213
Intracardiac and ascending aortic injuries can be approached through
the same incision, but cardiac injuries in conjunction with traumatic
rupture of the descending aorta cannot. Assuming that the need is to repair
both sites at the same setting (as opposed to nonoperative treatment or
stent-graft approaches to the aorta, for example), options include the
following: repair of the thoracic aorta via a posterolateral thoracotomy
before or after sternotomy, depending on which injury is thought to take
precedence; stent-graft repair of the thoracic aorta followed by or
preceding repair of the cardiac injuries; clamshell incision; or sternotomy
with left anterolateral extension as required.
277-279
The key point is that
using standard cardiopulmonary bypass, thereby allowing collapse of
both lungs and gaining hemodynamic stability, will allow retraction of the
left lung and exposure of the descending thoracic aorta. It may be possible
to repair these injuries in a staged fashion, treating the aortic injury
nonoperatively.
273
Coronary Artery
Coronary occlusion, dissection, and aneurysm have been described after
blunt trauma, along with the late complications of ventricular aneurysm,
septal defect, and myocardial infarction.
279-281
The left anterior descend-
ing coronary is by far the most common artery injured.
279
Coronary
occlusions are treated by formal bypass or, depending on the anatomy, by
coronary stents.
282
Thrombolysis is often contraindicated because of
associated injuries or concern that the hemorrhagic infarct may extend.
212
Many patients may be treated conservatively. Late complications of
posttraumatic occlusion include the development of ventricular aneurysm,
usually in the anterior wall in the distribution of the left anterior
descending artery. Repair is indicated for the usual indications, including
heart failure or the risk of rupture.
283
300 Curr Probl Surg, March 2004
Coronary dissection is less common but can lead to subsequent
occlusion and infarction. If diagnosed by angiography before any com-
plications develop (unusual in the setting of acute trauma), anticoagula-
tion (if not contraindicated) may be all that is required.
284
Left ventricular pseudoaneurysm and septal defect in the anterior
descending distribution also has been reported, presumably due the
muscular necrosis as a consequence of severe coronary injury and
occlusion.
285
Coronary arteriovenous stulas can manifest in a delayed
fashion with ischemia and may be treated by ligation or stenting,
depending on the need for other procedures and the specic anatomic
features.
278
Coronary-ventricular stulas also have been reported and are
treated in a similar fashion.
286
Although expectant treatment can be
performed, the risks of heart failure, endocarditis, and infarction have
prompted consideration for early intervention.
287,288
Friesen and col-
leagues
289
noted 5 cases of coronary artery to cardiac chamber stulas
after blunt trauma: left anterior descending to right ventricle RV in 3,
right coronary artery to right ventricle in 1, and left anterior descending
to left ventricle in 1. Closure of the stula from within the affected
chamber offers an opportunity to repair associated lesions and may have
a reduced risk of damaging the distal coronary artery, although other
surgeons have found external stula ligation acceptable.
Septal Defects
Patients with atrial septal defects, either congenital (eg, patent foramen
ovale) or acquired, can present with severe hypoxia.
208,257
In some cases,
the atrial defect may not require repair, since shunting is mild and
reverses as the patients cardiac function improves.
246
Atrioventricular
valve injury can be associated with atrial and/or ventricular septal defects
since their annuli form part of the septal structure of the heart. Repair of
atrioventricular septal defects, particularly those close to the septal leaet
of the tricuspid valve, can be complicated by complete heart block
requiring pacemaker placement.
290
The majority of traumatic ventricular septal defects occur in the
muscular portion of the septum, usually toward the apex.
291
Perimem-
branous injuries tend to be associated with tricuspid valve defects.
292
Tears in the ventricular septum, usually under the right coronary valve
and particularly if combined with aortic leaet injury, can result in
signicant left-to-right shunting.
275
Although usually acute, septal defects
can occur in a delayed fashion (a few days after injury) due to hematoma
and/or ischemic necrosis.
293,294
A new-onset systolic murmur at the left
sternal edge is pathognomonic.
294
These defects may be small enough to
Curr Probl Surg, March 2004 301
be repaired with interrupted pledgeted sutures.
275
Larger defects require
a patch.
295
Nonoperative treatment with serial echocardiographic fol-
low-up is appropriate for small lesions not associated with signicant
shunt (2:1) and not involving the infra-aortic septum (which leads to
progressive valve injury).
296
The natural history is to heal, since unlike
ischemic ventricular defects, the bulk of the septal muscle is healthy.
297
The exposure of the defect depends on associated injuries and the location
of the septal defect. Options can include repair via the right atrium,
through the aortic valve, through a ventricular defect or aneurysms, or via
an apical ventriculotomy.
292,295,298
Ideally, any ventricular incision
would be through an already damaged portion of myocardium.
299
Repair
can be assisted by biologic glues, particularly to assist the closure of any
ventriculotomy.
294
As with valve injuries, if operation can be delayed, the
procedure is better tolerated since brosis makes repair easier.
298,300
Several cardiac valvular lesions may manifest years after the injury.
Tricuspid valve injuries can be particularly insidious.
206
Progressive
mitral insufciency or aortic root dilation may require operation to
prevent irreversible heart failure or aortic rupture.
261,268
Intracardiac
lesions may be found in between 4% and 56% of patients who undergo
cardiorrhaphy and therefore, follow-up echocardiography is recom-
mended at 3 months.
238
Pericardium
Complications involving the pericardium are unpredictable and essen-
tially unavoidable but are occasionally difcult to diagnose and life-
threatening. A degree of suspicion is required to recognize the occurrence
of these complications, and liberal use of echocardiography, central
monitoring, and early operative exploration may be needed to prevent
acute cardiovascular collapse.
Pericardial Rupture. Pericardial rupture is associated with signicant
chest wall impact and usually is diagnosed either postmortem or as an
incidental nding.
301
Fulda and colleagues
302
described a series of 22
cases among a total of 20,000 trauma patients admitted during a 10-year
period. The majority occurred after an MVC; 4 (18%) were diagnosed by
subxiphoid window, whereas the remainder were diagnosed at the time of
operation for resuscitation or for treatment of other injuries. Associated
cardiac injuries were present in 5 patients (23%), all of whom died. The
overall mortality rate was 64%. Most series reect a preponderance of
left-sided injuries, usually in conjunction with diaphragmatic tears (Table
22).
303
302 Curr Probl Surg, March 2004
Rarely the diagnosis may be made preoperatively. A bruit de moulin
may be heard, signifying hemopneumopericardium.
302
The plain CXR
may demonstrate cardiac displacement, air in the pericardial sac, and/or
intestinal contents.
304,305
The ECG may show axis deviation (to the side
affected), or ST-segment changes or bundle branch block reecting
herniation and/or suggesting blunt injury (contusion).
305
This diagnosis
also has been established by chest CT scan for the assessment of other
injuries.
306,307
The reasons for establishing the diagnosis are because of the likelihood
of associated signicant injuries and to prevent cardiac herniation.
Herniation through the right side can result in a tamponade-like picture.
Herniation through the left side can lead to acute occlusion of the left
anterior coronary artery and acute left ventricular decompensation. When
suspected or diagnosed, this injury can be conrmed by subxiphoid or
thoracoscopic exploration, but there should be no hesitation in operative
exploration.
308
Pericardial herniation and subsequent deterioration can
occur in a delayed fashion, which adds to the difculty in establishing the
diagnosis.
308
If signicant unilateral associated injuries are present, a
posterolateral thoracotomy is warranted; otherwise, sternotomy offers the
most reliable exposure.
301
The defect can be repaired with interrupted
sutures but occasionally requires patch repair, with care to avoid the
phrenic nerve.
All patients should undergo follow-up echocardiography to detect
occult intracardiac lesions (eg, tricuspid injury noted in 3% of pa-
tients).
303
Delayed cardiac herniation also has been described in 1 case 6
months after injury and requires a high degree of suspicion to make the
diagnosis.
309
Pericarditis
Pericarditis has been noted to occur in as many as 22% of patients after
penetrating cardiac injury in survivors but has also been reported after blunt
injury.
205,237,310-314
The etiology has been predominantly attributed to an
autoimmune reaction with antibodies directed against the myocardium or
pericardium after injury.
315
In additional, the introduction of blood into the
TABLE 22. Location of pericardial lacerations after blunt injury
Left pleuropericardial 64%
Diaphragmatic 18%
Right pleuropericardial 9%
Superior mediastinal 9%
Curr Probl Surg, March 2004 303
pericardium also may set up a vigorous inammatory response.
316
Dressler
317
described the predominant clinical features of recurrent fever and
pleuropericardial pain. These symptoms usually are separated from the injury
by days or months. The fevers are low-grade (38C to 40C) and the pain
tends to be predominantly precordial, although it may radiate to the shoulder,
neck, or scapular area. In addition, the pain is aggravated by inspiration,
recumbency, and twisting the torso. Nonspecic, diffuse ST-segment
changes and elevated erythrocyte sedimentation rate also are noted often. A
pericardial friction rub may suggest the diagnosis but may be absent if the
effusion reaches a large enough volume to cause mufed heart sounds. Large
pericardial effusions with or without tamponade may result in compression
atelectasis of the base of the lower left lobe.
318
Although rarely becoming
clinically signicant, exudative, nonhemorrhagic, pericardial effusions lead-
ing to tamponade also have been reported.
205,245,313
Echocardiography is the most specic diagnostic modality. Not only
will echocardiography document the effusion but also it may demonstrate
pericardial thickening, consistent with inammation. Progressive tampon-
ade initially can be demonstrated by collapse of the right atrium and then
subsequently the right ventricle during diastole. Both have a predictive
accuracy for tamponade of 72%.
318
In most instances posttraumatic pericarditis is self-limiting, although
recurrences are not uncommon.
314
In the elective setting there is no
specic prophylaxis recommended, but after open massage in the trauma
setting it is reasonable to start treatment if there are no contraindications.
Initial treatment in the absence of tamponade includes anti-inammatory
agents. Nonsteroidal agents are often effective, although acetylsalicylic
acid can be tried as well; if relapses occur particularly if a growing
effusion is documented, steroids may be required.
310,311
Once the
effusion causes cardiac decompensation, drainage either by pericardio-
centesis or by operative approaches is required. Usually the most effective
approach is by subxiphoid drainage, but if the echocardiogram suggests
signicant loculation or if there is suspicion of secondary infection, a
non-rib-spreading anterolateral fourth intercostal incision may be safer
(Figure 15).
312,319
Constrictive pericarditis is even more uncommon after trauma and has
been related more to the effect of blood in the pericardial cavity.
312,316
Usually it occurs weeks but more often years after the event but on rare
occasion has been noted within days.
241,320
Constrictive pericarditis is
less common after elective cardiac procedures, possibly because the
pericardium is widely drained after elective cases. When it does occur,
especially years after the inciting event, extensive calcication is the
304 Curr Probl Surg, March 2004
rule.
201
One of us (R.K.-J.) has had occasion to operate on 3 patients for
this problem. All were women in their mid-30s, all had suffered some
form of signicant blunt chest injury associated with suspicion of sternal
fracture or contusion at least 10 years previously (1 from an MVC, the
other 2 as victims of intimate partner violence). The diagnosis was
established by noting clinical features of systemic venous plethora
(including jugular vein distension, pedal edema, and even liver engorge-
ment) and conrmed by echocardiography and measuring chamber
pressures at catheterization.
In the acute setting, simple pericardial resection can be performed as in
the setting of effusive tamponade. The treatment of chronic, calcied,
constrictive pericarditis requires pericardial resection, removing or cob-
ble-stoning the pericardium through a sternotomy from both phrenic
nerves laterally, opening the roots of the pulmonary artery and aorta, and
ensuring that both cava are decompressed. This latter objective may be
limited in cases of severe calcication to cracking open the anterior
surfaces. The left heart should be decompressed rst to prevent acute
Fig. 15. Patient with low-grade fever and dyspnea on exertion 2 weeks after blunt chest injury.
Echocardiogram revealed moderate right ventricular and atrial compromise that was relieved by
pericardial resection, which was performed by limited anterior thoracotomy, avoiding rib spreading.
CT scan demonstrates thickened pericardium (arrows).
Curr Probl Surg, March 2004 305
pulmonary edema that might occur if the right heart was decompressed
before freeing up the left ventricle enough to allow it to accept the sudden
increase in volume from the pulmonary circuit.
Cardiac Injury in the Pediatric Population
The pattern of cardiac injury in the pediatric patient is similar to that in
adults but with a slight preponderance of intracardiac injuries. An autopsy
study of patients under the age of 16 who died after traumatic injuries
noted cardiac injuries in 15% (41 of 282) of cases.
321
Deaths occurred at
the scene in 46%, in the ED in 37%, and during subsequent hospitaliza-
tion in 17%. In 16 cases cardiac rupture occurred and was the direct cause
of death in 8. Contusion without rupture was noted in 25 but was not the
cause of death.
The incidence of cardiac injury in children in clinical reviews is
generally approximately 5% but ranges from 0% to 43%.
62
Because of
multiple associated injuries the diagnosis is often delayed, even in the
setting of signicant intracardiac lesions.
322
Dowd and Krug
62
performed
a multicenter retrospective review and noted that 95% of the 184 cardiac
injuries diagnosed during a 10-year span were contusion. Five cases of
complex injury were noted: anteroseptal necrosis (1), papillary rupture
and mitral insufciency (2); ventricular septal defect (1); and ventricular
septal defect, papillary muscle dysfunction, and septal coronary artery
rupture (1). Four patients (2.1%) suffered laceration or rupture. Nearly
40% of cases were after pedestrian-auto impact, with 31% as passengers
in a vehicle. Eight patients had signicant residual cardiac defects,
including ventricular septal defect (2), mitral insufciency (2), tricuspid
insufciency (1), atrial septal defect (1), and signicant conduction
delays.
3
Echocardiography and ECG appeared to be much more sensitive
and useful than CK-MB levels. Isolated cardiac injury tended to manifest
with a lower incidence of shock, need for ED intubation, and use of
TABLE 23. Differences in presentation among pediatric patients with blunt cardiac injury
depending on whether or not there were associated injuries
Isolated cardiac
injury (N 23)
Cardiac and multiple
injuries (N 161)
Shock in ED 26% 56%
Intubation in ED 39% 63%
Need for vasopressors 13% 38%
ED, emergency department.
Adapted from Dowd MD, Krug S. Pediatric blunt cardiac injury: epidemiology, clinical features,
and diagnosis. Pediatric Emergency Medicine Collaborative Research Committee Working
Group on Blunt Cardiac Injury. J Trauma 1996;40:617.
62
Used with permission.
306 Curr Probl Surg, March 2004
vasopressors compared with those patients who presented with combina-
tion injuries (Table 23).
62
Karpas and colleagues
323
reviewed traumatic ventricular septal defects
in the pediatric population. In patients under age 16, these investigators
found reports detailing 12 cases.
323
Mechanisms included MVC (3), fall
(3), and individual miscellaneous causes in the remainder. The age range
was 5 months to 8 years; 3 were diagnosed postmortem, and 2 of 9 who
underwent operation died. One half presented with evidence of heart
failure, the remainder presented in shock, and 3 patients were noted to
have a large systolic murmur lateral to the sternum. Associated cardiac
lesions were present in 5 cases, including 2 cases of ventricular aneurysm.
The interval between injury and operation ranged from 12 hours to 12
years. Echocardiography has proven invaluable in the diagnosis and
treatment of these patients. Small septal defects may close spontaneous-
ly.
62
Other uncommon injuries include coronary artery thrombosis,
pulmonary artery lacerations, and septal aneurysms.
62,324-326
Commotio Cordis
Commotio cordis is a syndrome characterized by sudden cardiac death
in an otherwise healthy-appearing individual. The predominant mecha-
nism appears to be a blow directly over the heart just before the T-wave,
resulting in ventricular brillation.
327-329
Young adults and children are
more susceptible because of their narrower and underdeveloped chest
walls. Maron and colleagues
330
analyzed 128 cases entered into the US
Commotio Cordis registry as of September 1, 2003. Inclusion criteria
included a witnessed blunt, nonpenetrating blow to the chest followed by
cardiac collapse; absence of bony injury to the chest; and absence of
underlying cardiovascular disease. The patient age ranged from 3 months
to 45 years (13.6 8.2 years) and 95% involved males. Incidents
occurred during organized sporting events in 62% of cases (58% of which
occurred during softball/baseball and 16% during hockey) but the
remainder occurred during recreational activities. These included such
disparate events as shadow boxing, and in 1 case a 2-year-old child was
struck in the chest by the head of a pet dog. Overall, 81% of cases
involved projectiles and the remainder involved nonprojectile blows (eg,
body checking in hockey). Of the episodes occurring during organized
sports, 22 individuals (28%) were wearing commercially designed pro-
tective gear.
Underlying arrhythmias were analyzed in 82 cases. Ventricular bril-
lation was documented in 33 (40%) and asystole in 49%, although
asystole was thought to represent a later arrhythmia rather than the
Curr Probl Surg, March 2004 307
original inciting event. Twenty-one (16%) survived, 15 with complete
recovery and 6 with mild to moderate neurologic and/or cardiac disability.
Of 68 patients in whom resuscitation was started within 3 minutes, 15
(25%) survived; only 1 of 38 (3%) survived if resuscitation was started
later. The primary preventive strategy includes proper chest protectors.
The authors note that many protectors do not actually cover the chest wall
entirely all the time. In addition, in 7 cases the projectile struck the
protector. This was thought to reect inadequate padding but may also
represent a form of behind armour blunt trauma. Interestingly, because
there is a degree of uncertainty regarding which materials and construc-
tion are best for chest protectors, the American Academy of Pediatrics has
limited recommendations for protectors in youth baseball to catchers.
331
The authors concluded their report by stressing the importance of
recognizing the risk of chest blows (particularly in youths), the utility of
early resuscitation and debrillation, and a call for the development of
sport-specic effective chest-protective gear.
Traumatic Rupture of the Thoracic Aorta
The treatment of aortic rupture has signicantly evolved from the
mid-portion of the last century when aortic injuries were thought to be
fatal in essentially all cases unless immediately operated on, through an
evolution of early recognition based on mechanism and physical signs,
improved imaging, varied operative approaches (including the clamp-
and-sew versus bypass controversy), to the current era of selective
operative repair, nonoperative repair, and the emergence of endovascular
techniques.
332,333
These latter issues have been claried further by
recognizing that there are roughly 3 categories of patients: those who die
at the scene (70% to 80% of the whole); those who present unstable or
become unstable (2% to 5% of the whole, with mortality rates of 90% to
98%), and those who are hemodynamically stable and are diagnosed 4 to
18 hours after injury (15% to 25% of the whole, with mortality rates of
25% largely due to associated injuries).
333,334
Currently, blunt aortic rupture remains second only to head injury as a
cause of death after blunt trauma.
335
If there are 7,500 to 8,000 cases per
year in the United States and given that 80% to 85% of victims die at the
scene, then only 1,000 to 1,500 cases per year with blunt aortic rupture are
treated in US hospitals.
336
In the largest contemporary prospective study
available, 274 patients were admitted to 50 institutions during a 2.5-year
period; if these cases were evenly distributed the number would equate to
roughly 2.2 cases per year.
49
In practice some centers may see 8 to 15
cases per year whereas others encounter 1 or 2 per year at most. This
308 Curr Probl Surg, March 2004
highlights the difculty in maintaining expertise in this area, not only in
surgical treatment but also in diagnosis and general decision-making.
Mechanism and Incidence
It has been argued for decades that the predominant mechanisms for
blunt aortic disruption involve deceleration with shear forces applied
against points of xation (especially at the ligamentum arteriosum), acute
hypertension within the aorta, compression by the diaphragm, and/or
torsion of the aorta. More recently it has been argued that acute
compression of the aorta between the sternum and spine is a major
mechanism (the osseous pinch).
332,333,337
Because the mechanism is related to extreme acceleration/deceleration,
the primary incidents are MVCs, pedestrians struck, falls, and air
disasters. Burkhart and colleagues,
336
in an autopsy study of 242 patients,
noted that the responsible mechanisms included MVC in 68%, pedestrian
struck in 17%, motorcycle crash in 8%, and fall in 4%. The American
Association for the Surgery of Trauma (AAST) prospective multicenter
clinical study found that MVCs were the responsible mechanism in 81%
of cases.
49
Between 15% and 23% of MVC fatalities are found on autopsy
to have suffered a traumatic aortic transection.
338
The lack of seatbelt use
may result in greater force, perhaps reected by the increased incidence
of ascending aortic rupture found at autopsy in those without seatbelts
(53.5%) compared with those who were wearing seatbelts (39.2%).
17,18
Air bags may be protective in terms of frontal impact, but the less
frequent use (at this time) of side air bags may be associated with an
increased incidence of aortic rupture from lateral impact mechanisms.
339
However, seat belts have been credited with a reduction in fatalities from
aortic injury.
336
The overall incidence of traumatic aortic rupture in
pedestrian-struck victims has been estimated at approximately 13%, with
a markedly greater mortality rate among those who survive to admission
compared with injuries after MVC because of the greater severity of
associated injuries.
161
Aortic rupture is found in 30% or more of aircraft
crash fatalities, although perhaps 50% have other lethal injuries as
well.
333,340
In clinical series, the majority of lesions (usually quoted as more than 95%)
occur in the region of the aortic isthmus, dened radiographically by the
origin of the left subclavian artery.
49,332,336,341
Autopsy series are slightly
different, reecting in all probability the natural history of worse injuries.
Separate reviews have found the following incidence of locations: isthmus,
54% to 65%; arch and ascending aorta, 10% to 14%; distal descending aorta,
8% to 12%, diaphragmatic and/or abdominal, 7 to 9%; and multiple sites,
Curr Probl Surg, March 2004 309
16% to 13%.
18,336,342
It may be that isthmus injuries reect lesser degrees of
deceleration and/or injury severity and thus more survivable injuries.
18
The lesion is usually a pseudoaneurysm, but rarely a true dissection with
separation of the medial layers of the aorta is encountered.
343,344
These
ndings are associated with an increased severity of injury overall and
increased technical difculty in operative repair.
Diagnosis
The diagnosis of aortic rupture remains problematic because of trans-
port time, distraction by multiple injuries, and subtle clinical or radio-
graphic ndings. The AAST prospective study found that the average
time from trauma center admission to conrmed diagnosis was 4.7 6.9
hours and from diagnosis to thoracotomy, 10.1 73.3 hours, reecting
the difculty in diagnosis, treatment of multiple injuries, and those
patients who were treated by delayed repair.
49
Clinical Diagnosis. Physical ndings are unreliable because a substan-
tial number of patients present with nonspecic ndings that serve only to
alert the examiner to the possibility because of the mechanism and forces
implied. A substantial number of patients, perhaps more than one half,
have normal thoracic physical ndings.
345
Sternal bruising has been
described in 12% to 43% and pseudocoarctation has been reported in 6%
of patients.
341
Sternal fractures do not appear to be associated with a
signicantly increased risk of aortic injury.
346
Pseudocoarctation and/or
expanding neck hematoma in the setting of a widened mediastinum has
been associated (along with hemothorax more than 500 mL without
pneumothorax) with an increased risk of early rupture and if noted should
stimulate urgent evaluation and possibly exploratory thoracotomy without
delay for angiography.
347
Upper-extremity pulse decits or murmurs
have also been found in uncommon cases and warrant angiography to
exclude aortic rupture and/or great-vessel injury.
348,349
It is thought that
the most common specic physical ndings are intrascapular murmur
and/or pseudocoarctation.
340,350
Radiologic Diagnosis. Because in the majority of cases there are no
reliable clinical indicators, this diagnosis is most commonly suggested by
plain CXR evidence of mediastinal hematoma (Figure 16 and Table
24).
351
These ndings were initially based on the upright CXR, which
may not be possible in many patients because of associated injuries.
352,353
Thoracic bony injuries, including sternal and rst rib fractures, have a
very low association with thoracic aortic rupture and in isolation do not
warrant routine angiography.
74,346
310 Curr Probl Surg, March 2004
One retrospective review of patients who were found to have traumatic
aortic injury noted the following incidence of plain radiographic ndings:
widened mediastinum, 89%; obscured aortic knob, 82% (all with widened
mediastinum); loss of paraspinous stripe, 91% (all with widened medi-
astinum); loss of the aorto-pulmonary window, 25% (again all with
widened mediastinum); and bronchial depression, 25%.
354,355
These
authors concluded that the most reliable nding indicating injury was the
sense that the mediastinum was widened and/or that the aortic knob was
obscured. Woodring and King
356
argued the opposite, noting in their
Fig. 16. Widened mediastinum, apical cap, and effusion with no evidence of pneumothorax.
TABLE 24. Mediastinal abnormalities on chest radiograph that suggest the possibility of aortic
rupture
Mediastinum 0.4 thoracic diameter
Loss of aortic knob
Apical cap
Nasogastric tube shifted right
Left mainstem bronchus depressed
Widened right paratracheal stripe
Obscured aortopulmonary window
Displacement of either paraspinal line
Displaced superior vena cava
Curr Probl Surg, March 2004 311
review that 41% of patients with great-vessel or aortic injury had a
normal mediastinal width (less than 7.5 cm) and 69% had a mediasti-
nal-to-cardiac ratio of less than 3.8, implying that the assessment of
mediastinal widening was too insensitive to exclude aortic injury. To add
further confusion, it appears that a subjective impression that the
mediastinum is widened can be as accurate or more accurate than any
predetermined measurement.
357
Compounding these issues is the fact that
between 2% and 7% of patients with aortic rupture have a normal CXR
initially.
332,340
In 1 series, 4 of 9 patients with traumatic rupture had a
normal CXR.
358
These patients may present over the ensuing hours or
days with gradually enlarging mediastinal silhouettes.
359
A substantial
number of these patients appear to have small injuries, such as intimal
defects.
360
In the majority of patients who have a suspicious CXR, the question of
evaluation has evolved into choosing between angiography, CT followed
by angiography, or CT alone. Thoracic aortography has a sensitivity of
nearly 100% and specicity of 98%.
361
False-negative studies have been
attributed to small intimal lesions and false-positives to atheromatous
plaques and/or anatomic variants. CT scanning has been advocated as a
screening tool but more recently has been superseded by CTA . Helical
CTA has been credited with 100% sensitivity, 99.7% specicity, an 89%
positive predictive value, and a 100% negative predictive value.
362
Helical CTA appears to be more sensitive than angiography in detecting
small intimal injuries that are still signicant.
360
In 1 review of 1,561
patients admitted after blunt injury who underwent CT scanning during a
5.5-year period, the vast majority of CT ndings were indirect, with
TABLE 25. Computed tomography (CT) ndings in patients with blunt aortic injury
CT ndings
Total number
(%)
Mediastinal hematoma
Ill-dened fat plane(s) 524 (39%)
Mediastinal hemorrhage 240 (18%)
Perivascular hematoma 108 (8%)
Periaortic hematoma 83 (6%)
Direct evidence of aortic injury
Caliber change 20 (1.5%)
Intraluminal irregularity 33 (2.5%)
Abnormal contour of the aorta 50 (3.7%)
Adapted from Dyer DS, Moore EE, Ilke DN, McIntyre RC, Bernstein SM, Durham JD, et al.
Thoracic aortic injury: how predictive is mechanism and is chest computed tomography a
reliable screening tool? A prospective study of 1,561 patients. J Trauma 2000;48:67382;
discussion 6823.
360
Used with permission.
312 Curr Probl Surg, March 2004
evidence of mediastinal hematoma (Table 25).
360
A CT scan of the
abdomen also can suggest this diagnosis. Retroperitoneal hematoma
along the aorta at the level of the hiatus, separate from any other source
of bleeding, should alert the team that this could represent a hematoma
tracking inferiorly from the chest.
363
The question of whether CTA or aortography is the best test has
evolved from one of diagnostic sensitivity to whether or not operation
can be performed on the basis of CTA without angiography. Using
nonhelical and nonangiographic CT to screen for mediastinal hematoma
can be associated with an increased delay to treatment if angiography is
used routinely to conrm the diagnosis.
340,364,365
It had been recom-
mended that CTA be followed by angiography in all cases because of
concern that great-vessel injury might be missed and that angiography
provides better details with which to plan operation.
362,366,367
Currently,
CTA should be thought of as being a combination of angiography and
helical scanning and has a sensitivity and specicity approaching those of
Fig. 17. Same patient as in Figure 16. Three-dimensional reconstruction of CTA identied that aortic
tear extended into the arch midway between left common carotid and subclavian arteries (arrows).
This was repaired by an anterior clamshell approach with cardiopulmonary bypass established with
arterial return through both the ascending aorta and femoral artery.
Curr Probl Surg, March 2004 313
angiography.
368,369
In addition, current 3-dimensional reconstruction
gives valuable data with which to plan operative or endovascular
approaches (Figure 17).
360,370
If both modalities are available, angiog-
raphy is utilized ideally when it is required for another reason (eg, pelvic
embolization, concern for cerebrovascular injury, etc), whereas CTA can
be used if there is an indication for a CT scan (eg, to asses the abdomen)
or as the primary evaluation after CXR. TEE has a sensitivity and
specicity of 57% to 63% and of 84% to 91%, respectively.
371
The arch
extending to an area between the left common carotid and the left
subclavian artery often is obscured by the trachea.
367,372
The advantages
of TEE include its ability to be performed during laparotomy, obviating
the need for further evaluation; concomitant assessment of cardiac
function; and the ability to discriminate between ulcerated plaques and
true injuries.
344,373
In addition, this test may be used to monitor aortic
lesions that are being managed nonoperatively.
374
Intravascular ultra-
sound has been used in a similar fashion.
375
Both modalities appear to
have their greatest utility in assessing equivocal ndings on CTA or
angiography, for monitoring lesions that are not deemed immediately
operable, and in the case of intravascular ultrasound, for assisting in the
placement of stent-grafts.
262,376,377
Impact of Clinical Scenario on Determining the Best Diagnostic
Algorithm. There have been attempts to use the mechanism of injury to
help increase the sensitivity of screening tests. Patients with pelvic
fractures have been noted to have an increased incidence of aortic injury,
although whether or not a specic pelvic fracture pattern or crash
mechanism is involved (front versus lateral impact) remains debat-
ed.
378,379
When combined with a high degree of clinical suspicion based
on mechanism, plain CXR has a sensitivity of more than 98%, although
the specicity can be as low as 10% to 45%.
352,380
Hunink and Bos
381
argued that CT of the chest (in patients who would not otherwise undergo
CT) was cost-effective if the risk of injury was 0.5% to 5%. Blackmore
and colleagues
382
developed an algorithm based on a retrospective review
of diagnosed traumatic aortic ruptures, designed as a clinical prediction
rule. For this reason, the CXR appearance was not included in the
analysis. Composite predictors were constructed from individual predic-
tors (Tables 26 and 27). These authors recommended that in the presence
of 0 or 1 clinical predictors, CXR should be the primary screening tool,
whereas if at least 4 predictors were present (corresponding to a risk of
injury of more than 5%), aortography would be the most cost-effective
initial screening method.
314 Curr Probl Surg, March 2004
There has been an increasing reliance on helical CTA. The series
published by Dyer and colleagues
360
identied high-speed MVC (greater
than 60 miles per hour) a subjective mechanism of injury score, and an
ISS greater than 40 to be predictive of aortic injury, whereas specic
features (including side versus frontal impact, MVC versus other mech-
anisms, steering wheel collapse, etc) were not predictive. The authors
concluded that helical CTA should be used to screen all patients with a
widened mediastinum on the supine CXR and all with a mechanism of
injury score of 3 or greater, even if the initial CXR is normal.
TABLE 26. Likelihood of aortic rupture
Simple predictors
Composite
predictors
Odds ratio of aortic
injury (condence
intervals)
Age 50 Age 50 12.1 (1.834)
Unrestrained (including unknown) Unrestrained 5.9 (1.131)
Hypotension (SBP 90 mm Hg) Hypotension 9.9 (1.854)
Rib fracture Thoracic injury 12.1 (2.754)
Chest abrasion
Pneumothorax
Pulmonary contusion
Pelvic fracture Abdominopelvic injury 4.5 (1.119)
Lumbar spine fracture
Emergency laparotomy
Arm fracture Extremity fracture 8.4 (1.355)
Leg fracture
Skull fracture Head injury 4.9 (1.220)
Intracranial hematoma
LOC at evaluation
Brain parenchymal hemorrhage
SBP, systolic blood pressure; LOC, loss of cousciousness.
Adapted from Blackmore CC, Zweibel A, Mann FA. Determining risk of traumatic aortic injury:
how to optimize imaging strategy. Am J Roentgenol 2000;174:3437.
382
Used with permis-
sion.
TABLE 27. Composite score to determine liklihood of aortic rupture.
Number of
composite
predictors
Probability of aortic
injury (condence
intervals)
0 0 (00.0013)
1 0.0019 (0.00040.0054)
2 0.005 (00.021)
3 0.045 (0.0140.15)
47 0.3 (0.110.83)
Adapted from Blackmore et al. (
382
)
Curr Probl Surg, March 2004 315
As crash data become more specic and accurate, it may be possible to
relate the degree of deceleration with a relative risk of injury. Horton and
colleagues
338
argued that more specic details obtained from the scene of
an MVC could be useful in predicting the likelihood of aortic rupture. A
change in velocity of more than 20 miles per hour, near impact (impact
on same side as the victim), and intrusion of more than 15 inches were
found to be signicantly associated with an increased risk of aortic
rupture.
Summary. The vast majority of patients will present with few
obvious direct clinical signs of aortic injury but with an abnormal
CXR. The few patients with normal CXR ndings tend to have intimal
injuries. The concern raised in the literature has been which tests are
most appropriate for screening in a given scenario. As experience with
helical CTA and technology progresses, it appears that CTA can be
used if the CXR is abnormal, if there is an indication for CT of the
abdomen and/or other body compartments in a patient with a suspi-
cious mechanism, and that operation can be performed without
needing further studies in the majority of cases. If there is an
indication for angiography (eg, concern for great-vessel injury, pelvic
embolization, etc), then angiography should be performed. Ultimately,
each center must decide the degree of condence with which CTA is
held in terms of a screening tool and/or whether or not operation can
be planned without requiring angiography.
Initial Treatment
When the diagnosis is suspected on the basis of CXR, immediate
control of blood pressure is critical.
369
The target blood pressure has been
described as less than 120 mm Hg, but more recently it has been argued
that a pressure lower than admission is sufcient to signicantly reduce
the risk of rupture during evaluation.
333,383
Short-acting -blockers such
as esmolol or combination agents such as labetalol are excellent agents,
as are routine interventions including pain control. Pure vasodilating
agents (Nipride principally) are not favored because the reex increased
heart rate increases P/T and may aggravate spinal ischemia by causing
shunting of blood away from the cord. Pain control is often all that is
required.
Free rupture remains a leading cause of death when considering all
patients admitted with signs of life.
49
It is assumed that free rupture is a
catastrophic event characterized by complete loss of vital signs. Although
in the majority of cases this is true and the bulk of patients who present
with hypotension or who become hypotensive during the initial few hours
316 Curr Probl Surg, March 2004
do so because of associated injuries, in at least some cases the cause may
be intermittent bleeding from the aortic laceration itself.
384,385
One
scenario predicting a high risk of early free rupture includes the
combination of hemothorax more than 500 mL without pneumothorax,
supraclavicular hematoma, and/or pseudocoarctation.
347
Simon and
Leslie
385
described 11 patients who presented with a grossly widened
mediastinum, hemothorax, and transient hypotension. The mean time
between transient hypotension and free rupture was 25 minutes.
The initial treatment requires an integration of associated injuries,
degree of aortic disruption, ability to utilize blood pressure control, and
clinical assessment of the risk of early free rupture to determine whether
operative, nonoperative, or endovascular approaches should be used and
how to integrate the plan for the aortic injury into a comprehensive
overall strategy taking into account the need to treat other injuries.
Treatment of Patients with Multiple Injuries
As many as 30% to 50% of patients with aortic rupture require other
operative procedures.
334,384
Although hypotension in the setting of
massive mediastinal hematoma may indicate impending rupture, in the
majority of cases it is a consequence of associated injuries.
384,386
Patients
with grossly positive DPL or evidence of pelvic fracture with associated
bleeding should have these injuries treated rst.
386,387
Patients who are
stable and have only a positive DPL by cell count may undergo aortic
repair rst. One concern has been the risk of restarting the hemorrhage
if heparin is used for mechanical circulatory support. This risk can be
removed essentially if heparin-bonded circuits are used. In addition, even
full heparinization can be tolerated if there is no evidence of ongoing
bleeding. However, most surgeons would feel comfortable having re-
moved a severely shattered spleen or packed a deep liver laceration before
heparinization.
Closed head injury can be present in as many as 50% of patients, one
half of whom have intracranial hemorrhage.
49
Head injuries have been
considered a contraindication to operation. However, overall head trauma
appears to be a marker of poor outcome overall, rather than absolutely a
contraindication to operation. Two reasons to avoid operation would
include patients with such severe injury that survival is not expected or
patients with large intracranial hemorrhage.
388
Severe cardiac injury ranging from severe myocardial stunning to
valvular injury can occur simultaneously.
279,389
Patients who require
aortic or mitral valve replacement or repair acutely can be managed by an
anterior approach, either by sternotomy or sternotomy with an anterolat-
Curr Probl Surg, March 2004 317
eral extension. If valve replacement can be temporized, either operative or
stent-graft approaches could be used rst followed by interval valve
surgery.
273,277
If patients need an IABP after repair of the descending
aorta, it can be placed with attention to avoiding placing the balloon over
suture lines.
A nal unique scenario is the pregnant patient with traumatic aortic
rupture. There are very few reports, but it appears that repair with
circulatory support should be considered. Heparin is not teratogenic in the
second and third trimester. There is concern that because of hormonal
changes the media of the aorta is weakened in pregnancy. This may
suggest that elective caesarian section be used after repair to avoid stress
during vaginal delivery, but successful vaginal delivery has been reported
after aortic repair.
390
Nonoperative or Delayed Treatment
The concept that all aortic injuries required immediate operative repair
has undergone signicant modication with the recognition that delayed
operative repair is feasible and can allow time to correct associated
injuries that would preclude or signicantly increase the risk of opera-
tion.
391
Although initially considered anathema because of Parmleys
data suggesting almost universal death if operation were delayed, it is
now recognized that although these data alerted trauma centers to the
importance and prevalence of the injury, as an autopsy report it may have
been biased by reecting the natural history of the worst injuries of
patients who received no treatment (including blood pressure control). In
current clinical practice, 20% to 50% of patients may not be candidates
for immediate operative repair because of associated injuries. Akins and
colleagues
393
noted a reduction in mortality rate from 24% in a group
undergoing immediate operation to 14% when there was a deliberate
delay (2 to 79 days) to allow stabilization. This most likely reected, at
TABLE 28. Contraindications to immediate operative repair of aortic rupture
Physiologic contraindications
Closed head injury (GCS 6 or intracranial hemorrhage)
Acute lung injury (PaO
2
/FiO
2
200 or inability to tolerate single-lung ventilation)
Cardiac injury (requirement for inotropes or evidence of ongoing ischemia)
Coagulopathy (PT
INR
/APTT 1.5 or diffuse nonoperative bleeding)
Anatomic contraindications
Extensive calcications
Aortic arch involvement when circulatory arrest contraindicated
GCS, Glasgow coma scale; PT, prothrombin time; INR, international normalized ratio; APTT,
activated partial thromboplastin time.
318 Curr Probl Surg, March 2004
least in part, less malignant aortic lacerations. However, selective
operative intervention has become accepted under certain circumstances
(Table 28).
384,391,394
In 4 series published between 1992 and 2000, a cumulative number of
172 patients were admitted with aortic rupture, of whom 74 (43%)
underwent deliberate delay ranging from 1 day to several months before
operative repair.
391,394-396
There were 4 (5%) free ruptures in this
combined experience, all occurring within 72 hours.
The cornerstone of therapy becomes careful blood pressure control, or
hypotensive therapy. Mattox and Wall
333
have noted that in their
literature review of 500 patients treated by delayed or nonoperative
therapy, rupture occurred in only 12 (2.4%) whose blood pressure became
severely hypertensive. Whether or not the risk of free rupture during this
period can be determined by the extent of injury is not clear. Minimal
injuries, usually intimal aps, appear to have a high probability of
spontaneous resolution if blood pressure control is achieved.
375
Kepros
and colleagues
374
described 5 patients in whom an intimal ap of less
than 20 mm was detected, which resolved between 3 and 19 days when
the systolic blood pressure was maintained at less than 90 mm Hg. What
these previous 2 studies illustrate is that the diagnosis of minimal injury
and how they are monitored are critically related to the tool used (ie, TEE
versus CTA versus intravascular ultrasound). As a simple summary, the
risk of rupture when -blockade is possible appears to be less than 5%,
but it can occur even with minimal injury, particularly if strict blood
pressure control is not possible or instituted.
333,370,384,394
One review
noted that the risk of expansion or rupture was greatest in the rst 5 to 7
days, after which the natural history of aortic rupture was similar to that
of nontraumatic aneurysmal disease, presumably due to the secondary
brotic reaction.
370
Serial studies (such as helical CTA) every 48 to 72
hours for the rst 7 days can be used to monitor the lesion and assure
stability. Evidence of growth would prompt earlier intervention, even if
the risk is greater.
Hypotensive therapy itself can be associated with complications.
Patients with closed head injury and elevated intracranial pressure may
have the cerebral perfusion pressure affected, leading to secondary brain
injury. These patients may be better treated aggressively to allow the
cerebral perfusion pressure to be driven.
384
Prolonged lower pressure
may result in end-organ dysfunction. Therefore, urgent repair should still
be considered the standard of care unless there are specic indications to
delay operation.
Curr Probl Surg, March 2004 319
Operative Repair
Technique. Although a variety of options have been described to
expose the proximal descending aorta, in the vast majority of cases a
posterolateral fourth intercostal space approach provides the best expo-
sure and access. Lower incisions will not allow access to the root of the
left subclavian artery. The left lung must be able to be collapsed and this
usually is achieved with a double-lumen endotracheal tube, although
newer endobronchial blockers that allow suctioning can be tried if airway
edema or other issues contraindicate changing from a single-lumen to a
double-lumen tube.
Proximal exposure requires an appreciation of the likelihood that a tear
extends proximal to or beyond the origin of the left subclavian artery into
the aortic arch. Lesions within 1 cm of the origin pose specic anatomic
concerns. Some patients (estimated at 14% in 1 review) will have occult
proximal extension or a separate tear such that clamping distal to the
origin of the left subclavian would not allow operative correction and
might lead to acute aortic disruption.
46
This possibility emphasizes the
importance of obtaining aortic control proximal to the left subclavian
artery in any case in which there is any doubt about the proximity of the
tear and the vessel. Tears close to the left subclavian artery also are
associated with an increased risk of rupture during proximal dissection,
possibly due to a combination of factors: proximal extension already
noted; larger size of tears; or inadvertent dissection distally along the
medial aspect of the arch entering the injury site.
46
In addition, the
exposure of these more proximal injuries is slightly more difcult, leading
to longer cross-clamp times. Compounding these issues, proximal dissec-
tion requires mobilization of the vagus nerve proximal to the point where
the recurrent nerve originates, leading to a greater incidence (10% to
20%) of vocal cord paralysis. In patients who are not actively bleeding it
is advisable to institute bypass rst and then perform distal exposure and
mobilize the subclavian artery, leaving the proximal exposure to the last
so that if bleeding occurs, everything is in readiness for repair.
46
A variety of techniques have been described, ranging from graft
interposition to resection and end-to-end anastomosis to patch repair and
to primary repair. In as many as 50% of cases (depending on the series)
primary repair (construed as either end-to-end reconstruction or debride-
ment followed by reapproximation of the injured portion of the vessel)
has been performed, the argument in favor being shorter cross-clamp
times and a reduced risk of prosthetic graft infection.
397-401
This option is
less likely the closure the injury is to the curvature of the arch, as marked
320 Curr Probl Surg, March 2004
by the left subclavian artery, where the tears tend to be more com-
plex.
46,402
Clearly, judgment is required for cases with extensive longi-
tudinal tears to avoid excessive tension. If a graft is used, sizing the graft
on the basis of the distal aortic diameter and then trimming the proximal
portion of the graft at an angle while laying it out so that the graft lies in
a straight attitude will prevent angulation, distortion, and problems with
oversizing the graft.
The aortic wall in young patients can be surprisingly friable. In
emergent situations some have advocated proximal clamping with con-
trolled distal exsanguination, allowing bleeding from the distal lumen
particularly if the injury is at the diaphragmatic level and/or if heparin is
contraindicated. This usually has been applied to nontraumatic complex
thoracic aortic rupture but in rare circumstances can be considered in the
trauma setting.
403
Mechanical Circulatory Support. Mechanical circulatory support has
been advocated (although this position is not fully supported) as the key
method to reduce the risk of paralysis. In fact, there are several other
issues to consider. The goals of bypass are not simply to provide distal
perfusion to the spinal cord but also to the abdominal organs and to
reduce myocardial strain and possibly allow rewarming and enhanced
oxygenation.
402,404
The 2 traditional manners of establishing bypass are
by atrial-femoral or thoracic partial bypass and femoral-femoral bypass.
Classically the former uses no or minimal heparin and does not allow
oxygenation, whereas the latter can be used as a form of full cardiopul-
monary bypass, with systemic heparinization and full oxygenation.
405
The advantage of providing some additional oxygenation is that if
patients have compromised pulmonary function, this may allow the
operation to proceed.
406
The addition of an oxygenator requires full
heparinization with activated clotting times of 400 seconds. One
variant, introducing an oxygenator into a partial left heart bypass circuit,
has been described allowing lower levels of heparinization (250 to 300
seconds).
407
It must be recalled that unlike elective cardiac operation, the
entire cardiac output cannot be diverted or else critical cerebral ischemia
would result. Thus, two third to one third perfusion is aimed for, with
the goal of maintaining one third of the cardiac output to the aortic arch.
Performing left heart bypass using a pulmonary vein appears to be
associated with a lower complication rate than the more friable left atrial
appendage. This includes a reduction in the incidence of atrial and
ventricular arrhythmias and pericarditis.
408
Rarely, circulatory arrest might be required. This is more often the case
in chronic settings in which complex anatomic features, aortic arch
Curr Probl Surg, March 2004 321
involvement, and/or extensive calcications suggest that exposure and
cerebral and cord protection will be difcult. If recognized before the start
of the operation femoral-femoral bypass can be used or, less commonly,
jugular-to-ascending aortic cannulation.
402,409
If the situation changes
during posterolateral thoracotomy particularly after clamps have been
applied, then the only way to institute full bypass is to cannulate the
pulmonary vein (if left heart bypass has been instituted) or the aortic arch
or ascending aorta with a Y-connector (if femoral-femoral bypass has
been instituted).
410
One of the main concerns regarding the use of bypass has been the risk
of heparinization.
388
With the levels required for left heart bypass
(activated clotting times of more than 150 seconds) it is apparent that the
risk of rebleeding from most abdominal injuries is overstated.
404,411
A
major risk, however, is the presence of severe pulmonary contusions
especially in the setting of deep lung lacerations, in which case hepa-
rinization is associated with a marked risk of intraparenchymal hemor-
rhage.
404,411
Recently, the increased use of heparin-bonded circuits has
allowed left heart bypass to be performed with no or as little as 1,000
units of heparin (the latter to reduce the risk of thrombus at the cannula
insertion sites).
411,412
This procedure requires that the patient be able to
tolerate single-lung ventilation but does provide a means of reducing the
risk of bleeding in multiply injured patients.
Outcome. The overall mortality rate and causes of death vary depending
on the volume of patients and the extent of time that encompasses the
review. Von Oppell and colleagues
411
performed a meta-analysis of
articles published between 1972 and 1992 of admitted patients who
underwent thoracotomy. Of 1,742 patients reaching the hospital, the
overall mortality rate was 32% (10.3% preoperative, 3.5% who under-
went emergency thoracotomy, 6.7% intraoperative, and 11.5% postoper-
ative deaths). The overall mortality rate for patients who underwent
emergency thoracotomy because of frank rupture or shock was almost
94%. The AAST prospective study found an overall mortality rate in all
patients of 31%; nearly two thirds of deaths were attributable to free
rupture.
49
If one concentrates on patients who are stable and who are
diagnosed in an elective fashion (ie, CXR abnormalities that prompt
further diagnostic tests), Mattox and Wall
333
estimated that the overall
mortality rate was roughly 25%, due to associated injuries in the majority
of cases . It is clear that the mortality rate, both overall and considering
those undergoing operative repair, is critically linked to stability. For
patients who present with systolic blood pressures greater than 90 mm Hg
and who do not require resuscitation, the operative mortality rate ranges
322 Curr Probl Surg, March 2004
from 7% to 18% compared with 70% to 98% if unstable.
332,333,384,385,400
It is intriguing (and frustrating) that the operative mortality rate for
patients who undergo delayed repair tends to be less than for those who
undergo urgent repair, although this probably reects intangible factors
(eg, smaller aortic lesions and better physiologic status).
384,391,402
Of
those patients who survive the operation but subsequently die, the most
common causes are respiratory failure and/or complications arising from
head injury.
404
Complications. The primary complication that is always considered is
the fear of paralysis. There have been several discussions focused on
whether or not some form of bypass can signicantly reduce the risk of
paralysis, as well as the risk of extended cross-clamp time. Sufce it to
say that mechanical circulatory support can reduce but not eliminate the
risk of paralysis and that clamp-and-sew technique can be used safely by
skilled surgeons in the appropriate setting.
332
The AAST prospective
study documented that among those patients who survived, the overall
incidence of paraplegia was 11.3% (19% in clamp-and-sew and 5.2%
when circulatory support was employed).
49
A meta-analysis recorded the
risk of new-onset paraplegia to be 25% after clamp-and-sew, 15.6% after
passive shunts, and 2.5% after active shunts were used.
411
Single-
institution series also reect the benet of bypass.
402,413
Keeping the
cross-clamp time to less than 30 minutes also has been stressed as a
critical goal.
49,414
Many authors believe that mechanical circulatory
support may allow some liberalization of the cross-clamp time, assuming
that adequate ows can be maintained distally so that the cross-clamp
time becomes less critical.
49
This should not be taken to imply that the
surgeon can take it easy but rather that attention can be given to difcult
suture lines instead of rushing through the repair or graft anastomosis,
resulting in excessive suture line bleeding. Interestingly, paraplegia can
occur with shorter cross-clamp times as well as on bypass. The left
subclavian artery through vertebral and other collaterals can be an
important supplier of collateral ow, and repositioning the proximal
clamp once the proximal anastomosis is performed may be a useful
adjunct.
46
The issue of patient stability is also critical. Patients who
require resuscitation or who exhibit severe oxygen debt appear to have
experienced an initial ischemic stress that puts them at risk of cord
injury.
46,404
In the context of ischemia/reperfusion injury, clamping then
provides a second insult. This can be aggravated by the use of vasodila-
tors preoperatively and during clamping, as well as uncontrolled inter-
costal back bleeding, both of which represent a steal phenomenon with
perfusion to the cord being reduced.
404
Pate and colleagues
404
elegantly
Curr Probl Surg, March 2004 323
have listed the options available to reduce the risk of signicant
ischemia/reperfusion injury to the cord, but in the emergent setting
probably the only other adjunct is preclamp steroid administration,
although hypothermia may become used more commonly as well. There
has been a great deal of emphasis placed on measuring ow and pressure
distally in elective and traumatic aortic aneurysm repair, but in practical
terms with left heart bypass it is difcult to manipulate ows other than
by administering volume and ensuring proper cannula placement. The
data available would support the following conclusions: mechanical
circulatory support reduces signicantly but not completely the risk of
paraplegia and should be used unless there are specic technical consid-
erations that contraindicate institution; the operating team should be very
focused to keep cross-clamp times as short as possible; intercostal arteries
that are back-bleeding should be controlled to prevent steal phenomena;
and in most circumstances the low level of heparin required for left heart
bypass will not cause rebleeding from associated injuries.
Pulmonary complications are the most common, including specically
pneumonia, ARDS, empyema, and hemorrhage, affecting roughly 25% of
postoperative patients.
49
Operation in general, possibly aggravated by
inammation associated with mechanical circulatory support, can lead to
deterioration in pulmonary function.
384,411,415
Vocal cord paresis also is
relatively common, especially when control proximal to the origin of the
left subclavian artery is required, which can lead to aspiration and poor
cough.
46
This complication can be treated with cord injections. Other
complications include renal failure (approximately 6%) that occurs more
frequently in unstable patients who have undergone repair without some
form of bypass and those with abdominal compartment syndrome.
Endovascular Stent-Graft Repair
Endovascular approaches have become an increasingly viable option for
treating traumatic aortic rupture (Figure 18). This approach is particularly
attractive in patients with severe lung and/or cardiac injures that preclude
open repair but who are judged at increased risk of rupture with
nonoperative treatment.
416
Dake and colleagues
417
extended the experi-
ence with stent-grafts used for infrarenal aortic aneurysms to the thoracic
aorta. Initially used predominantly for lesions that could wait at least 24
hours, it is now acknowledged that stent-grafts can be placed emer-
gently.
418-420
There was concern, however, that noncommercial de-
vices might not be reliable with prolonged follow-up, particularly if
signicant infection were present.
418
More contemporary studies of
commercial self-expanding devices are more promising.
421
324 Curr Probl Surg, March 2004
As experience is gained some anatomic issues have been resolved, whereas
others have been raised. To achieve a reliable seal, landing zones of at least
1.5 cm are recommended.
421
This situation is problematic since approxi-
mately one half of aortic ruptures occur within 1 to 2 cmof the left subclavian
artery, implying that the origin of this vessel will have to be crossed in a
substantial number of cases.
422
However, the clinical experience suggests
that this does not provide an acute risk of limb ischemia, and late a steal
phenomenon can be treated electively with carotid-subclavian bypass when
the patient has stabilized.
423,424
The left subclavian artery, however, is an
important indicator of the distal end of the aortic arch, and signicant
curvature can prevent passing the stiff deployment device across the site of
the injury and can, particularly with the stiffer noncommercial devices, lead
to stent deformation and increased frequency of endoleak.
421,425
In addition,
self-expanding commercial devices appear to provide more consistent lateral
tension against the aortic wall with better apposition. In addition, some grafts
have an uncovered proximal portion that can be placed across arch vessels
without impeding perfusion. Currently, commercial stent- grafts used for the
Fig. 18. Three-dimensional CT reconstruction of an endovascular stent- graft placed to occlude aortic
laceration after blunt trauma
Curr Probl Surg, March 2004 325
infrarenal aorta are widely available. These include the Ancure and AnueRx
cuff extender.
426
The route of placement can be problematic. Because currently available
devices are designed for intra-abdominal placement, in many instances a
conduit must be placed onto the iliac artery or infrarenal aorta. This is not
an insurmountable problem, since a retroperitoneal approach can be used,
and many patients have just undergone a laparotomy, so that using the
transaortic route is not physiologically unreasonable.
There are specic thoracic devices under study (including the Talent
[World Medical Manufacturing Corp, Sunrise, Fla]; Cook-Zenith [Cook
Australia, Brisbane, Australia]; and Gore [W.L. Gore and Associates
Flagstaff, Ariz]), but these are not currently available in the United States
outside clinical trials. However, the growing experience with these
devices suggests that they will overcome the majority of the issues raised
previously.
421,427
When choosing the size of the device, it is critical to oversize them by
20%.
419
Some centers nd that placing a left brachial guidewire helps to
identify the subclavian orice and to stabilize the device.
421
When
deploying the graft, adenosine is useful to induce transient systolic arrest,
thereby preventing the device from being pushed distally.
426
Appropriate follow-up evaluation to identify endoleak is critical. There
is concern that over time subtle but signicant distal migration can occur.
Helical CTA is probably the most efcient tool for determining if there is
an endoleak of migration and should be performed after placement
(within a few days) and then yearly for 1 to 2 years after discharge. The
use and utility of endovascular stent-grafts will continue to increase as
more experience is gained with devices specically designed for thoracic
deployment. At this point there are no denitive long-term follow-up data
to recommend absolutely this approach over open repair in patients who
are acceptable operative candidates. However, even with this caveat, it is
apparent that stent-grafts have added an extremely important tool to the
treatment options for aortic rupture.
Traumatic Aortic Rupture in the Pediatric Population
Estimates of the incidence of aortic rupture in the pediatric population
vary, depending on the population studied. Lowe and colleagues
428
noted
an incidence of 0.06% among all patients admitted after blunt trauma,
whereas Spouge and colleagues
429
described a 7.4% incidence among
children admitted with blunt chest injury. The majority of patients present
after MVC, and not wearing seat belts may result in a higher risk.
350,430
Compared with those in adults, chest injuries in children initially may not
326 Curr Probl Surg, March 2004
be apparent clinically, although pseudocoarctation may be more preva-
lent.
350
The diagnosis is suggested by abnormal ndings on CXR and can
be conrmed by angiogram, CT, and/or TEE, depending on institutional
experience.
350,429-431
Operative repair remains the standard treatment,
and mechanical circulatory support is favored but not mandated.
350
Some
patients can undergo primary repair, but the majority have graft recon-
struction.
350,429,430
As for the adult population, commonly there are
multiple associated injuries.
350,430
This may prompt temporization with
-blockade.
431
Operative repair remains the initial standard, but in select
patients nonoperative treatment or endovascular stent-grafting can be
considered.
Ascending and Arch Injuries
Injuries involving the aortic arch and/or ascending aorta are rare,
occurring in less than 5% of series that can extend for at least a 25-year
period.
332,405,406
This may reect a greater mortality rate at the scene
from these injuries.
17
Apart from frank rupture, ascending aortic injuries
may manifest as acute dissection with aortic insufciency and/or coronary
ostial obstruction.
213
The importance of these tears is that the operative
approach is via sternotomy, and hypothermic circulatory arrest is re-
quired. Occasionally when the injury is noted to involve the distal arch,
a combined approach utilizing a dedicated submammary incision with
cardiopulmonary bypass (utilizing ascending aortic and femoral arterial
cannulation) may permit repair without the need for circulatory arrest
(Figure 17). In patients surviving to operation the lesions are usually
small, and primary repair can be performed.
406
Diagnosis is usually made
in the same manner that tears of the descending thoracic aorta are
identied: CXR followed by CTA or angiogram. Three-dimensional
reconstruction can be very useful in dening the exact anatomy.
432
There
is very limited experience with nonoperative treatment of these lesions,
since the natural history is thought to follow that of acute ascending
dissection, with early free rupture. If there are major contraindications to
operation, however, nonoperative therapy can be used in rare circum-
stances when blood pressure control is feasible to allow time for
optimization.
433
Chronic Pseudoaneurysms
Originally considered a rarity, chronic pseudoaneurysms arising from
minimal or missed aortic injuries are being recognized with increasing
frequency. The denition of chronic varies, although Pate and col-
leagues
404
argue that any lesion detected after 8 days or treated nonop-
Curr Probl Surg, March 2004 327
eratively for 8 days should be considered a chronic pseudoaneurysm. This
would t with the concept that after 5 to 7 days there is an intense brotic
reaction that limits the potential for acute rupture and that the lesion
follows the natural history of chronic atherosclerotic aneurysmal dis-
ease.
370
This can include late dissection, rupture, erosion, or even distal
embolization that has been noted with nontraumatic aneurysms.
434
Patients with chronic pseudoaneurysms should, at the very least, be
treated with blood pressure control. Patients with large saccular aneu-
rysms should be considered for either resection or endovascular ap-
proaches. Operation can be made more challenging by dense adhesions
within the chest as well as calcication and inammation involving the
vessel itself.
435
In general, patients with symptomatic and/or enlarging
lesions should undergo repair or endografting. Treatment should be more
aggressive in younger patients who are more likely to have progressive
growth.
Great-Vessel Injury
Blunt injuries involving the intrathoracic great vessels are difcult to
diagnose and treat and are commonly associated with signicant associ-
ated injuries (including the airway, heart, brachial plexus, and central
nervous system) that impact the outcome. As with aortic injury, the
incidence and location of blunt injury of the great vessels differ between
autopsy and clinical series. It has been argued that the majority of patients
who suffer blunt disruption of the great vessels die at the scene or before
transport.
369,436
Dosios and colleagues
437
in an autopsy study noted the
following incidence of great-vessel injury based on mechanism: MVC,
8.9% (drivers 8.3% and rear passengers 25%); pedestrian struck, 25%;
and falls, 11.8%. Multiple injuries involving both aortic branches and the
aorta proper were present in 13.4% of cases. Interestingly, pedestrians
struck had a higher incidence of great-vessel injury compared with
automobile occupants (17.6% versus 4.6%, P 0.04) but a lower
incidence of isthmus rupture (50% versus 67.8%, P 0.04).
437
Chen and
colleagues
366
described 166 patients who underwent angiography for
indeterminate mediastinum. Nine patients (5%) had great-vessel injury,
which included 4 innominate, 4 left common carotid, 3 left subclavian, 1
internal mammary artery, and 1 left vertebral artery injury. Great vessel
injury in conjunction with aortic laceration was found in 3 (1%) cases.
Nine of the vessels had intimal defects and 4 had pseudoaneurysm. Ahrar
and colleagues
367
reported a similar study that documented 24 great
vessel injuries among 17 of 89 patients (19%) undergoing angiography, 3
328 Curr Probl Surg, March 2004
of whom (18% of those with great vessel injury, 3% of the whole
population) had combined aortic laceration as well.
Overall, innominate artery rupture is considered the second most
common thoracic vascular injury after aortic rupture, although the
experience varies between individual series.
438
Rosenberg and col-
leagues
439
found that one half of the blunt injuries involved the innom-
inate, the remainder being divided equally among left common carotid
and subclavian arteries. During an 8-year period Pretre and colleagues
440
treated 14 cases, 2 involving the innominate, 1 the right common carotid,
and the remainder the subclavian artery.
Mechanism
The mechanism of injury to the innominate artery is similar to that of
aortic rupture, in that acute deceleration is the principal cause and
includes a combination of traction injury as the head is forced to the left
and sternal compression against the spine with cardiac displace-
ment.
439,441-443
Because the innominate artery is relatively mobile com-
pared with the aortic arch, this results in force being applied primarily to
the root of the artery, which explains that the most common site of injury
is at the origin of the vessel.
366
A direct blow compressing the manubrium
against the innominate artery may also be a major mechanism. Clavicular
fractures remain an important mechanism of injury for subclavian artery
ruptures in the thoracic outlet and are the cause in approximately 50% of
cases. Traction injury (usually encountered after MVC) is applied against
the xed origin of the vessel.
444
Diagnosis
The majority of patients who do present for evaluation with intratho-
racic great vessel injury are stable, although they often have associated
injuries.
445
This scenario is in contrast to those admitted after penetrating
injury and who are more likely to be unstable. The most common
associated injuries appear to be rib fractures (46%) and pneumothorax
(36%).
445
The diagnosis can be suggested by clinical examination (ie,
bruit, supraclavicular hematoma, pulse decit).
446
The shoulder-belt
sign, a vivid bruise following the pattern of the restraining belt running
from the base of the right neck inferiorly and to the left, has also been
noted to suggest the diagnosis of intrathoracic or cervical carotid
injury.
445,447
Brachial plexus injuries also are relatively common, partic-
ularly when the subclavian artery is injured.
443
Patients who survive to be
admitted are usually hemodynamically stable, and the diagnosis is
suggested by a widened mediastinum on CXR.
369,441
The CT scan will
Curr Probl Surg, March 2004 329
usually demonstrate hematoma around the arch and the great ves-
sels.
439,443
Earlier CT scans were associated with only a 55% sensitivity
and specicity for the diagnosis of great vessel injury.
448
Whether more
contemporary helical CTA is sufcient to diagnose accurately the specic
injury is not as clear, and angiography is still recommended as the
standard of care for diagnosing these injuries.
358,366,449
Nonoperative Treatment
Nonoperative treatment may be appropriate in a small subset of patients
who present with intimal defects without surrounding hematoma and
when there are no contraindications to anticoagulation. These patients
should be monitored with transcranial Doppler studies to identify micro-
emboli that may result in stroke.
450
Patients who have complete occlusion
of the carotid vessels extending into the cerebral circulation and who do
not have a neurologic decit also may be treated by anticoagulation,
although there is a risk of delayed thrombosis or embolism leading to
cerebral infarction.
Endovascular Approaches
Rarely, proximal occlusive catheters can be used to control bleeding
before operative repair, although concerns should include prolonged
delay in transporting the patient to the operating room, continued bleeding
due to collaterals, and possible ischemic insult.
451,452
Endovascular stent-
grafts have been reported in isolated cases of innominate, carotid, and
subclavian artery emergencies.
453,454
Experience with these devices is
still accruing, but they offer the hope of an alternative to operative repair
in patients with severe coexistent injuries.
Operative Repair of Innominate Artery Rupture
The majority of injuries to the innominate artery are located at or very
close to the origin.
366,436
Control and repair are usually performed via
sternotomy, usually with a right neck extension and employing a graft
from the ascending aorta to the innominate artery anastomosed end-to-
end after which the proximal injury is controlled with pledgeted su-
tures.
209
Injuries in the mid-region of the artery can be repaired with an
interposition graft.
445
Occasionally more distal injuries require
Y-grafts.
455
Resection and primary anastomosis can be performed for
injuries not associated with extensive tissue loss or tension.
369
Cardio-
pulmonary bypass is rarely required unless there is evidence of heart
failure once partial clamping on the ascending aorta is performed (eg,
cardiac distension, low cardiac output, and/or arrhythmias), to manage
330 Curr Probl Surg, March 2004
specic associated injuries (eg, cardiac valve rupture), or even more
rarely if there are associated airway lesions that prevent oxygen-
ation.
267,369,456
In some cases the preoperative angiogram may document an adequate
collateral supply via the circle of Willis, which may reduce concern
regarding the need for aortic-carotid shunting.
441
The majority of authors
have not found shunting necessary in any case, particularly since most of
the injuries are proximal and the distal clamp can be placed proximal to
the bifurcation, allowing some collateral supply from the vertebral
artery.
209,457
The method of choice has evolved into performing an
ascending aortic (side-to-end) to distal innominate (end-to-end) graft
followed by closure of the proximal injury.
209,436
This allows reduced
cross-clamp time. However, in our institutional experience, 4 of 6 patients
with proximal injury presented with active bleeding requiring control of
the injury rst. If a patient has extensive aortic calcication, simple
side-clamping may not be possible and other options, including possibly
hypothermic circulatory arrest, may be required.
433
When operating for distal tracheal rupture, if great-vessel injury is
suspected, sternotomy provides the most versatile approach.
441
The
tracheobronchial tree can be approached between the superior vena cava
and ascending aorta, incising the pericardium and reecting the right main
pulmonary artery.
458
If there has not been time to identify the specic site
of great vessel injury or a large hematoma is encountered, proximal
control of the great vessels is best obtained by opening the pericardium
(and thus staying out of the hematoma) and dissecting along the curvature
of the aorta, exposing the origin of the great vessels in turn.
62
Combined blunt innominate and left common carotid rupture is
rare.
220,459-461
This injury pattern may be more common when there is a
common origin of the vessels. The reviews of both Johnston and
colleagues
209
and Graham and colleagues
436
noted that the incidence of
this anomaly is 11% in the general population but is present in 29% of
patients with blunt innominate rupture. The treatment of this combined
injury is made difcult by the need for cerebral protection. If the injury
in the common trunk variety is distal to the origin of the left common
carotid, simple repair with or without an aortic-to-right carotid shunt can
be performed.
220
Aortic-to-right common carotid shunting also can be
used for injuries that require simultaneous clamping of both innominate
and common carotid injuries (whether from a common trunk or not) or,
if the injury is complex, by circulatory arrest.
459-461
Ruebben and
colleagues
462
reported a unique approach in which the left common
Curr Probl Surg, March 2004 331
carotid artery was transposed to the left subclavian artery, permitting
deployment of a stent-graft to correct the innominate artery laceration.
Operative Repair of Left Common Carotid Artery Rupture
The origin of the left common carotid artery also is approached via
sternotomy (with left neck extension) and the basic concerns are similar
to those for repair of innominate artery rupture. Operative options can
include ligation with subclavian-carotid bypass or interposition graft-
ing.
463
The underlying consideration in the treatment of carotid artery
injuries is cerebral protection, since the brain tolerates ischemia for only
a few minutes. Although many patients with penetrating carotid artery
injury present with exsanguinating hemorrhage, ligation should, if possi-
ble, be reserved for patients with established neurologic decits in the
presence of complete occlusion of the entire carotid artery. Although the
view was once held that ligation is preferable to repair in all patients with
neurologic decits so as to avoid mortality, the consensus is now rmly
in favor of carotid reconstruction in cases of both blunt and penetrating
injuries as long as antegrade ow is present. The concern that deteriora-
tion may be caused by reperfusion into infarcted tissue always must be
borne in mind; however, hemorrhage of some degree often occurs within
infarcted tissue regardless of reperfusion. In general the consensus is that
patients presenting with neurologic ndings and great vessel injury may
be helped more often than harmed by aggressive restoration of perfusion.
Combined morbidity and mortality rates are signicantly lower in patients
undergoing primary repair compared with ligation (15% versus 50%).
426
The role of anticoagulation in these situations remains variable and will
be moderated by the extent and nature of traumatic injuries. In general
systemic administration of heparin is acceptable in a patient with an
isolated carotid artery injury even when signs of cerebral ischemia are
present. If preoperative angiography demonstrates complete occlusion,
magnetic resonance angiography may be useful in determining the
patency of the distal vessel.
464
Cerebral CT with contrast or diffusion
magnetic resonance imaging will be helpful in assessing the potential risk
for hemorrhagic conversion of an infarct. Established thrombus must be
removed by a balloon catheter before repair or insertion of a shunt. The
presence of pulsatile backow from the internal carotid artery implies
satisfactory cerebral perfusion.
Operative Repair of the Subclavian Artery
Injuries involving the proximal left subclavian artery represent a
different spectrum of issues compared with more distal injuries. A variety
332 Curr Probl Surg, March 2004
of approaches are possible, determined by the nature of the injury and the
surgeons comfort with specic approaches (Table 29).
443,450,463
Patients who present with active intrathoracic bleeding may be managed
best by an anterolateral second intercostal space thoracotomy, which
allows packing of the apex and then subsequent repair as dictated by the
extent of injury (Figure 19).
446
Tears involving the root of the vessel may
be approached best by posterolateral thoracotomy as with aortic rupture if
TABLE 29. Operative repair of left subclavian arterial injuries
Operative exposure
Trap-door
Sternotomy supraclavicular extension
Posterolateral neck incision
Anterolateral supraclavicular incision
Repair options
Graft interposition
Saphenous vein interposition
Transposition to carotid
Carotid-subclavian bypass
Bifurcated carotid-subclavian graft
Fig. 19. Exposure of the proximal left subclavian injury from anterolateral approach. The subclavian
artery is looped with vascular tape. (Color version of gure is available online.)
Curr Probl Surg, March 2004 333
there is any doubt that the aortic wall is signicantly damaged. In other
instances when the proximal portion is involved, sternotomy with
supraclavicular extension is an acceptable alternative to the trap-door
incision.
463
Injuries in the thoracic outlet may require sternotomy for initial
proximal control, but more commonly division of the clavicle provides
excellent exposure.
443
Primary repair is possible is some injuries, but the
majority of patients will require graft interposition.
443,465
Ligation be-
cause of the extensive collateralization is acceptable if the patient is in
extremis.
63
Outcome
The mortality rate and procedure-related complication rate for patients
who undergo operation for blunt innominate rupture may be as high as
30% and 40%, respectively.
209
The overall complication rate has been
100% in some series, but the bulk of these complications are due to
associated injuries.
209,369
Patients with central nervous system injuries
have a worse prognosis.
209
In general survival after great vessel injury is
related to the stability of the patient and the absence of associated major
airway and/or central nervous system trauma.
436,441,443,454
Internal Mammary Artery Injury
Blunt traumatic injury of the internal mammary artery is extremely
rare.
454,466,467
In 1 series of patients who underwent thoracotomy within
48 hours of injury, internal mammary injuries were found in 7 of 142
blunt trauma cases.
4
Injuries may manifest as occlusion, contained
hematoma with a characteristic D shape with the base against the sternum,
contained pseudoaneurysm, or hemothorax.
454,466
Most patients with
active hemorrhage and hemothorax will be diagnosed and undergo
ligation at thoracotomy or thoracoscopy. If diagnosed by angiography,
options may included embolization.
454
Azygous Vein Rupture
The azygous vein, as a tributary of the superior vena cava, should be
considered a great vessel.
468
Rib fractures are not always present and
it has been argued that axial rotation results in tearing of the
vein.
469,470
Bowles and colleagues
468
presented a case report and
reviewed the literature, identifying 12 cases in total. Their summary
found that 11 cases were related to MVC, that 11 presented with
hemothorax and hypotension, and that the injury involved the junction
334 Curr Probl Surg, March 2004
of the azygous with the superior vena cava in 5 (the arch in the
remainder). Two patients died.
Tracheobronchial Injury
The rst description of tracheobronchial rupture from blunt trauma may
be from an 1874 article by W.H. Winslow, as quoted by Mills and
colleagues
471
:
The cook was preparing two of them (canvas back ducks) for baking, when she
notice [sic] something abnormal in one of them, and called my attention to it.
On examination, it was evident that at some previous remote period the left
bronchus of the duck had been ruptured on the outer side, where it joined the
trachea at the bifurcation. . .yet in this wild bird life and health had
apparently existed with the injury for many months, and repair had made good
progress, until interrupted by the sportsman.
In 1928 Krinitzki reported autopsy ndings in a 31-year-old woman
who had an occluded right mainstem bronchus from traumatic stricture,
apparently the result of trauma at age 10 years.
471
The rst successful
primary repair of bronchial rupture resulting from blunt trauma was
reported by Kinsella and Johnsrud in 1947.
472
The occurrence of
traumatic tracheobronchial rupture is unusual, ranging from 1% to 3% of
reports of severe blunt chest trauma. Four Los Angeles urban trauma
centers reported only 9 such cases between 1980 and 1987.
473
Two
autopsy reports have documented a 0.85% and a 2.8% incidence of
tracheobronchial rupture after blunt thoracic injury.
471
Iatrogenic causes
of tracheal rupture are most commonly due to endotracheal intubation and
overination of the tracheal cuff.
474
Blunt tracheobronchial disruption occurs in only 1% to 3% of MVCs
and more than 80% of victims die before reaching the hospital.
383,475
Overall, intrathoracic ruptures occur in 1% to 2% of thoracic trauma
admissions.
476
Kiser and colleagues
475
in their review of the literature
found that the injury was within 2 cm of the carina in 76% of cases, within
1 cm in 58%, and specically in the right main stem within 2 cm of the
carina in 43%. Approximately 50% of airway injuries are circumferen-
tial.
477
Right-sided injuries are more likely to be diagnosed within 24
hours (52%) compared with tracheal injuries (43%) or left main stem
disruption (14%).
475
One reason may be that the left mainstem bronchus
is relatively more buried by mediastinal structures, including the arch of
the aorta, with signicantly more investing peribronchial tissue to
maintain ventilation for a time.
478
Curr Probl Surg, March 2004 335
Mechanism
Blunt tracheal or bronchial injuries are often due to compression of the
airway between the sternum and the vertebral column. Such a decelerat-
ing steering wheel incident results in 3 typical and distinct patterns of
tracheobronchial injury: a shearing of the right main stem bronchus from
the carina; a transverse laceration of the trachea; or a blowout of the
membranous trachea if the glottis is closed. The membranous blowout can
extend from the subcricoid area to the carina.
479
Every level of the trachea
and all major bronchi have been involved, but 80% of injuries are within
2.5 cm of the carina and the injuries are equally divided between the right
and left sides.
471
Kirsh and colleagues
480
have postulated 3 distinct
mechanism of injury: tracheal traction injury at the carina from antero-
posterior compression and lateral expansion of the thorax; shearing at
xation points (cricoid and carina); and elevated intratracheal pressure
(closed glottis).
In a 10-year review of thoracic trauma cases from University of Texas
at San Antonio, 14 patients were treated for major tracheal or bronchial
injuries and only 5 of these were due to blunt trauma.
481
Three were
avulsions of the right main bronchus and in 2 there was a stellate tear of
the distal trachea. The dominant physical nding was subcutaneous
emphysema in all but 1 patient. This was a 3-year-old with an avulsed
right mainstem bronchus and large air leak into the right pleural space.
Bronchoscopy was diagnostic in the 3 blunt trauma patients in whom it
was performed and aided in the establishment of an airway in 1. The 3
patients with complete but simple avulsions were repaired primarily; the
2 stellate lacerations required a combination of pneumonectomy and
repair.
Major injuries are present in 40% to 100% of patients with tracheo-
bronchial rupture. Although the majority of injuries are orthopedic in
nature, as many as one half have concomitant facial fractures, pulmonary
contusion, and/or abdominal injuries. In addition closed head injuries
have been described in 10% to 20% of cases, spinal cord injury may be
present in 10%, and esophageal rupture in some reports is present in 20%
of cases.
482
Diagnosis
Patients with tracheal injuries typically present with mediastinal and
deep cervical emphysema or, less commonly, with pneumothorax and
massive air leak (Figure 20). The deep cervical fascia appears to contain
the air, causing massive subcutaneous emphysema while preventing a
336 Curr Probl Surg, March 2004
pneumothorax. In 1 series all of the patients with injury to the cervical and
mediastinal trachea had subcutaneous emphysema, and 6 of 11 had
mediastinal emphysema, but only 4 of the 11 had a pneumothorax.
481
Hemoptysis, hemopneumothorax, subcutaneous crepitus, and respiratory
distress are also frequent. Respiratory distress seems to be more common
in blunt trauma injuries than with penetrating tracheobronchial wounds.
When accompanied by acute airway obstruction, the immediate priority is
establishment of an effective airway. If possible this should be combined
with endoscopic evaluation of the injury before blind endotracheal
intubation, although this is rarely possible.
CXR can demonstrate pneumothorax and pneumomediastinum or oc-
casionally the fallen lung sign in which the lung is seen to drop away
Fig. 20. Patient admitted after MVC. Pneumothorax (arrow) and subcutaneous emphysema are
prominent.
Curr Probl Surg, March 2004 337
from the hilum within the hemithorax.
285
Spiral CT also can demonstrate
important details, including focal disruption or avulsion of the airway-
(Figure 21).
483
However, a denitive diagnosis can be difcult since
many patients have an underlying parenchymal lung injury that can
account for an air leak or pneumomediastinum. Alternatively, mediastinal
tissues, blood clot, or airway enfolding may occlude an airway disruption,
preventing the anticipated air leak and masking the injury. This can result
in the radiographic appearance of a persistent pneumothorax despite
placement of a chest tube.
285
Injuries of the carina or within the fth ring
of either mainstem bronchus more commonly appear to be associated
with pneumomediastinum, which may help localization.
484
The denitive diagnosis of tracheal and/or bronchial injury usually
requires conrmation by bronchoscopy. Patients with persistent air leak
and/or persistent pneumothorax without air leak despite an appropriately
placed chest tube should undergo bronchoscopy.
156
In some cases the
injury will be obvious, but in many the injury will be small, perhaps only
a ap with some air bubbling. In many cases the injury will be obscured
by sputum and/or blood and may appear initially like extrinsic compres-
sion.
Injuries may be missed owing to distraction by associated injuries, or partial
Fig. 21. CT scan of patient in Figure 20. Small contained rupture of the distal trachea (arrow) is noted.
338 Curr Probl Surg, March 2004
injuries may manifest since scar tissue leads to stricture formation. Late
recognition of tracheobronchial disruption more than 24 hours after injury
often manifests with obstructive pneumonitis with hemoptysis and/or signs of
pulmonary sepsis. At least 20% of these patients will present with late
stricture formation and corresponding symptoms of wheezing, dyspnea, or
recurrent pneumonia.
285
New-onset asthma or dyspnea in a previously
healthy individual with a history of blunt chest injury should raise the
possibility of the diagnosis, even if there was a bronchoscopy at the initial
hospitalization. Flow-volume loops and pulmonary function tests may
suggest a xed obstruction that would prompt further evaluation, including
bronchoscopy and/or CT. CT bronchography reformatting may be more
sensitive for evaluating airway anatomy than conventional CT and has been
used both for diagnostic purposes and for planning operation complicated by
congenital abnormalities and airway tumors, as well as in 1 case report for the
diagnosis of a tracheal rupture.
96,485,486
Initial Treatment
Emergency treatment consists of inserting the endotracheal tube beyond
the injury to facilitate ventilation and prevent the aspiration of blood.
Diagnosis of the exact injury can follow by using small exible
bronchoscopes or beroptic laryngoscopes inserted around the endotra-
cheal tube. Alternatively, ne-cut CT scans of the upper mediastinum can
delineate the extent of injury. Tube thoracostomy is clearly indicated in
the presence of a hemothorax or pneumothorax. If endotracheal intubation
is not possible or if the anatomy is signicantly distorted, operative entry
into the trachea for placement of a tracheostomy tube may be necessary.
The most critical aspect is to secure the airway. Patients who present in
extremis should have an initial attempt at oral intubation, but there should
be no delay in performing tracheostomy. There is usually a great
temptation to accomplish this over a beroptic bronchoscope, which does
have the advantage of not requiring neck extension (when cervical spine
injuries have are suspected). Furthermore, beroptic bronchoscopy can
help dene the injury and can direct the endotracheal tube across the site
of the injury or into the uninjured main bronchus. However, the urgency
of airway and oxygenation takes precedence over denitive diagnosis of
the injury. Although cricothyroidotomy is usually advocated for emer-
gency airway control after trauma, suspicion of a tracheal injury partic-
ularly if the larynx is involved should prompt tracheotomy. The injury is
usually distal to the cricothyroid membrane and if the injury involves the
larynx, a cricothyroidotomy can convert a partial injury into a complete
separation.
482
Occasionally the soft tissues of the neck are lleted open
Curr Probl Surg, March 2004 339
with the tracheal injury, allowing direct tracheal intubation through the
wound. Except in elective circumstances or if the injury is known to be
small, a single-lumen 8.0-mm or larger endotracheal tube is preferred, but
a double-lumen tube is too large.
44
When an early diagnosis is made, the contralateral bronchus is intubated
and primary repair is performed. Recent authors have reported using a
brin glue plug inserted endoscopically to occlude the injured bronchus
and thereby decrease tidal volume loss.
487,488
Although small lesions may
be treated initially without operation, delayed healing invites stricture
formation, resulting in recurrent atelectasis, infection, and bronchiectasis,
and parenchymal destruction will be the nal result. For an early stricture
either resection or a bronchoplastic procedure may be performed. After
permanent parenchymal damage pulmonary resection should be per-
formed.
Operative Repair
Usually standard ventilation through an oral endotracheal tube or via a
sterile tube placed through the operative eld into the distal airway or
opposite mainstem bronchus is possible. High-frequency jet ventilation
delivered through small catheters advanced across the injury site is also
effective, particularly in the setting of carinal injury.
482
Cardiopulmonary
bypass is rarely required except when coexisting cardiac injuries require
its use.
Patients with associated great vessel injuries are best approached via
sternotomy (Figure 22).
441
In other cases the incision is dictated by the
location of injury. The proximal two thirds of the trachea is best exposed
by a low collar incision that also provides exposure to the cervical
esophagus and neck vessels. Extending this with a T-incision with
manubrial split provides greater exposure of the mid-portion of the
trachea as well as better exposure of the innominate artery and vein.
Injuries of the distal trachea, carina, and right mainstem bronchus are
approached via a right fourth intercostal space posterolateral thoracot-
omy. Injuries of the left mainstem bronchus are exposed via a left
posterolateral thoracotomy, although division of the ligamentum arterio-
sum and mobilization of the aortic arch may be required. A clamshell
incision through the fourth interspace provides excellent exposure to both
hemithoraces and the anterior mediastinum and may be the approach of
choice if associated injuries are present.
Operative repair varies depending on the timing of operation and the
extent of injury. Small injuries, usually ones in which the membrane has
torn away from the cartilage, can be repaired primarily with simple,
340 Curr Probl Surg, March 2004
interrupted, absorbable sutures. Signicant injuries require debridement
and are best treated with end-to-end anastomosis rather than wedge
resection. Dissection should be limited to the area of injury so as not to
interrupt the blood supply. As much as 50% of the trachea can be resected
and have primary repair still possible. Airway release procedures that
assist in reducing tension in cervical reconstruction include simple neck
exion and anterior release (blunt development of the pretracheal plane
as performed during mediastinoscopy); on occasion suprahyoid release
will provide an additional 2 cm of mobilization.
482
Relaxation procedures
for intrathoracic tracheobronchial repairs include dividing the inferior
pulmonary ligament and hilar release. This latter technique is performed
by creating a U-division of the pericardium around the inferior pulmonary
vein and hilum. Distal airway injuries associated with lobar destruction,
either acute from trauma or chronic from infection, can be treated by
simple lobectomy.
489
Muscle aps can be used as an adjunct to allow
reconstruction of the membranous portion of the airway.
156
Severe
tracheal injuries or injuries in unstable patients can be treated by
Fig. 22. Relationships between the tracheobronchial tree and great vessels. (From Wood DE,
Karmy-Jones R. In: Pearson FG, Cooper JD, Deslaurier J, Ginsberg RJ, Hiebert CA, Patterson GA,
Urschel HC Jr, eds. Thoracic Surgery: Tracheobronchial Trauma. 2nd ed. Philadelphia, Pa: Churchill
Livingstone; 2002. Used with permission.).
Curr Probl Surg, March 2004 341
tracheostomy placed through the site of injury. Pneumonectomy is rarely
required for airway rupture unless there is extensive distal injury or
associated severe parenchymal injury.
44
Postoperative care is similar to that for elective resections. Ideally patients
should be extubated at the end of the case. Pulmonary toilet is important.
Patients with laryngeal and/or recurrent nerve injuries and those who required
a cervical release procedure are at risk of aspiration and decreased cough.
Liberal use of bedside bronchoscopy to help clear secretions should be
considered. Bronchoscopy should be performed 7 to 10 days postoperatively
to assure healing without excessive granulation tissue.
Stricture and dehiscence occur in 3% of patients after tracheobronchial
reconstruction, the former manifesting in many instances as new-onset
wheezing.
285
If the stricture is limited dilation and temporary stenting to
allow remodeling can provide a permanent patent and functional airway. In
the rare setting of combined tracheal and esophageal injury, prevention of a
stula after reconstruction requires interposition with viable tissue and even
the use of a sternocleidomastoid ap if no other tissue is available. Once an
anastomotic breakdown has occurred, options depend on the extent of
pneumonia and tissue loss. Ideal options include resection of the tracheal
rings involved, reconstruction of the esophagus (usually gastric pull-up in this
setting), and/or cervical drainage of the esophageal leak with later recon-
struction. Placing stents in 1 or the other organ may be useful to temporize,
but kissing stents (ie, in both trachea and esophagus) should be avoided
since this will simply increase the tendency of the stula to increase in size.
Occasionally patients will have a delayed manifestation of the tracheo-
bronchial injury, which is diagnosed usually by recurrent pneumonia. If
irreversible parenchymal destruction has not yet occurred, airway recon-
struction should be attempted. Endobronchial airway stenting may be
possible as a temporizing or even denitive approach in select settings
when healthy airway past the point of injury can be seen clearly at
bronchoscopy.
477
In many instances preoperative studies (eg, CT with
contrast) will suggest minimal or no perfusion to the affected lung, but
this is most likely due to reex vasoconstriction that resolves with
restoration of ventilation. In the absence of destroyed lung, operation or
stenting should be performed in anticipation that perfusion will be
restored when ventilation is resumed.
Outcome
The overall mortality rate after repair in the acute setting is 10% to 25%
and usually is determined by associated injuries. Early primary repair
results in a good airway in more than 90% of cases.
482
Dehiscence or
342 Curr Probl Surg, March 2004
stricture occurs in up to 6% of cases and can be treated by endoluminal
or tracheal T-tube stenting followed by reconstruction once the inam-
mation has subsided.
482
Esophageal Rupture
Blunt injury to the esophagus is exceedingly rare, and few surgeons
have direct experience with treating these injuries. Beal and colleagues
490
noted that between 1900 and 1988 there were 96 cases reported in the
literature. One autopsy study of MVCs noted only 1 case among 585
fatalities.
491
A 9-year review from Harbor General Hospital in Los
Angeles (1966 to 1975) documented only 1 case of esophageal perfora-
tion after blunt trauma due to a hypertrophic cervical vertebral bone spur
injury during a exion/hyperextension (whiplash) injury. A 1990 article
reviewed 10 cases from a review of the worlds literature and added a
single case of pharyngoesophageal perforation due to blunt neck trau-
ma.
492
Two representative clinical series encompassing 69 cases of
esophageal trauma noted a blunt mechanism in only 5 (7%), predomi-
nantly in the cervical region.
458,493
The most common cause of blunt traumatic esophageal rupture is a
direct blow against a hyperextended neck, with the esophagus being
crushed against the vertebra. The most common cause is MVC, but the
incidence may be increasing with motorcycle injuries.
490,494
Patients with
cervical osteophytes are at increased risk.
495
Rarely intrathoracic or
subdiaphragmatic ruptures are encountered, and in these instances either
acute increases in intraluminal pressure or laceration by rib or vertebral
fragments have been implicated.
496,497
Diagnosis. Because the vast majority of esophageal injuries are in the
cervical region, most if not all patients present with associated laryngeal
or tracheal injuries.
458
In the absence of airway injury, full-thickness
perforation usually manifests initially with subcutaneous emphysema,
pneumomediastinum, pneumothorax, or free air under the diaphragm,
depending on the site of injury. If undetected, progressive uid collection,
infection, and sepsis will develop within 6 to 12 hours. This may be
difcult to appreciate in the multiply injured victim and in fact the
diagnosis is missed initially in nearly 80% of cases.
490
Based on the
experience with nontraumatic perforations, there may be rare cases when
the diagnosis is established when gastric contents are drained after
placing a chest tube or by eroding into adjacent structures.
154,498
The most common symptom of esophageal perforation is extreme pain
with the slow evolution of fever several hours later. Regurgitation of
blood, hoarseness, dysphagia, or respiratory distress also may be present
Curr Probl Surg, March 2004 343
because of concomitant injuries to the trachea. Suspicious radiographic
ndings are air and mediastinal widening. Pleural effusion or hydropneu-
mothorax is frequently noted and should be a call for action. There is
controversy about the relative merits of rigid esophagoscopy, contrast
esophagography, and exible beroptic endoscopy (EGD) in examining
the injured or potentially injured esophagus.
Both endoscopy and esophagography have reported sensitivities that
vary from 50% to 90%.
499,500
Flexible EGD was performed on 31
patients at the Maryland Institute for Emergency Medical Services
Systems for the purpose of diagnosing esophageal trauma between 1991
and 1994.
501
Seven of these patients had a blunt mechanism of injury and
24 had penetrating wounds. Esophageal trauma was found by exible
EGD in 5 patients: true-positive in 4 patients and false-positive in 1. A
true-negative EGD, conrmed by exploration in 5 patients and the clinical
course in 21, was found in 26 patients. The sensitivity of exible EGD
was 100%, the specicity was 96%, and the accuracy was 97%. The
positive predictive value was 80%. The advantages noted by these authors
for exible EGD were the high resolution, magnied image, the porta-
bility of examination, safety, lack of need for general anesthesia in most
cases (61% in this series, although 77% were intubated), and low
morbidity rate (0.2% complication rate, 0.03% perforation rate). Despite
these excellent results, the number of esophageal injuries noted was
small. In addition the authors note that less than one half (4 of 9) of the
patients with esophageal injuries treated at that institution over this time
period underwent exible EGD.
TABLE 30. Diagnosis of penetrating esophageal trauma
Esophageal
injury present
Esophageal
injury absent
Barium swallow Sensitivity, 89%
Positive 8 0
Negative 1 103
None 1 5
Flexible EGD Sensitivity, 37.5%
Positive 3 1
Negative 5 97
None 2 10
Rigid endoscopy Sensitivity, 89%
Positive 8 5
Negative 1 102
None 1 1
EGD, beroptic endoscopy.
Reprinted with permission from Weigelt JA, Thal ER, Snyder WID 3rd, Foy RE, Meier DE, Kilman
WJ. Diagnosis of penetrating cervical esophageal injuries. Am J Surg 1987;154:61922.
499
344 Curr Probl Surg, March 2004
The largest reported series examining the diagnostic modalities in
esophageal trauma is from Weigelt and colleagues
499
at the University of
Texas Southwestern Medical Center in Dallas. All 118 patients in this
report suffered penetrating injuries to the neck. One hundred twelve
patients had barium swallows, 106 had a exible EGD, and 116 had rigid
esophagoscopy. Ninety-three patients had all 3 studies. This report is less
enthusiastic about the sensitivity of exible EGD in diagnosing penetrat-
ing esophageal injures (Table 30 ). In this study the single patient with a
false-negative barium swallow result was diagnosed by endoscopy, and
the patient with a false-negative rigid endoscopy was diagnosed by
barium swallow. Although rigid endoscopy was more sensitive in this
study, it requires general anesthesia, is more technically demanding, and
has a higher complication (perforation) rate than exible EGD.
A comparison of the literature on the accuracy of exible versus rigid
esophagoscopy was conducted by Flowers and colleagues.
501
Their
review of 14 articles published between 1975 and 1996 summarizes the
sensitivity, specicity, and accuracy of these 2 diagnostic modalities in
270 patients. Six articles reported only on patients with penetrating
injuries. Not every article had enough data to calculate sensitivity and the
diagnostic examination used was not always mentioned (Table 31).
Water-soluble contrast esophagography is often suggested to prevent
barium contamination if a perforation has occurred. However, this
technique is less accurate and initially negative water-soluble contrast
radiographs should be followed by barium studies. Nesbitt and Saw-
yers
502
reported that contrast radiographs diagnosed esophageal perfora-
tion in 76 of 78 patients (97.4% sensitivity). Regardless of which
diagnostic method is chosen initially, endoscopy and esophagography
should be considered complementary studies; if there is any question
TABLE 31. Comparison between the ability of exible and rigid esophagoscopy to diagnose
esophageal trauma
501
No. of
patients
Sensitivity,
%
Specicity,
%
Accuracy,
%
Flexible 106 37.5 99 94
13 100 83 85
31 100 96 97
Rigid 116 89 95 94
6 75 NA NA
12 100 NA NA
11 82 NA NA
Reprinted with permission from Flowers JL, Graham SH, Ugarte MA, Sartor WM, Rodriguez A,
Gens DR, et al. Management of blunt and penetrating external esophageal trauma. J Trauma
1996;40:2615; discussion 2656.
501
Curr Probl Surg, March 2004 345
regarding the accuracy of a test, either a different diagnostic modality
should be added or the patient should undergo operative exploration.
Treatment. The majority of experience with esophageal perforation
occurs after iatrogenic or spontaneous rupture. The approach is deter-
mined primarily by the quality of the tissue, the stability of the patient,
and the presence of underlying lesions. Although a diagnosis that is
delayed (12 to 24 or more hours) often results in signicant sepsis, the
timing of the repair is no longer considered the predominant factor in
determining the optimal approach. In the trauma population treatment is
also affected critically by the presence or absence of associated injuries.
That being said, most surgeons believe that esophageal perforations
require immediate debridement, suture closure, and drainage. The mor-
bidity of delay is great. Nesbitt and Sawyers
502
reported that delays of
more than 24 hours in the operative treatment of esophageal perforation
increased the mortality rate from 11% to 26%, and if the delay was greater
than 48 hours the mortality rate was 44%. Therefore, the diagnosis of
esophageal injuries is vital.
Lesions that involve less than 50% of the circumference should be
either repaired primarily with tissue buttressing or closed with tissue
aps.
493
In practical terms longitudinal tears often can be closed primar-
ily, whereas transverse ruptures may require resection and end-to-end
anastomosis. This latter approach rarely occurs in the neck, and it is
critical to ensure that both ends of the esophagus are indeed viable and
that minimal dissection is performed so that the blood supply, which runs
longitudinally, is not compromised. Buttressing the repair is particularly
important to avoid leak and airway stulas. Available aps, depending on
the site of injury, include sternocleidomastoid, intercostal muscle, dia-
phragm, omentum, and gastric fundus.
493,503,504
If the patient is hemo-
dynamically unstable (due to either sepsis or blood loss) and the defect is
not too extensive, drainage can be achieved with a large tracheal T-tube.
A chest tube (usually 28 F) can be inserted over or into the T-limb and 2
more chest tubes placed in close proximity. An early swallow to ensure
that there is no leak around the T-tube is critical. With recovery it is
possible to extract the T-tube via rigid esophagoscopy and then gradually
to downsize the chest drain until the stula seals.
503,504
In general if the
injury is too extensive to repair or drain with a T-tube, we prefer
esophagectomy (with or without immediate reconstruction depending on
stability) over diversion/exclusion procedures. Many of these diversion/
exclusion procedures that have been described, although valid, take as
long or longer to perform than esophagectomy, and reconstruction
afterward can be signicantly more complicated than simple gastric or
346 Curr Probl Surg, March 2004
colon interposition at a delayed date. If a diversion procedure is judged to
be needed, however, we favor proximal diversion with nasogastric tube
drainage (with or without spit stula) in conjunction with gastrostomy
and jejunostomy tubes rather than stapling above and below the injury site
(exclusion/diversion) since this adds operative time and complexity to
later treatment. Of course, in extremely unstable patients, simple wide
drainage with chest tubes and a nasogastric tube may be all that can be
performed and should be considered a damage-control approach.
The operative approach is clearly related to the level of injury. Cervical
injuries, especially those associated with laryngeal or tracheal disruption,
are best explored by a transverse approach, which leaves room for various
degrees of inferior extension. Intrathoracic injuries of the upper two thirds
of the esophagus are approached via right fth to sixth intercostal
posterolateral thoracotomy, whereas intrathoracic injuries below the level
of the inferior pulmonary vein are best exposed via left seventh to eighth
intercostal posterolateral incisions.
The treatment of esophageal leaks that are not recognized early is
largely inuenced by the degree of sepsis. In stable patients primary
repair or resection is still preferred, whereas T-tube drainage remains the
best option in unstable patients. Whichever approach is taken, it is
critical to debride the lung of any inammatory peel that restricts full
parenchymal expansion. One of the best methods of combating a leak is
to have a fully expanded lung that can seal the injury site. Late-appearing
stulas in the neck, with systemic sepsis probably are treated best simply
by wide open cervical drainage. Rarely there may be traumatic esopha-
geal stulas that are adequately decompressed by adjacent chest tubes,
without signs of sepsis or undrained uid collections, that can be treated
expectantly until resolution or until the patients conditions allows
thoracotomy.
The outcome of patients with these injuries is linked to associated
injuries and whether or not a delay in diagnosis has occurred. Unfortu-
nately as many as 10% of patients will die of sepsis related to delayed
diagnosis after blunt perforation, reinforcing the importance of clinical
suspicion.
490
Tracheoesophageal Fistulas
Combined esophageal and tracheal rupture after blunt injury is exceed-
ingly uncommon, but it can occur after crush injury to the extended neck
and airway just at or proximal to the carina.
167,505,506
The incidence has
been estimated to be less than 0.001% of all blunt trauma admissions.
507
Reed and colleagues
507
reviewed 61 reported cases, the majority involv-
Curr Probl Surg, March 2004 347
ing steering wheel or air bag incidents, and again noted that the most
common site was at or just above the carina. It has been hypothesized that
simultaneous compression of the structures between the sternum and
vertebral column results in contusion or injury to the anterior esophagus
and membranous airway. The latter heals but the former becomes necrotic
over time, resulting in delayed manifestation 10 days or more after
injury.
507
The diagnosis can be suggested by new-onset cough or
pneumonia after swallowing or evidence of aspiration of tube feeds.
Operative treatment is associated with a mortality rate of 10% to 15%,
whereas nonoperative treatment carries mortality rates as high as 80%,
but this may reect greater underlying lung disease, later manifestation,
sepsis, etc.
167
In general operative repair through a fourth right intercostal posterolat-
eral thoracotomy with tracheal resection and esophageal repair with
viable tissue (eg, omentum) or gastric pull-up is performed. If there is
severe pneumonia or ARDS that precludes operative repair, gastric
decompression (with a nasogastric and/or G-tube), a feeding J-tube, and
temporization are appropriate. Ventilation may be complicated by air leak
into the esophagus, and if possible the endotracheal tube can be advanced,
but if this is not feasible or there is concern that occluding the stula
requires prolonged pressure by the tube or cuff, then earlier repair should
be undertaken.
Diaphragmatic Injuries
Injury to the diaphragm is relatively uncommon, comprising only 3% of
the total number of injuries sustained from trauma. Blunt injuries usually
occur due to high-speed MVCs.
508
Penetrating injuries such as gunshot
wounds and stab wounds probably occur more frequently, but these have
been cited less often in the literature. The diaphragm alone is rarely
injured. Blunt trauma with diaphragmatic tears is often associated with
head injury, pelvic and long bone fracture, and splenic and hepatic
lacerations, as well as thoracic aortic disruption. Overall the associated
injury rate has been reported as high as 80% to 100%, particularly after
blunt trauma.
509
Anatomic Features. The diaphragm is a musculoaponeurotic apron that
divides the thoracic and abdominal cavities.
508
The internal attachments
of the diaphragm extend from the sternum anteriorly to the rst 3 lumbar
vertebrae posteriorly. The lateral attachments of the diaphragm extend
from ribs 6 through 12 in an anterior to posterior orientation as well. The
blood supply to the diaphragm derives from pericardiophrenic arteries, as
well as multiple branches from both the abdominal aorta and intercostals.
348 Curr Probl Surg, March 2004
The phrenic nerves, which arise from the third, fourth, and fth cervical
roots, are responsible for the diaphragmatic innervation. The diaphragm
normally contains 3 openings for important visceral structures. These
include the inferior vena cava at the eighth thoracic vertebral level, the
esophageal hiatus at the tenth level, and the aortic hiatus at the twelfth.
The esophagus is accompanied by both right and left vagi, and the aorta
is accompanied by the thoracic duct and the azygous vein. The size of the
diaphragmatic defect can be scaled (Table 32).
199
The anatomic location of the diaphragmatic injury appears to be more
common on the left side. One reason may be that after blunt injury the liver
affords some degree of protection to lacerations of the diaphragm. In addition
the radiographic signs of a left-sided injury are much easier to notice and are
more likely to be detected.
508
Bilateral injuries to the diaphragm reportedly
occur in only 2%of all patients sustaining diaphragmatic trauma. Tears of the
central tendon of the diaphragm with herniation of abdominal contents into
the pericardium are uncommon but have been reported.
510
Occasionally,
particularly in patients with a preexisting hiatal hernia, abdominal contents
can be forced through the hiatus.
Physiologic Findings. The diaphragm is the main respiratory muscle in
the body. It moves inferiorly during inhalation and superiorly during
exhalation. Constant diaphragmatic motion preserves normal negative
intrathoracic pressure. A sudden increase in the pressure gradient between
the pleural and peritoneal cavities that occurs with high-speed blunt
trauma will lead to disruptions of the diaphragm.
508
This same pleuro-
peritoneal pressure gradient will also promote migration of intraperitoneal
structures into the pleural space after disruption has occurred. Once the
viscera have been displaced into the pleural space, both cardiovascular
and respiratory functions are compromised. Venous return and ventricular
lling are often impaired, which leads to a reduction of cardiac output.
TABLE 32. Diaphragm organ injury scale
Grade
*
Denition ICD-9 AIS-90
I Contusion 862.0 2
II Laceration 2 cm 862.1 3
III Laceration 210 cm 862.1 3
IV Laceration 10 cm with tissue loss 25 cm 862.1 3
V Laceration with tissue loss 25 cm 862.1 3
*
Advance 1 grade for bilateral injuries. ICD, International Classication of Diseases; AIS,
abbreviated injury score.
Reprinted with permission from Moore EE, Malangoni MA, Cogbill TH, Shackfora SR, Champion
HR, Jurkovich GJ, et al. Organ injury scaling, IV: Thoracic vascular, lung, cardiac, and
diaphragm. J Trauma 1994;36:299300.
199
Curr Probl Surg, March 2004 349
The ventilation of the lung on the involved side is often markedly reduced
as well, which leads to profound hypoxemia. The combination of
diminished venous return and impaired ventilation can lead to a clinical
picture very similar to tension pneumothorax with all of its adverse
circumstances.
509
Diagnosis. Diaphragmatic injuries most commonly are diagnosed
incidentally during the time of laparotomy for associated intra-abdominal
injuries. In those in whom this diagnosis is isolated or in those presenting
in a delayed fashion, the symptoms are nonspecic and varied. Patients
may present with chest or abdominal pain, dyspnea, and orthopnea. A
history of rib fractures, contusions, or wounds of the chest and upper
abdomen should alert one to the possibility of diaphragmatic injury. In the
more acute setting it is not uncommon that intra-abdominal hemorrhage
is being evacuated through a diaphragmatic rent and out a chest tube.
Patients with pericardial defects and those with a transhiatal protrusion of
abdominal contents may present with signs of tamponade.
Initial CXRs are usually normal in 50% of patients and show a pneumo-
thorax or hemothorax in most of the remaining 50% of patients with
diaphragmatic injury. Abnormalities that can be detected on the portable
CXR that suggest diaphragmatic tears include elevation or obscuration of the
diaphragmand visceral herniation. The nding of the nasogastric tube coiling
in the left hemithorax is pathognomonic for diaphragmatic injury but rarely
is seen.
509,511,512
The need for positive- pressure ventilation can obscure a
diaphragm injury by keeping abdominal contents out of the chest. In 1 series,
patients who were not intubated were 25 times more likely to have a
diagnostic or suggestive CXR than were those intubated before arrival in the
ED.
513
As ventilator support is weaned progressive herniation of the
abdominal contents occurs.
143
This underlines the importance of reviewing
CXRs in sequence in injured patients.
CT has become the primary diagnostic modality in the evaluation of
patients sustaining abdominal injury. It is very accurate for the detection of
intra-abdominal uid, solid-organ injury, fractures, intraperitoneal air, pneu-
mothorax, and retroperitoneal injury. Unfortunately it has not been able
consistently to demonstrate diaphragmatic lacerations in several reports in the
literature.
509
Laparoscopy or thoracoscopy is ideal for conrming the
diagnosis but is not particularly useful as a screening tool. If suspicion for
diaphragmatic injury and need for immediate diagnosis are great, these
minimally invasive procedures offer the best diagnostic option.
Operative Exploration and Repair of Acute Injuries. Diagnostic
laparoscopy and rigid or videothoracoscopy have been reported to be
highly successful in the identication of diaphragmatic injury.
4,514-516
350 Curr Probl Surg, March 2004
Occasionally a patient with a small defect can be repaired successfully by
these access techniques as well. However, most acute diaphragmatic
injuries are approached best by a laparotomy, particularly since the
majority will have associated abdominal injuries. A chest tube often will
be required before operation in those patients with either hemothorax or
pneumothorax. The chest tube should be inserted carefully in those
patients with suspected diaphragmatic injury to avoid inadvertent injury
to any potentially herniated abdominal viscera. The smaller injuries
without tissue loss (class I through III) can be repaired with a continuous
or an interrupted 1- 0 or larger braided suture, which may be less prone
than a monolament suture to fracturing with repetitive diaphragmatic
motion.
508
The edges of the diaphragm should be grasped and elevated by
long Allis clamps before suturing. This helps prevent inadvertent suturing
of the underlying lung and facilitates identication of the full extent of the
injury. Class IV injuries usually can be repaired in this manner as well,
although the repair may facilitated by placing some interrupted sutures
rst to realign the edges before repair with a continuous suture.
On occasion the defect along the lateral chest wall can be extensive
and/or there may be combined loss of chest wall integrity. In this setting
resuspending the diaphragm from the ribs at a higher level can allow
closure.
508
If the diaphragm is torn away from its attachments to the chest
wall, it can be resuspended by placing mattress sutures around the ribs.
More central defects especially those involving the crura or pericardial
reection may not be reparable completely. In the setting of abbreviated
thoracotomy or laparotomy diaphragm repair can be delayed, but if there
is a question of abdominal compartment syndrome, it is better to leave the
abdomen open to avoid cardiopulmonary compromise by herniated
viscera, which cannot be overcome by increasing PEEP.
Chronic Diaphragmatic Hernia. Delayed posttraumatic chronic dia-
phragmatic hernias usually are dened as those for which the diagnosis is
made more than 1 month after the injury.
512
The onset of symptoms can
be delayed as much as 40 years. Shah and colleagues
512
reviewed 980
patients with traumatic diaphragmatic injuries reported in the English
literature and noted that the diagnosis was made preoperatively in 43.5%
of cases and at operation or autopsy in 41.3%, and in the remaining 14.6%
the diagnosis was delayed. Maekawa and colleagues
517
noted that during
an 18-year period in Japan, 297 cases of blunt traumatic diaphragmatic
hernia were reported, of which 47 (32 left, 15 right) were delayed. In the
acute setting chronic traumatic diaphragmatic hernia appears to be more
common involving the left side. Mansour
509
noted that of 15 chronic
Curr Probl Surg, March 2004 351
posttraumatic diaphragmatic hernias, 13 involved the left side and 4
occurred after penetrating trauma.
The key in the diagnosis of posttraumatic diaphragmatic hernia is obtaining
a history of trauma. It is important to note that acute diaphragmatic injuries
can be missed at laparotomy and a history of laparotomy therefore does not
exclude the injury.
509
Chronic diaphragmatic hernia can manifest with a
variety of symptoms, ranging from asymptotic radiographic changes to
shock.
518,519
Traumatic chronic diaphragmatic hernia may be asymptotic in
up to 20% of cases, occasionally may masquerade as acute pneumonia,
and/or may manifest with gastrointestinal symptoms of varying severity in up
to 70%, including incarcerated abdominal viscera in 30% to 50% of cases.
511
The broad ranges of patient complaints in the setting of chronic diaphrag-
matic hernia represent the variety of herniated structures found in these
patients. Notably many patients present not to surgeons but rather to internists
or pediatricians.
520
In the series by Hegarty and colleagues
518
72% of
patients presented with a herniated colon, 40% presented with a herniated
stomach, 16% presented with a small bowel herniation, and 8% presented
with spleen herniations.
It is the risk of developing intestinal incarceration or severe cardiopul-
monary compromise that stimulates aggressive evaluation when a chronic
diaphragmatic hernia is suspected. CXRs are diagnostic in 25% to 50% of
cases.
511
Patients who present with primarily intestinal complaints and a
pattern suggesting gas above the diaphragm should be evaluated with a
barium enema and/or upper gastrointestinal series to evaluate the stomach
and small bowel. Patients who present with less specic complaints and
who have soft signs of diaphragmatic herniation or who present with
complex pleural space problems with no gastrointestinal signs or
symptoms should be evaluated by a CT scan with oral contrast.
If the CT scan is suggestive magnetic resonance imaging may provide
better visualization of small defects. Fluoroscopy is useful for determin-
ing an abnormal diaphragmatic excursion that might suggest an injury or
defect, but it has no better sensitivity or specicity than plain CXR.
512
As
in the acute setting, thoracoscopy and occasionally laparoscopy have
proven to be effective minimally invasive methods of conrming the
diagnosis.
520
Thoracoscopy is used in patients who have soft ndings on
the CXR, often after an equivocal CT scan, and can be used to repair
defects in some cases in which adhesions are not severe.
When traumatic chronic diaphragmatic hernia is diagnosed repair is
usually performed via the ipsilateral chest, since usually there are dense
adhesions between the viscera and lung that preclude a safe transabdom-
inal reduction. Reducing a herniated viscus through an abdominal
352 Curr Probl Surg, March 2004
approach risks excessive pulling and tearing of the viscus, potentially
spilling intestinal contents into the pleural space. Rarely a thoracoabdomi-
nal incision is needed, although it is preferable to avoid this because of the
risk of phrenic nerve injury as well as creating another diaphragmatic
defect. Primary repair can be performed in most cases (with or without
pledgets), but in up to 50% articial material will be required.
512
There is
some experimental evidence that suggests that repairing the defect with
prosthetic material may result in better respiratory muscle function, but
this has not been studied clinically, and in general we prefer to avoid the
risk of foreign material if a tension-free repair can be achieved.
521
Conclusion
In conclusion blunt chest injury continues to pose a signicant burden
on trauma systems and requires aggressive diagnostic and therapeutic
approaches. Patients often have multiple injuries that compete for
priority, and in a large proportion these injuries may not be operable.
Ongoing research into biomechanics offers some hope in reducing both
the incidence and severity of injuries. Other clinical research efforts are
introducing newer diagnostic modes to our armamentarium, as well as
developing other therapeutic options, such as nonoperative or endovas-
cular approaches that provide greater exibility in the treatment of
patients with these complex injuries.
41,392
REFERENCES
1. Boyd AD, Glassman LR. Trauma to the lung. Chest Surg Clin North Am
1997;7:263-84.
2. Calhoon JH, Trinkle JK. Pathophysiology of chest trauma. Chest Surg Clin North
Am 1997;7:199-211.
3. Peterson RJ, Tepas JJ 3rd, Edwards FH, Kissoon N, Pieper P, Ceithaml EL.
Pediatric and adult thoracic trauma: age-related impact on presentation and
outcome. Ann Thorac Surg 1994;58:14-8.
4. Karmy-Jones R, Jurkovich GJ, Nathens AB, Shatz DV, Brundage S, Wall MJ Jr, et
al. Timing of urgent thoracotomy for hemorrhage after trauma: a multicenter study.
Arch Surg 2001;136:513-8.
5. Crankson SJ, Fischer JD, Al-Rabeeah AA, Al-Jaddan SA. Pediatric thoracic
trauma. Saudi Med J 2001;22:117-20.
6. Garcia VF, Gotschall CS, Eichelberger MR, Bowman LM. Rib fractures in
children: a marker of severe trauma. J Trauma 1990;30:695-700.
7. Viano DC, Lau IV, Andrzejak DV, Asbury C. Biomechanics of injury in lateral
impacts. Accid Anal Prev 1989;21:535-51.
8. Viano DC, Lau IV, Asbury C, King AI, Begeman P. Biomechanics of the human
chest, abdomen, and pelvis in lateral impact. Accid Anal Prev 1989;21:553-74.
9. Shorr RM, Crittenden M, Indeck M, Hartunian SL, Rodriguez A. Blunt thoracic
trauma: analysis of 515 patients. Ann Surg 1987;206:200-5.
Curr Probl Surg, March 2004 353
10. National Center for Statistics and Analysis. National Highway Trafc Safety
Administration. For Ref 10, please provide URL and date site was last accessed, as
per AMA Style.
11. McGwin G Jr, Reiff DA, Moran SG, Rue LW 3rd. Incidence and characteristics of
motor vehicle collision-related blunt thoracic aortic injury according to age.
J Trauma 2002;52:859-65 ; discussion 865-6.
12. Scally JT, McCullough CA, Brown LJ, Eppinger R. Development of the Crash
Injury Research and Engineering Network. Int J Trauma Nurs 1999;5:136-8.
13. Crash Injury Research and Engineering Network (CIREN): an update. Ann Emerg
Med 2001;38:181-2.
14. Ossiander EM, Cummings P. Freeway speed limits and trafc fatalities in
Washington state. Accid Anal Prev 2002;34:13-8.
15. Newman RJ. Chest wall injuries and the seat belt syndrome. Injury 1984;16:110-3.
16. Newman RJ, Jones IS. A prospective study of 413 consecutive car occupants with
chest injuries. J Trauma 1984;24:129-35.
17. Arajarvi E, Santavirta S. Chest injuries sustained in severe trafc accidents by
seatbelt wearers. J Trauma 1989;29:37-41.
18. Arajarvi E, Santavirta S, Tolonen J. Aortic ruptures in seat belt wearers. J Thorac
Cardiovasc Surg 1989;98:355-61.
19. Valent F, McGwin G Jr, Hardin W, Johnston C, Rue LW 3rd. Restraint use and
injury patterns among children involved in motor vehicle collisions. J Trauma
2002;52:745-51.
20. Sharma OP, Mousset XR. Review of tricuspid valve injury after airbag deployment:
presentation of a case and discussion of mechanism of injury. J Trauma 2000;48:
152-6.
21. Kraus JF, Peek-Asa C, Cryer HG. Incidence, severity, and patterns of intrathoracic
and intra-abdominal injuries in motorcycle crashes. J Trauma 2002;52:548-53.
22. Bulger EM, Copass MK, Maier RV, Larsen J, Knowles J, Jurkovich GJ. An
analysis of advanced prehospital airway management. J Emerg Med 2002;23:
183-9.
23. Karch SB, Lewis T, Young S, Hales D, Ho CH. Field intubation of trauma patients:
complications, indications, and outcomes. Am J Emerg Med 1996;14:617-9.
24. Butler FK Jr, Hagmann J, Butler EG. Tactical combat casualty care in special
operations. Mil Med 1996;161(suppl):3-16.
25. Mines D, Abbuhl S. Needle thoracostomy fails to detect a fatal tension pneumo-
thorax. Ann Emerg Med 1993;22:863-6.
26. Baird RE, McAninch GW, Ungersma J. High altitude penetrating chest trauma: a
case report. Mil Med 1989;154:337-40.
27. Butler KL, Best IM, Weaver WL, Bumpers HL. Pulmonary artery injury and
cardiac tamponade after needle decompression of a suspected tension pneumotho-
rax. J Trauma 2003;54:610-1.
28. McSwain NE Jr, Frame SB, editors. PHTLS: Prehospital Trauma Life Support, 5th
ed. St. Louis: Mo: Mosby; 2003.
29. Advanced Trauma Life Support for Doctors. 6th ed. Chicago, Ill: American College
of Surgeons; 1997.
30. Cuschieri J. Tube thoracostomy. In: Karmy-Jones R, Nathens A, Stern E, editors.
Thoracic Trauma and Critical Care. Boston, Mass: Kluwer Academic Publishers;
2002. 45-7.
354 Curr Probl Surg, March 2004
31. Bailey RC. Complications of tube thoracostomy in trauma. J Accid Emerg Med
2000;17:111-4.
32. Romanoff H. Prevention of infection in war chest injuries. Ann Surg 1975;182:
144-9.
33. Luchette FA, Barrie PS, Oswanski MF, Spain DA, Mullins CD, Palumbo F, et al.
Practice management guidelines for prophylactic antibiotic use in tube thoracos-
tomy for traumatic hemopneumothorax: the EAST practice management guidelines
work group. Eastern Association for Trauma. J Trauma 2000;48:753-7.
34. Gonzalez RP, Holevar MR. Role of prophylactic antibiotics for tube thoracostomy
in chest trauma. Am Surg 1998;64:617-20 ; discussion 620-1.
35. Stern E. Imaging of blunt and penetrating trauma to the pulmonary parenchyma. In:
Karmy-Jones R, Stern E, Nathens A, editors. Thoracic Trauma and Critical Care.
Boston, Mass: Kluwer Academic Publishers; 2002. 159-64.
36. Carrillo EH, Heniford BT, Senler SO, Dykes JR, Maniscalco SP, Richardson JD.
Embolization therapy as an alternative to thoracotomy in vascular injuries of the
chest wall. Am Surg 1998;64:1142-8.
37. Thourani VH, Pettitt BJ, Schmidt JA, Cooper WA, Rozycki GS. Validation of
surgeon-performed emergency abdominal ultrasonography in pediatric trauma
patients. J Pediatr Surg 1998;33:322-8.
38. Dulchavsky SA, Schwarz KL, Kirkpatrick AW, Billica RD, Williams DR, Diebel
LN, et al. Prospective evaluation of thoracic ultrasound in the detection of
pneumothorax. J Trauma 2001;50:201-5.
39. Rhee PM, Acosta J, Bridgeman A, Wang D, Jordan M, Rich N. Survival after
emergency department thoracotomy: review of published data from the past 25
years. J Am Coll Surg 2000;190:288-98.
40. Durham LA 3rd, Richardson RJ, Wall MJ Jr, Pepe PE, Mattox KL. Emergency
center thoracotomy: impact of prehospital resuscitation. J Trauma 1992;32:775-9.
41. Lorenz HP, Steinmetz B, Lieberman J, Schecoter WP, Macho JR. Emergency
thoracotomy: survival correlates with physiologic status. J Trauma 1992;32:780-5
; discussion 785-8.
42. Perchinsky MJ, Long WB, Hill JG. Blunt cardiac rupture: the Emanuel Trauma
Center experience. Arch Surg 1995;130:852-6 ; discussion 856-7.
43. Cuschieri J, Kralovich KA, Patton JH, Horst HM, Obeid FN, Karmy-Jones R.
Anterior mediastinal abscess after closed sternal fracture. J Trauma 1999;47:551-4.
44. Wagner JW, Obeid FN, Karmy-Jones RC, Casey GD, Sorensen VJ, Horst HM.
Trauma pneumonectomy revisited: the role of simultaneously stapled pneumonec-
tomy. J Trauma 1996;40:590-4.
45. McNamara JJ, Messersmith JK, Dunn RA, Molot MD, Stremple JF. Thoracic
injuries in combat casualties in Vietnam. Ann Thorac Surg 1970;10:389-401.
46. Carter Y, Meissner M, Bulger E, Demerir S, Brundage S, Jurkovich G, et al.
Anatomical considerations in the surgical management of blunt thoracic aortic
injury. J Vasc Surg. 2001;34:628-33.
47. DiBardino DJ, Brundage SI. Abbreviated thoracotomy: the evolving role of damage
control in thoracic trauma. In: Karmy-Jones R, Nathens A, Stern E, editors.
Thoracic Trauma and Critical Care. Boston, Mass: Kluwer Academic Publishers;
2002. 69-76.
48. Shapiro MB, Jenkins DH, Schwab CW, Rotondo MF. Damage control: collective
review. J Trauma 2000;49:969-78.
Curr Probl Surg, March 2004 355
49. Fabian TC, Richardson JD, Croce MA, Smith JS, Rodman G, Kearney PA, et al.
Prospective study of blunt aortic injury: multicenter trial of the American
Association for the Surgery of Trauma. J Trauma 1997;42:374-80 ; discussion
380-3.
50. Mashiko K, Matsumoto H, Mochizuki T, Takuhiro K, Hara Y, Katada S. Damage
control for thoracic injuries. Nippon Geka Gakkai Zasshi 2002;103:511-6.
51. Vargo DJ, Battistella FD. Abbreviated thoracotomy and temporary chest closure:
an application of damage control after thoracic trauma. Arch Surg 2001;136:21-4.
52. Nirula R, Nathens A. Timing of long bone fracture xation in patients with blunt
thoracic trauma. In: Karmy-Jones R, Nathens A, Stern E, editors. Thoracic Trauma
and Critical Care. Boston, Mass: Kluwer Academic Publishers; 2002. 523-7.
53. Behrman SW, Fabian TC, Kudsk KA, Taylor JC. Improved outcome with femur
fractures: early vs. delayed xation. J Trauma 1990;30:792-7; discussion 797-8.
54. Willis BH, Carden DL, Sadasivan KK. Effect of femoral fracture and intramedul-
lary xation on lung capillary leak. J Trauma 1999;46:687-92.
55. Pape HC, Dwenger A, Grotz M, Kaever V, Negatsch R, Kleemann W, et al. Does
the reamer type inuence the degree of lung dysfunction after femoral nailing
following severe trauma? an animal study. J Orthop Trauma 1994;8:300-9.
56. Pell AC, Christie J, Keating JF, Sutherland GR. The detection of fat embolism by
transesophageal echocardiography during reamed intramedullary nailing: a study of
24 patients with femoral and tibial fractures. J Bone Joint Surg Br 1993;75:921-5.
57. Pape HC, AufmKolk M, Paffrath T, Regel G, Sturm JA, Tscherne H. Primary
intramedullary femur xation in multiple trauma patients with associated lung
contusion: a cause of posttraumatic ARDS? J Trauma 1993;34:540-7 ; discussion
547-8.
58. Charash WE, Fabian TC, Croce MA. Delayed surgical xation of femur fractures
is a risk factor for pulmonary failure independent of thoracic trauma. J Trauma
1994;37:667-72.
59. Brundage SI, McGhan R, Jurkovich GJ, Mack CD, Maier RV. Timing of femur
fracture xation: effect on outcome in patients with thoracic and head injuries.
J Trauma 2002;52:299-307.
60. Weresh MJ, Stover MD, Bosse MJ, Jeray K, Kellam JF, Sims SH, et al. Pulmonary
gas exchange during intramedullary xation of femoral shaft fractures. J Trauma
1999;46:863-8.
61. Mitchell ME, Muakkassa FF, Poole GV, Rhodes RS, Griswold JA. Surgical
approach of choice for penetrating cardiac wounds. J Trauma 1993;34:17-20.
62. Dowd MD, Krug S. Pediatric blunt cardiac injury: epidemiology, clinical features,
and diagnosis. Pediatric Emergency Medicine Collaborative Research Committee:
Working Group on Blunt Cardiac Injury. J Trauma 1996;40:61-7.
63. Abouljoud MS, Obeid FN, Horst HM, Sorensen VJ, Fath JJ, Chung SK. Arterial
injuries of the thoracic outlet: a ten-year experience. Am Surg 1993;59:590-5.
64. Karmy-Jones R, Vallieres E, Kralovich K, Gasparri M, Sorensen VJ, Horst HM, et
al. A comparison of rigid-v-video thoracoscopy in the management of chest trauma.
Injury 1998;29:655-9.
65. Karmy-Jones R, Jurkovich GJ, Shatz DV, Brundage S, Wall MJ Jr, Engelhardt S,
et al. Management of traumatic lung injury: a Western Trauma Association
multicenter review. J Trauma 2001;51:1049-53.
66. Meyer DM, Jessen ME, Wait MA, Estrera AS. Early evacuation of traumatic
356 Curr Probl Surg, March 2004
retained hemothoraces using thoracoscopy: a prospective, randomized trial. Ann
Thorac Surg 1997;64:1396-400 ; discussion 1400-1.
67. Schermer CR, Matteson BD, Demarest GB 3rd, Albrecht RM, Davis VH. A
prospective evaluation of video-assisted thoracic surgery for persistent air leak due
to trauma. Am J Surg 1999;177:480-4.
68. Park SH, Song HH, Park JM, Song KS, Sohn HS, Lee HJ, et al. Impact of a primary
readers opinion on the detection of rib fractures. Invest Radiol 1992;27:785-9.
69. Mayberry JC, Trunkey DD. The fractured rib in chest wall trauma. Chest Surg Clin
North Am 1997;7:239-61.
70. Lee RB, Bass SM, Morris JA Jr, MacKenzie EJ. Three or more rib fractures as an
indicator for transfer to a level I trauma center: a population-based study. J Trauma
1990;30:689-94.
71. Healey MA, Brown R, Fleiszer D. Blunt cardiac injury: is this diagnosis necessary?
J Trauma 1990;30:137-46.
72. Reynolds MA, Richardson JD. Chest wall and diaphragmatic injuries. In: Maull KI,
Rodriguez A, Wiles CE III, editors. Complications in Trauma and Critical Care.
Philadelphia, Pa: WB Saunders; 1996. 313-24.
73. Ziegler DW, Agarwal NN. The morbidity and mortality of rib fractures. J Trauma
1994;37:975-9.
74. Lee J, Harris JH Jr, Duke JH Jr, Williams JS. Noncorrelation between thoracic
skeletal injuries and acute traumatic aortic tear. J Trauma 1997;43:400-4.
75. Poole GV. Fracture of the upper ribs and injury to the great vessels. Surg Gynecol
Obstet 1989;169:275-82.
76. Bergeron E, Lavoie A, Clas D, Moore L, Ratte S, Tetreault S, et al. Elderly trauma
patients with rib fractures are at greater risk of death and pneumonia. J Trauma
2003;54:478-85.
77. Bulger EM, Arneson MA, Mock CN, Jurkovich GJ. Rib fractures in the elderly.
J Trauma 2000;48:1040-6 ; discussion 1046-7.
78. Shorr RM, Rodriguez A, Indeck MC, Crittenden MD, Hartunian S, Cowley RA.
Blunt chest trauma in the elderly. J Trauma 1989;29:234-7.
79. Clark GC, Schecter WP, Trunkey DD. Variables affecting outcome in blunt chest
trauma: ail chest vs. pulmonary contusion. J Trauma 1988;28:298-304.
80. Freedland M, Wilson RF, Bender JS, Levison MA. The management of ail chest
injury: factors affecting outcome. J Trauma 1990;30:1460-8.
81. Albaugh G, Kann B, Puc MM, Vemulapalli P, Marra S, Ross S. Age-adjusted
outcomes in traumatic ail chest injuries in the elderly. Am Surg 2000;66:978-81.
82. Rodriguez JL, Gibbons KJ, Bitzer LG, Dechert RE, Steinberg SM, Flint LM.
Pneumonia: incidence, risk factors, and outcome in injured patients. J Trauma
1991;31:907-12 ; discussion 912-4.
83. Easter A. Management of patients with multiple rib fractures. Am J Crit Care
2001;10:320-7 ; quiz 328-9.
84. Karmakar MK, Ho AM. Acute pain management of patients with multiple fractured
ribs. J Trauma 2003;54:615-25.
85. Mackersie RC, Shackford SR, Hoyt DB, Karagianes TG. Continuous epidural
fentanyl analgesia: ventilatory function improvement with routine use in treatment
of blunt chest injury. J Trauma 1987;27:1207-12.
86. Mackersie RC, Karagianes TG, Hoyt DB, Davis JW. Prospective evaluation of
epidural and intravenous administration of fentanyl for pain control and restoration
Curr Probl Surg, March 2004 357
of ventilatory function following multiple rib fractures. J Trauma 1991;31:443-9 ;
discussion 449-51.
87. Wisner DH. A stepwise logistic regression analysis of factors affecting morbidity
and mortality after thoracic trauma: effect of epidural analgesia. J Trauma
1990;30:799-804 ; discussion 804-5.
88. Ullman DA, Fortune JB, Greenhouse BB, Wimpy RE, Kennedy TM. The treatment
of patients with multiple rib fractures using continuous thoracic epidural narcotic
infusion. Reg Anesth 1989;14:43-7.
89. Moon MR, Luchette FA, Gibson SW, Crews J, Sudarshan G, Hurst JM, et al.
Prospective, randomized comparison of epidural versus parenteral opioid analgesia
in thoracic trauma. Ann Surg 1999;229:684-91 ; discussion 691-2.
90. Shackford SR, Smith DE, Zarins CK, Rice CL, Virgilio RW. The management of
ail chest: a comparison of ventilatory and nonventilatory treatment. Am J Surg
1976;132:759-62.
91. Voggenreiter G, Neudeck F, Aufmkolk M, Obertacke U, Schmit-Neuerburg KP.
Operative chest wall stabilization in ail chest: outcomes of patients with or
without pulmonary contusion. J Am Coll Surg 1998;187:130-8.
92. Tanaka H, Yukioka T, Yamaguti Y, Shimizu S, Goto H, Matsuda H, et al. Surgical
stabilization of internal pneumatic stabilization? a prospective randomized study of
management of severe ail chest patients. J Trauma 2002;52:727-32 ; discussion 732.
93. Ahmed Z, Mohyuddin Z. Management of ail chest injury: internal xation versus
endotracheal intubation and ventilation. J Thorac Cardiovasc Surg 1995;110:1676-80.
94. Beal SL, Oreskovich MR. Long-term disability associated with ail chest injury.
Am J Surg 1985;150:324-6.
95. Landercasper J, Cogbill TH. Long-term follow-up after traumatic asphyxia.
J Trauma 1985;25:838-41.
96. Nakamori Y, Hayakata T, Fujimi S, Satou K, Tanaka C, Ogura H, et al. Tracheal
rupture diagnosed with virtual bronchoscopy and managed nonoperatively: a case
report. J Trauma 2002;53:369-71.
97. Slater MS, Mayberry JC, Trunkey DD. Operative stabilization of a ail chest six
years after injury. Ann Thorac Surg 2001;72:600-1.
98. Cacchione RN, Richardson JD, Seligson D. Painful nonunion of multiple rib
fractures managed by operative stabilization. J Trauma 2000;48:319-21.
99. Buckman R, Trooskin SZ, Flancbaum L, Chandler J. The signicance of stable
patients with sternal fractures. Surg Gynecol Obstet 1987;164:261-5.
100. Wojcik JB, Morgan AS. Sternal fractures: the natural history. Ann Emerg Med
1988;17:912-4.
101. Rambaud G, Desachy A, Francois B, Allot V, Cornu E, Vignon P. Extrapericardial
cardiac tamponade caused by traumatic retrosternal hematoma. J Cardiovasc Surg
(Torino) 2001;42:621-4.
102. Rashid MA, Ortenwall P, Wikstrom T. Cardiovascular injuries associated with
sternal fractures. Eur J Surg 2001;167:243-8.
103. White C, Isik F. Reconstruction of complex chest wall defects. In: Karmy-Jones R,
Nathens A, Stern E, editors. Thoracic Trauma and Critical Care. Boston, Mass:
Kluwer Academic Publishers; 2002. 247-51.
104. Losanoff JE, Metzler MH, Richman BW, Cotton BA, Jones JW. Necrotizing chest
wall infection after blunt trauma: case report and review of the literature. J Trauma
2002;53:787-9.
358 Curr Probl Surg, March 2004
105. Kao L. Traumatic lung hernia. In: Karmy-Jones R, Nathens A, Stern E, editors.
Thoracic Trauma and Critical Care. Boston, Mass: Kluwer Academic Publishers;
2002. 257-59.
106. Di Bartolomeo S, Sanson G, Nardi G, Scian F, Michelutto V, Lattuada L. A
population-based study on pneumothorax in severely traumatized patients.
J Trauma 2001;51:677-82.
107. Rommens PM, Carlier H, Delooz HH. Early mortality following multiple trauma:
a retrospective study. Acta Chir Belg 1988;88:375-9.
108. Council IR. Prehospital trauma care: approcio e trattamento preospedaliero al
traumatizzo. Italian Resusitation Council; Rome, Italy, 1988.
109. Schmidt U, Stalp M, Gerich T, Blauth M, Maull KI, Tscherne H. Chest tube
decompression of blunt chest injuries by physicians in the eld: effectiveness and
complications. J Trauma 1998;44:98-101.
110. Deakin CD, Davies G, Wilson A. Simple thoracostomy avoids chest drain insertion
in prehospital trauma. J Trauma 1995;39:373-4.
111. Collins JA, Samra GS. Failure of chest x-rays to diagnose pneumothoraces after
blunt trauma. Anaesthesia 1998;53:74-8.
112. Hill SL, Edmisten T, Holtzman G, Wright A. The occult pneumothorax: an
increasing diagnostic entity in trauma. Am Surg 1999;65:254-8.
113. Neff MA, Monk JS Jr, Peters K, Nikhilesh A. Detection of occult pneumothoraces
on abdominal computed tomographic scans in trauma patients. J Trauma 2000;49:
281-5.
114. Enderson BL, Abdalla R, Frame SB, Casey MT, Gould H, Maull KI. Tube
thoracostomy for occult pneumothorax: a prospective randomized study of its use.
J Trauma 1993;35:726-9 ; discussion 729-30.
115. Helling TS, Gyles NR 3rd, Eisenstein CL, Soracco CA. Complications following
blunt and penetrating injuries in 216 victims of chest trauma requiring tube
thoracostomy. J Trauma 1989;29:1367-70.
116. Woodring JH, Baker MD, Stark P. Pneumothorax ex vacuo. Chest 1996;110:
1102-5.
117. Florman S, Young B, Allmon JC, Diethelm L, Raafat A. Traumatic pneumothorax
ex vacuo. J Trauma 2001;50:147-8.
118. Capizzi PJ, Martin M, Bannon MP. Tension pneumopericardium following blunt
injury. J Trauma 1995;39:775-80.
119. Hudgens S, McGraw J, Craun M. Two cases of tension pneumopericardium
following blunt chest injury. J Trauma 1991;31:1408-10.
120. Paillard A. Lecons orales clinique chirurgicale de M. Dupuytren. Paris, France.
Germer Baillere Libraire 1839;6:308-18.
121. Johnson JA, Cogbill TH, Winga ER. Determinants of outcome after pulmonary
contusion. J Trauma 1986;26:695-7.
122. Cohn SM. Pulmonary contusion: review of the clinical entity. J Trauma 1997;42:
973-9.
123. Tranbaugh RF, Elings VB, Christensen J, Lewis FR. Determinants of pulmonary
interstitial uid accumulation after trauma. J Trauma 1982;22:820-6.
124. Guerrero-Lopez F, Vazquez-Mata G, Alcazar-Romero PP, Fernandez-Mondejar E,
Aguayo-Hoyos E, Linde-Valverde CM. Evaluation of the utility of computed
tomography in the initial assessment of the critical care patient with chest trauma.
Crit Care Med 2000;28:1370-5.
Curr Probl Surg, March 2004 359
125. Sattler S, Maier RV. Pulmonary contusion. In: Karmy-Jones R, Nathens A, Stern
E, editors. Thoracic Trauma and Critical Care. Boston, Mass: Kluwer Academic
Publishers; 2002. 235-45.
126. Kelly ME, Miller PR, Greenhaw JJ, Fabian TC, Proctor KG. Novel resuscitation
strategy for pulmonary contusion after severe chest trauma. J Trauma 2003;55:94-105.
127. Vidhani K, Kause J, Parr M. Should we follow ATLS guidelines for the
management of traumatic pulmonary contusion: the role of non-invasive ventilatory
support. Resuscitation 2002;52:265-8.
128. Miller PR, Croce MA, Bee TK, Qaisi WG, Smith CP, Collins GL, et al. ARDS after
pulmonary contusion: accurate measurement of contusion volume identies high-
risk patients. J Trauma 2001;51:223-8 ; discussion 229-30.
129. Bulger EM. Adult respiratory distress syndrome. In: Karmy-Jones R, Nathens A,
Stern E, editors. Thoracic Trauma and Critical Care. Boston, Mass: Kluwer
Academic Publishers; 2002. 439-51.
130. Nelson LD. Ventilatory support of the trauma patient with pulmonary contusion.
Respir Care Clin North Am 1996;2:425-47.
131. Hickling KG. Low volume ventilation with permissive hypercapnia in the adult
respiratory distress syndrome. Clin Intensive Care 1992;3:67-78.
132. Ventilation with lower tidal volumes as compared with traditional tidal volumes for
acute lung injury and the acute respiratory distress syndrome. The Acute Respira-
tory Distress Syndrome Network. N Engl J Med 2000;342:1301-8.
133. Eisner MD, Thompson T, Hudson LD, Luce JM, Hayden D, Schoenfeld D, et al.
Efcacy of low tidal volume ventilation in patients with different clinical risk
factors for acute lung injury and the acute respiratory distress syndrome. Am J
Respir Crit Care Med 2001;164:231-6.
134. Riou B, Zaier K, Kalfon P, Puybasset L, Coriat P, Rouby JJ. High-frequency jet
ventilation in life-threatening bilateral pulmonary contusion. Anesthesiology 2001;
94:927-30.
135. Parikshak M, Gurkin MA, Horst HM. High frequency ventilation. In: Karmy-Jones
R, Nathens A, Stern E, editors. Thoracic Trauma and Critical Care. Boston, Mass:
Kluwer Academic Publishers; 2002. 453-62.
136. Gurkin MA, Parikshak M, Horst HM. Pressure controlled, inverse ratio mechanical
ventilation. In: Karmy-Joes R, Nathens A, Stern E, editors. Thoracic Trauma and
Critical Care. Boston, Mass: Kluwer Academic Publishers; 2002. 463-66.
137. Sharma S, Mullins RJ, Trunkey DD. Ventilatory management of pulmonary
contusion patients. Am J Surg 1996;171:529-32.
138. Stocker R, Neff T, Stein S, Ecknauer E, Trentz O, Russi E. Prone postioning and
low-volume pressure-limited ventilation improve survival in patients with severe
ARDS. Chest 1997;111:1008-17.
139. Sinclair SE, Albert RK. Thoracic trauma and critical care. In: Karmy-Jones R,
Nathens A, Stern E, editors. Thoracic Trauma and Critical Care. Boston, Mass:
Kluwer Academic Publishers; 2002. 467-78.
140. Neff MA. The role of nitric oxide in sepsis and respiratory failure. In: Karmy-Jones
R, Nathens A, Stern E, editors. Thoracic Trauma and Critical Care. Boston, Mass:
Kluwer Medical Publishers; 2002. 497-501.
141. Dellinger RP, Zimmerman JL, Taylor RW, Straube RC, Hauser DL, Criner GJ, et
al. Effects of inhaled nitric oxide in patients with acute respiratory distress
360 Curr Probl Surg, March 2004
syndrome: results of a randomized phase II trial. Inhaled Nitric Oxide in ARDS
Study Group. Crit Care Med 1998;26:15-23.
142. Johannigman JA, Campbell RS, Davis K Jr, Hurst JM. Combined differential lung
ventilation and inhaled nitric oxide therapy in the management of unilateral
pulmonary contusion. J Trauma 1997;42:108-11.
143. Alpard SK, Zwischenberger JB. ECMO in the surgical patient. In: Karmy-Jones R,
Nathens A, Stern E, editors. Thoracic Trauma and Critical Care. Boston, Mass:
Kluwer Academic Publishers; 2002. 479-90.
144. Bartlett RH, Gazzaniga AB, Toomasian J, Coran AG, Roloff D, Rucker R, et al.
Extracorporeal membrane oxygenation (ECMO) in neonatal respiratory failure: 100
cases. Ann Surg 1986;204:236-45.
145. Zwischenberger JB, Wang D, Lick SD, Deyo DJ, Alpard SK, Chambers SD. The
paracorporeal articial lung improves 5-day outcomes from lethal smoke/burn-
induced acute respiratory distress syndrome in sheep. Ann Thorac Surg 2002;74:
1011-6 ; discussion 1017-8.
146. Cinnella G, Dambrosio M, Brienza N, Giuliani R, Bruno F, Fiore T, et al.
Independent lung ventilation in patients with unilateral pulmonary contusion:
monitoring with compliance and EtCO
2
. Intensive Care Med 2001;27:1860-7.
147. Miller RS, Nelson LD, Rutherford EJ, Morris JA Jr. Synchronized independent
lung ventilation in the management of a unilateral pulmonary contusion with
massive hemoptysis. J Tenn Med Assoc 1992;85:374-5.
148. Carrillo EH, Block EF, Zeppa R, Sosa JL. Urgent lobectomy and pneumonectomy.
Eur J Emerg Med 1994;1:126-30.
149. Asensio JA, Demetriades D, Berne JD, Velmahos G, Cornwell EE 3rd, Murray J,
et al. Stapled pulmonary tractotomy: a rapid way to control hemorrhage in
penetrating pulmonary injuries. J Am Coll Surg 1997;185:486-7.
150. Robison PD, Harman PK, Trinkle JK, Grover FL. Management of penetrating lung
injuries in civilian practice. J Thorac Cardiovasc Surg 1988;95:184-90.
151. Stewart KC, Urschel JD, Nakai SS, Gelfand ET, Hamilton SM. Pulmonary
resection for lung trauma. Ann Thorac Surg 1997;63:1587-8.
152. Stanic V. The advantages of limited resection vs. suture in the primary management
of penetrating lung war wounds. Vojnosanit Pregl 1998;55:583-90.
153. Cothren C, Moore EE, Bif WL, Franciose RJ, Offner PJ, Burch JM. Lung-sparing
techniques are associated with improved outcome compared with anatomic resec-
tion for severe lung injuries. J Trauma 2002;53:483-7.
154. Asaoka M, Usami N, Sasaki M, Masumoto H, Kajiyama M, Seki A. Combined
rupture of trachea and esophagus following blunt trauma: a case report. Jpn
J Thorac Cardiovasc Surg 1998;46:215-9.
155. Gasparri M, Karmy-Jones R, Kralovich KA, Patton JH Jr, Arbabi S. Pulmonary
tractotomy versus lung resection: viable options in penetrating lung injury.
J Trauma 2001;51:1092-5; discussion 1096-7.
156. Jones WS, Mavroudis C, Richardson JD, Gray LA Jr, Howe WR. Management of
tracheobronchial disruption resulting from blunt trauma. Surgery 1984;95:319-23.
157. Eddy AC, Luna GK, Copass M. Empyema thoracis in patients undergoing emergent
closed tube thoracostomy for thoracic trauma. Am J Surg 1989;157:494-7.
158. Coselli JS, Mattox KL, Beall AC Jr. Reevaluation of early evacuation of clotted
hemothorax. Am J Surg 1984;148:786-90.
159. Rosenblatt M, Lemer J, Best LA, Peleg H. Thoracic wounds in Israeli battle
Curr Probl Surg, March 2004 361
casualties during the 1982 evacuation of wounded from Lebanon. J Trauma
1985;25:350-4.
160. Velmahos GC, Demetriades D, Chan L, Tatevossian R, Cornwell EE 3rd, Yassa N,
et al. Predicting the need for thoracoscopic evacuation of residual traumatic
hemothorax: chest radiograph is insufcient. J Trauma 1999;46:65-70.
161. Brundage SI, Harruff R, Jurkovich GJ, Maier RV. The epidemiology of thoracic
aortic injuries in pedestrians. J Trauma 1998;45:1010-4.
162. Kempainan R, Pierson D. Evaluation and management of persistent air leaks in
trauma patients. In: Karmy-Jones R, Stern E, Nathens A, editors. Thoracic Trauma
and Critical Care. Boston, Mass: Kluwer Academic Publishers; 2003. 503-11.
163. Cerfolio RJ. The incidence, etiology, and prevention of postresectional broncho-
pleural stula. Semin Thorac Cardiovasc Surg 2001;13:3-7.
164. Pierson DJ, Horton CA, Bates PW. Persistent bronchopleural air leak during
mechanical ventilation: a review of 39 cases. Chest 1986;90:321-3.
165. Regel G, Sturm JA, Neumann C, Schueler S, Tscherne H. Occlusion of broncho-
pleural stula after lung injury: a new treatment by bronchoscopy. J Trauma
1989;29:223-6.
166. McManigle JE, Fletcher GL, Tenholder MF. Bronchoscopy in the management of
bronchopleural stula. Chest 1990;97:1235-8.
167. Sebastian MW, Wolfe WG. Traumatic thoracic stulas. Chest Surg Clin North Am
1997;7:385-400.
168. Aguilar MM, Battistella FD, Owings JT, Su T. Posttraumatic empyema: risk factor
analysis. Arch Surg 1997;132:647-50 ; discussion 650-1.
169. Lemmer JH, Botham MJ, Orringer MB. Modern management of adult thoracic
empyema. J Thorac Cardiovasc Surg 1985;90:849-55.
170. Richardson JD, Carrillo E. Thoracic infection after trauma. Chest Surg Clin North
Am 1997;7:401-27.
171. Weissberg D, Refaely Y. Pleural empyema: 24-year experience. Ann Thorac Surg
1996;62:1026-9.
172. Robinson LA, Moulton AL, Fleming WH, Alonso A, Galbraith TA. Intrapleural
brinolytic treatment of multiloculated thoracic empyemas. Ann Thorac Surg
1994;57:803-13 ; discussion 813-4.
173. Wait MA, Sharma S, Hohn J, Dal Nogare A. A randomized trial of empyema
therapy. Chest 1997;111:1548-51.
174. Karmy-Jones R, Vallieres E, Harrington R. Surgical management of necrotizing
pneumonia. Clin Pul Med 2003;10:17-25.
175. Hagan JL, Hardy JD. Lung abscess revisited: a survey of 184 cases. Ann Surg
1983;197:755-62.
176. Stathopoulos G, Chrysikopoulou E, Kalogeromitros A, Papakonstantinou K,
Poulakis N, Polyzogopoulos D, et al. Bilateral traumatic pulmonary pseudocysts:
case report and literature review. J Trauma 2002;53:993-6.
177. Svane S. Multiple persistent circumscribed pulmonary hematomas due to a blunt
chest trauma. Ann Thorac Surg 2001;72:1752-3.
178. Ikonomidis JS, Boulanger BR, Brenneman FD. Chylothorax after blunt chest
trauma: a report of 2 cases. Can J Surg 1997;40:135-8.
179. Chamberlain M, Ratnatunga C. Late presentation of tension chylothorax following
blunt chest trauma. Eur J Cardiothorac Surg 2000;18:357-9.
362 Curr Probl Surg, March 2004
180. McCormick J 3rd, Henderson SO. Blunt trauma-induced bilateral chylothorax.
Am J Emerg Med 1999;17:302-4.
181. Dulchavsky SA, Ledgerwood AM, Lucas CE. Management of chylothorax after
blunt chest trauma. J Trauma 1988;28:1400-1.
182. Vallieres E, Karmy-Jones R, Wood DE. Early complications: chylothorax. Chest
Surg Clin North Am 1999;9:609-16, ix.
183. Lindhorst E, Miller HA, Taylor GA, Gotzen L. On the possible role of positive
end-expiratory pressure ventilation in the treatment of chylothorax caused by blunt
chest trauma. J Trauma 1998;44:540-2.
184. Vallieres E, Shamji FM, Todd TR. Postpneumonectomy chylothorax. Ann Thorac
Surg 1993;55:1006-8.
185. Ramos W, Faintuch J. Nutritional management of thoracic duct stulas: a
comparative study of parenteral versus enteral nutrition. J Parenter Enteral Nutr
1986;10:519-21.
186. Pratap U, Slavik Z, Ofoe VD, Onuzo O, Franklin RC. Octreotide to treat
postoperative chylothorax after cardiac operations in children. Ann Thorac Surg
2001;72:1740-2.
187. Au M, Weber TR, Fleming RE. Successful use of somatostatin in a case of neonatal
chylothorax. J Pediatr Surg 2003;38:1106-7.
188. Mikroulis D, Didilis V, Bitzikas G, Bougioukas G. Octreotide in the treatment of
chylothorax. Chest 2002;121:2079-80 ; author reply 2080-1.
189. Hoffer EK, Bloch RD, Mulligan MS, Borsa JJ, Fontaine AB. Treatment of
chylothorax: percutaneous catheterization and embolization of the thoracic duct.
Am J Roentgenol 2001;176:1040-2.
190. Marts BC, Naunheim KS, Fiore AC, Pennington DG. Conservative versus surgical
management of chylothorax. Am J Surg 1992;164:532-4 ; discussion 534-5.
191. Cable DG, Deschamps C, Allen MS, Miller DL, Nichols FC, Trastek VF, et al.
Lobar torsion after pulmonary resection: presentation and outcome. J Thorac
Cardiovasc Surg 2001;122:1091-3.
192. Schamaun M. Postoperative pulmonary torsion: report of a case and survey of the
literature including spontaneous and posttraumatic torsion. Thorac Cardiovasc Surg
1994;42:116-21.
193. Warburg E. Myocardial and pericardial lesions due to non-penetrating injury. Br
Heart J 1940;10:271-80.
194. Borch O. Cited by Warburg. Acta Med Hafn IV, Obs XLVII 1676:150.
195. Fischer G. Arch Klin Chir 1867;9:571.
196. Fulton JO, Nel L, de Groot KM, von Oppell UO. Blunt cardiac rupture. S Afr J Surg
1998;36:132-5.
197. Desforges G, Ridder WP, Lenoci RJ. Successful suture of ruptured myocardium
after non-penetrating injury. N Engl J Med 1955;252:567-9.
198. Mattox KL, Flint LM, Carrico CJ, Grover F, Meredith J, Morris J, et al. Blunt
cardiac injury. J Trauma 1992;33:649-50.
199. Moore EE, Malangoni MA, Cogbill TH, Shackford SR, Champion HR, Jurkovich
GJ, et al. Organ injury scaling, IV: thoracic vascular, lung, cardiac, and diaphragm.
J Trauma 1994;36:299-300.
200. Lancey RA, Monahan TS. Correlation of clinical characteristics and outcomes with
injury scoring in blunt cardiac trauma. J Trauma 2003;54:509-15.
Curr Probl Surg, March 2004 363
201. Tenzer ML. The spectrum of myocardial contusion: a review. J Trauma 1985;25:
620-7.
202. Bif WL, Moore FA, Moore EE, Sauaia A, Read RA, Burch JM. Cardiac enzymes
are irrelevant in the patient with suspected myocardial contusion. Am J Surg
1994;168:523-7; discussion 527-8.
203. Kupferschmid JP, Stein D, Aldea GS, Lazar HL. Rupture of the right atrium
secondary to blunt cardiac injury. J Card Surg 1995;10(pt 1):285-7.
204. Clements RH, Fischer PJ 2nd. Blunt injury of the intrapericardial great vessels.
J Trauma 2001;50:129-31.
205. Liedtke AJ, DeMuth WE Jr. Nonpenetrating cardiac injuries: a collective review.
Am Heart J 1973;86:687-97.
206. Zakynthinos EG, Vassilakopoulos T, Routsi C, Roussos C, Zakynthinos S. Early-
and late-onset atrioventricular valve rupture after blunt chest trauma: the usefulness
of transesophageal echocardiography. J Trauma 2002;52:990-6.
207. Lyon RT, Levett JM, Sheridan JM, Glagov S, Anagnostopoulos CE. Myocardial
rupture, III: chamber pressure, rate of distention, and ventricular disruption in
isolated hearts. Ann Thorac Surg 1979;27:554-8.
208. Pretre R, Bednarkiewicz M, Faidutti B. Blunt cardiac injury: in achieving a
practical diagnostic classication. J Trauma 1994;36:462-3.
209. Johnston RH Jr, Wall MJ Jr, Mattox KL. Innominate artery trauma: a thirty-year
experience. J Vasc Surg 1993;17:134-9 ; discussion 139-40.
210. DiMarco RF, Layton TR, Manzetti GW, Pellegrini RV. Blunt traumatic rupture of
the right atrium and the right superior pulmonary vein. J Trauma 1983;23:353-5.
211. Baxter BT, Moore EE, Synhorst DP, Reiter MJ, Harken AH. Graded experimental
myocardial contusion: impact on cardiac rhythm, coronary artery ow, ventricular
function, and myocardial oxygen consumption. J Trauma 1988;28:1411-7.
212. Marek A, Rey JL, Jarry G, Hermida JS, Avinee P, Bernasconi P, et al. Myocardial
infarction caused by closed thoracic injury: pathogenic and angiocoronarographic
aspects: apropos of 4 cases and review of the literature. Ann Cardiol Angiol (Paris)
1991;40:111-21.
213. Cheng I, McLellan BA, Joyner C, Christakis G. Aortic root trauma: serious injuries
requiring early recognition and management. J Trauma 2000;48:525-9.
214. Lindstaedt M, Germing A, Lawo T, von Dryander S, Jaeger D, Muhr G, et al. Acute
and long-term clinical signicance of myocardial contusion following blunt
thoracic trauma: results of a prospective study. J Trauma 2002;52:479-85.
215. van Wijngaarden MH, Karmy-Jones R, Talwar MK, Simonetti V. Blunt cardiac
injury: a 10 year institutional review. Injury 1997;28:51-5.
216. Macdonald RC, ONeill D, Hanning CD, Ledingham IM. Myocardial contusion in
blunt chest trauma: a ten-year review. Intensive Care Med 1981;7:265-8.
217. Malangoni MA, McHenry CR, Jacobs DG. Outcome of serious blunt cardiac injury.
Surgery 1994;116:628-32 ; discussion 632-3.
218. Bodor GS, Portereld D, Voss EM, Smith S, Apple FS. Cardiac troponin-I is not
expressed in fetal and healthy or diseased adult human skeletal muscle tissue. Clin
Chem 1995;41(pt 1):1710-5.
219. Bertinchant JP, Polge A, Mohty D, Nguyen-Ngoc-Lam R, Estorc J, Cohendy R, et al.
Evaluation of incidence, clinical signicance, and prognostic value of circulating
cardiac troponin I and T elevation in hemodynamically stable patients with suspected
myocardial contusion after blunt chest trauma. J Trauma 2000;48:924-31.
364 Curr Probl Surg, March 2004
220. Roberts CS, Sadoff JD, White DR. Innominate arterial rupture distal to anomalous
origin of left carotid artery. Ann Thorac Surg 2000;69:1263-4.
221. Ferjani M, Droc G, Dreux S, Arthaud M, Goarin JP, Riou B, et al. Circulating
cardiac troponin T in myocardial contusion. Chest 1997;111:427-33.
222. Helm M, Hauke J, Weiss A, Lampl L. Cardiac troponin T as a biochemical marker
of myocardial injury early after trauma: diagnostic value of a qualitative bedside
test. Chirurg 1999;70:1347-52.
223. Velmahos GC, Karaiskakis M, Salim A, Toutouzas KG, Murray J, Asensio J, et al.
Normal electrocardiography and serum troponin I levels preclude the presence of
clinically signicant blunt cardiac injury. J Trauma 2003;54:45-50; discussion
50-1.
224. Hobbs FD, Davis RC, Roalfe AK, Hare R, Davies MK, Kenkre JE. Reliability of
N-terminal pro-brain natriuretic peptide assay in diagnosis of heart failure: cohort
study in representative and high risk community populations. BMJ 2002;324:1498.
225. Sela B. Monitoring heart failure with brain natriuretic peptide. Harefuah 2003;142:
25-31, 78.
226. Redeld MM, Rodeheffer RJ, Jacobsen SJ, Mahoney DW, Bailey KR, Burnett JC
Jr. Plasma brain natriuretic peptide concentration: impact of age and gender. J Am
Coll Cardiol 2002;40:976-82.
227. Orliaguet G, Jacquens Y, Riou B, Le Bret F, Rouby JJ, Viars P. Combined severe
myocardial and pulmonary contusion: early diagnosis with transesophageal echo-
cardiography and management with high-frequency jet ventilation: case report.
J Trauma 1993;34:455-7.
228. Helling TS, Duke P, Beggs CW, Crouse LJ. A prospective evaluation of 68 patients
suffering blunt chest trauma for evidence of cardiac injury. J Trauma 1989;29:
961-5; discussion 965-6.
229. Kantor G, Devitt JH. Blunt cardiac injury and intraoperative hypoxaemia. Can J
Anaesth 1993;40:515-7.
230. Pontillo D, Capezzuto A, Achilli A, Serraino L, Savelli S, Guerra R. Bifascicular
block complicating blunt cardiac injury: a case report and review of the literature.
Angiology 1994;45:883-90.
231. Flancbaum L, Wright J, Siegel JH. Emergency surgery in patients with post-
traumatic myocardial contusion. J Trauma 1986;26:795-803.
232. Utley JR, Doty DB, Collins JC, Spaw EA, Wachtel C, Todd EP. Cardiac output,
coronary ow, ventricular brillation and survival following varying degrees of
myocardial contusion. J Surg Res 1976;20:539-43.
233. Miller FA Jr, Seward JB, Gersh BJ, Tajik AJ, Mucha P Jr. Two-dimensional
echocardiographic ndings in cardiac trauma. Am J Cardiol 1982;50:1022-7.
234. Torres-Mirabal P, Gruenberg JC, Brown RS, Obeid FN. Spectrum of myocardial
contusion. Am Surg 1982;48:383-92.
235. Timberlake GA, McSwain NE Jr. Thromboembolism as a complication of
myocardial contusion: a new capricious syndrome. J Trauma 1988;28:535-40.
236. Shyu MY, Lee AY, Lee BJ, Chang Y, Wei HJ, Chang MC, et al. Right atrial and
ventricular thrombi after blunt chest trauma. J Trauma 2002;52:765-6.
237. Pretre R, Chilcott M. Blunt trauma to the heart and great vessels. N Engl J Med
1997;336:626-32.
238. End A, Rodler S, Oturanlar D, Domanig E, Havel M, Kassal H, et al. Elective
surgery for blunt cardiac trauma. J Trauma 1994;37:798-802.
Curr Probl Surg, March 2004 365
239. Sturaitis M, McCallum D, Sutherland G, Cheung H, Driedger AA, Sibbald WJ.
Lack of signicant long-term sequelae following traumatic myocardial contusion.
Arch Intern Med 1986;146:1765-9.
240. Carrillo EH, Schirmer TP, Sideman MJ, Wallace JM, Spain DA. Blunt hemoperi-
cardium detected by surgeon-performed sonography. J Trauma 2000;48:971-4.
241. Bif WL, Moore EE. Blunt cardiac injury. In: Karmy-Jones R, Nathens A, Stern E,
editors. Thoracic Trauma and Critical Care. Boston, Mass: Kluwer Academic
Publishers; 2002. 281-8.
242. Gunewardene HO. Traumatic rupture of the heart without external injuries. BMJ
1934;2:942.
243. Driscoll RW. Right atrial and right ventricular rupture with cardiac tamponade
secondary to nonpenetrating blunt trauma to the chest: report of case of survival and
review of the literature. J Am Osteopath Assoc 1973;72:1061-9.
244. Brown J, Grover FL. Trauma to the heart. Chest Surg Clin North Am 1997;7:325-41.
245. Mangram A, Kozar RA, Gregoric I, Grant P, Cocanour CS, Moore FA. Blunt
cardiac injuries that require operative intervention: an unsuspected injury. J Trauma
2003;54:286-8.
246. Baumgartel ED. Cardiac rupture from blunt trauma with atrial septal defect. Arch
Surg 1992;127:347-8.
247. Fulda G, Brathwaite CE, Rodriguez A, Turney SZ, Dunham CM, Cowley RA.
Blunt traumatic rupture of the heart and pericardium: a ten-year experience
(1979-1989). J Trauma 1991;31:167-72 ; discussion 172-3.
248. Krejci CS, Blackmore CC, Nathens A. Hemopericardium: an emergent nding in
a case of blunt cardiac injury. Am J Roentgenol 2000;175:250.
249. May AK, Patterson MA, Rue LW 3rd, Schiller HJ, Rotondo MF, Schwab CW.
Combined blunt cardiac and pericardial rupture: review of the literature and report
of a new diagnostic algorithm. Am Surg 1999;65:568-74.
250. Martin TD, Flynn TC, Rowlands BJ, Ward RE, Fischer RP. Blunt cardiac rupture.
J Trauma 1984;24:287-90.
251. Pevec WC, Udekwu AO, Peitzman AB. Blunt rupture of the myocardium. Ann
Thorac Surg 1989;48:139-42.
252. Hendel PN, Grant AF. Blunt traumatic rupture of the heart: successful repair of
simultaneous rupture of the right atrium and left ventricle. J Thorac Cardiovasc
Surg 1981;81:574-6.
253. Varghese D, Patel H, Cameron EW, Robson M. Repair of pulmonary vein rupture
after deceleration injury. Ann Thorac Surg 2000;70:656-8.
254. Ambrose G, Barrett LO, Angus GL, Absi T, Shaftan GW. Main pulmonary artery
laceration after blunt trauma: accurate preoperative diagnosis. Ann Thorac Surg
2000;70:955-7.
255. van de Wal HJ, Draaisma JM, Vincent JG, Goris RJ. Rupture of the supradiaphrag-
matic inferior vena cava by blunt decelerating trauma: case report. J Trauma
1990;30:111-3.
256. Mazzucco A, Rizzoli G, Faggian G, Aru G, Bortolotti U, Sorbara C, et al. Acute
mitral regurgitation after blunt chest trauma. Arch Intern Med 1983;143:2326-9.
257. Banning AP, Pillai R. Non-penetrating cardiac and aortic trauma. Heart 1997;78:
226-9.
258. Hanna KM, Weiman DS, Pate JW, Wolf BA, Fabian TC. Aortic valve injury
secondary to blunt trauma from an air bag. Tenn Med 1997;90:195-6.
366 Curr Probl Surg, March 2004
259. Maisano F, Lorusso R, Sandrelli L, Torracca L, Coletti G, La Canna G, et al. Valve
repair for traumatic tricuspid regurgitation. Eur J Cardiothorac Surg 1996;10:867-73.
260. Banning AP, Durrani A, Pillai R. Rupture of the atrial septum and tricuspid valve
after blunt chest trauma. Ann Thorac Surg 1997;64:240-2.
261. Cuadros CL, Hutchinson JE 3rd, Mogtader AH. Laceration of a mitral papillary
muscle and the aortic root as a result of blunt trauma to the chest: case report and
review of the literature. J Thorac Cardiovasc Surg 1984;88:134-40.
262. Brooks SW, Young JC, Cmolik B, Schina M, Dianzumba S, Townsend RN, et al.
The use of transesophageal echocardiography in the evaluation of chest trauma.
J Trauma 1992;32:761-5 ; discussion 765-8.
263. Cho MC, Kim DW, Hong JM, Ahn JH, Hong JS. Left ventricular and papillary
muscle rupture following blunt chest trauma. Am J Cardiol 1995;76:424-6.
264. Guhathakurta S, Chen Q, Nalladaru Z, Squire BH, Sharma AK. Delayed traumatic
mitral regurgitation after blunt chest trauma. J Trauma 1999;47:982-4.
265. Bardy GH, Talano JV, Meyers S, Lesch M. Acquired cyanotic heart disease
secondary to traumatic tricuspid regurgitation: case report with a review of the
literature. Am J Cardiol 1979;44:1401-6.
266. Matthews RV, French WJ, Criley JM. Chest trauma and subvalvular left ventricular
aneurysms. Chest 1989;95:474-6.
267. Pretre R, Bruschweiler I, Faidutti B. Blunt injuries to the innominate artery. Ann
Vasc Surg 1993;7:470-3.
268. Pretre R, Faidutti B. Aortic valve rupture in closed trauma: the extent of the
damage. J Thorac Cardiovasc Surg 1993;106:371-3.
269. Murray EG, Minami K, Kortke H, Seggewiss H, Korfer R. Traumatic sinus of
Valsalva stula and aortic valve rupture. Ann Thorac Surg 1993;55:760-1.
270. DeSaNeto A, Padnick MB, Desser KB, Steinhoff NG. Right sinus of Valsalva-
right atrial stula secondary to nonpenetrating chest trauma: a case report with
description of noninvasive diagnostic features. Circulation 1979;60:205-9.
271. Misfeld M, Ehlermann P, Sievers HH. Transaortic repair of blunt traumatic cardiac
wall and papillary muscle rupture. J Thorac Cardiovasc Surg 2001;122:834-5.
272. Chang JP, Chu JJ, Chang CH. Aortic regurgitation due to aortic root intimal tear as
a result of blunt chest trauma. J Formos Med Assoc 1990;89:41-3.
273. Girardi L, Isom OW. Repair of traumatic aortic valve disruption and descending
aortic transection. Ann Thorac Surg 2000;69:1251-3.
274. Pretre R, Faidutti B. Surgical management of aortic valve injury after nonpenetrat-
ing trauma. Ann Thorac Surg 1993;56:1426-31.
275. Aris A, Delgado LJ, Montiel J, Subirana MT. Multiple intracardiac lesions after
blunt chest trauma. Ann Thorac Surg 2000;70:1692-4.
276. Okita Y, Miki S, Kusuhara K, Ueda Y, Tahata T, Yamanaka K, et al. Long-term
results of aortic valvuloplasty for aortic regurgitation associated with ventricular
septal defect. J Thorac Cardiovasc Surg 1988;96:769-74.
277. Paone RF, Kidd JN, Dobrin DJ, DiDonna GJ. Traumatic aortic incompetence
associated with transection of the thoracic aorta. Chest 1996;109:1118-9.
278. Pellegrini RV, Layton TR, Dimarco RF, Grant KJ, Marrangoni AG. Multiple
cardiac lesions from blunt trauma. J Trauma 1980;20:169-73.
279. Pretre R, Kursteiner K, Khatchatourian G, Faidutti B. Traumatic occlusion of the
left anterior descending artery and rupture of the aortic isthmus. J Trauma
1995;39:388-90.
Curr Probl Surg, March 2004 367
280. Gillebert T, van de Werf F, Piessens J, de Geest H. Post-traumatic infarction due
to blunt chest trauma: report of two cases. Acta Cardiol 1980;35:445-53.
281. Gaspard P, Clermont A, Villard J, Amiel M. Non-iatrogenic trauma of the coronary
arteries and myocardium: contribution of angiographyreport of six cases and
literature review. Cardiovasc Intervent Radiol 1983;6:20-9.
282. Ginzburg E, Dygert J, Parra-Davila E, Lynn M, Almeida J, Mayor M. Coronary
artery stenting for occlusive dissection after blunt chest trauma. J Trauma
1998;45:157-61.
283. Candell J, Valle V, Paya J, Cortadellas J, Esplugas E, Rius J. Post-traumatic
coronary occlusion and early left ventricular aneurysm. Am Heart J 1979;97:509-
12.
284. Fu M, Wu CJ, Hsieh MJ. Coronary dissection and myocardial infarction following
blunt chest trauma. J Formos Med Assoc 1999;98:136-40.
285. Stamm C, Feit LR, Geva T, del Nido PJ. Repair of ventricular septal defect and left
ventricular aneurysm following blunt chest trauma. Eur J Cardiothorac Surg
2002;22:154-6.
286. Sareli P, Goldman AP, Pocock WA, Colsen P, Casari A, Barlow JB. Coronary
artery-right ventricular stula and organic tricuspid regurgitation due to blunt chest
trauma. Am J Cardiol 1984;54:697-9.
287. Lowe JE, Adams DH, Cummings RG, Wesly RL, Phillips HR. The natural history
and recommended management of patients with traumatic coronary artery stulas.
Ann Thorac Surg 1983;36:295-305.
288. Renzulli A, Wren C, Hilton CJ. Coronary artery-left ventricular stula and multiple
ventricular septal defects due to blunt chest trauma. Thorax 1989;44:1055-6.
289. Friesen CH, Howlett JG, Ross DB. Traumatic coronary artery stula management.
Ann Thorac Surg 2000;69:1973-82.
290. Amorim MJ, Almeida J, Santos A, Bastos PT. Atrioventricular septal defect
following blunt chest trauma. Eur J Cardiothorac Surg 1999;16:679-82.
291. Pierli C, Iadanza A, Del Pasqua A, Sinicropi G. Unusual localisation of a
ventricular septal defect following blunt chest trauma. Heart 2001;86:E6.
292. Moront M, Lefrak EA, Akl BF. Traumatic rupture of the interventricular septum
and tricuspid valve: case report. J Trauma 1991;31:134-6.
293. Berkery W, Hare C, Warner RA, Battaglia J, Potts JL. Nonpenetrating traumatic
rupture of the tricuspid valve: formation of ventricular septal aneurysm and
subsequent septal necrosis: recognition by two-dimensional Doppler echocardiog-
raphy. Chest 1987;91:778-80.
294. Genoni M, Jenni R, Turina M. Traumatic ventricular septal defect. Heart 1997;78:
316-8.
295. Stahl RD, Liu JC, Walsh JF. Blunt cardiac trauma: atrioventricular valve disruption
and ventricular septal defect. Ann Thorac Surg 1997;64:1466-8.
296. Pirzada FA, McDowell JW, Cohen EM, Saini VK, Berger RL. Traumatic
ventricular septal defect: sequential hemodynamic observations. N Engl J Med
1974;291:892-5.
297. Ilia R, Goldfarb B, Wanderman KL, Gueron M. Spontaneous closure of a traumatic
ventricular septal defect after blunt trauma documented by serial echocardiography.
J Am Soc Echocardiogr 1992;5:203-5.
298. Wu JJ, Yu TJ, Wang JJ, Wen YS, Liu M, Lee CH. Early repair of traumatic
ventricular septal defect and mitral valve regurgitation. J Trauma 1995;39:1191-3.
368 Curr Probl Surg, March 2004
299. Pevec WC, el-Hillel M, McArdle DQ, Walsh C, Peitzman AB. Rupture of the left
ventricle and interventricular septum by blunt trauma. Crit Care Med 1989;17:
837-8.
300. Pickard LR, Mattox KL, Beall AC Jr. Ventricular septal defect from blunt chest
injury. J Trauma 1980;20:329-31.
301. Janson JT, Harris DG, Pretorius J, Rossouw GJ. Pericardial rupture and cardiac
herniation after blunt chest trauma. Ann Thorac Surg 2003;75:581-2.
302. Fulda G, Rodriguez A, Turney SZ, Cowley RA. Blunt traumatic pericardial rupture:
a ten-year experience 1979 to 1989. J Cardiovasc Surg (Torino) 1990;31:525-30.
303. Clark DE, Wiles CS 3rd, Lim MK, Dunham CM, Rodriguez A. Traumatic rupture
of the pericardium. Surgery 1983;93:495-503.
304. Borrie J, Lichter I. Pericardial rupture from blunt chest trauma. Thorax 1974;29:
329-37.
305. Mattila S, Silvola H, Ketonen P. Traumatic rupture of the pericardium with luxation
of the heart: case report and review of the literature. J Thorac Cardiovasc Surg
1975;70:495-8.
306. Place RJ, Cavanaugh DG. Computed tomography to diagnose pericardial rupture.
J Trauma 1995;38:822-3.
307. Schir F, Thony F, Chavanon O, Perez-Moreira I, Blin D, Coulomb M. Blunt
traumatic rupture of the pericardium with cardiac herniation: two cases diagnosed
using computed tomography. Eur Radiol 2001;11:995-9.
308. Thomas P, Saux P, Lonjon T, Viggiano M, Denis JP, Giudicelli R, et al. Diagnosis
by video-assisted thoracoscopy of traumatic pericardial rupture with delayed
luxation of the heart: case report. J Trauma 1995;38:967-70.
309. Watkins BM, Buckley DC, Peschiera JL. Delayed presentation of pericardial
rupture with luxation of the heart following blunt trauma: a case report. J Trauma
1995;38:368-9.
310. Bellanger D, Nikas D, Freeman J, Izenberg S. Delayed posttraumatic tamponade.
S Med J 1996;89:1197-9.
311. Symbas PN. Traumatic injury of the pericardium. In: Symbas PN, editor. Cardio-
thoracic Trauma. Philadelphia, Pa: WB Saunders; 1989. 77-88.
312. Karmy-Jones R, Yen T, Cornejo C. Pericarditis after trauma resulting in delayed
cardiac tamponade. Ann Thorac Surg 2002;74:239-41.
313. Tabatznick B, Issaca J. Postpericardiotomy syndrome following traumatic hemo-
pericardium. Am J Cardiol 1961;7:83-96.
314. Wiegand L, Zwillich CW. The post-cardiac injury syndrome following blunt chest
trauma: case report. J Trauma 1993;34:445-7.
315. McCabe JC, Ebert PA, Engle MA, Zabriskie JB. Circulating heart-reactive
antibodies in the postpericardiotomy syndrome. J Surg Res 1973;14:158-64.
316. Erenhaft J, Taft R. Hemopericardium and constrictive pericarditis. J Thorac Surg
1952;24:355-85.
317. Dressler W. A post-myocardial infarction syndrome. JAMA 1956;160:1379-83.
318. Chong HH, Plotnick GD. Pericardial effusion and tamponade: evaluation, imaging
modalities, and management. Compr Ther 1995;21:378-85.
319. Sato TT, Geary RL, Ashbaugh DG, Jurkovich GJ. Diagnosis and management of
pericardial abscess in trauma patients. Am J Surg 1993;165:637-41.
320. Schweitzer J, Nirula R, Romero J, Vogel J, Waxman K. Successful emergent
Curr Probl Surg, March 2004 369
thoracotomy for pericardial tamponade caused by late constrictive pericarditis after
trauma. J Trauma 2001;50:945-8.
321. Scorpio RJ, Wesson DE, Smith CR, Hu X, Spence LJ. Blunt cardiac injuries in
children: a postmortem study. J Trauma 1996;41:306-9.
322. Bromberg BI, Mazziotti MV, Canter CE, Spray TL, Strauss AW, Foglia RP.
Recognition and management of nonpenetrating cardiac trauma in children.
J Pediatr 1996;128:536-41.
323. Karpas A, Yen K, Sell LL, Frommelt PC. Severe blunt cardiac injury in an infant:
a case of child abuse. J Trauma 2002;52:759-64.
324. Bliss DW, Newth CJ, Stein JE. Blunt traumatic injury to the coronary arteries and
pulmonary artery in a child. J Trauma 2000;49:550-2.
325. Cizmarova E, Simkovic I, Zelenay J, Masura J. Post-traumatic coronary occlusion
and its consequences in a young child. Pediatr Cardiol 1988;9:117-20.
326. Harel Y, Szeinberg A, Scott WA, Frand M, Vered Z, Smolinski A, et al. Ruptured
interventricular septum after blunt chest trauma: ultrasonographic diagnosis.
Pediatr Cardiol 1995;16:127-30.
327. Maron BJ, Poliac LC, Kaplan JA, Mueller FO. Blunt impact to the chest leading to
sudden death from cardiac arrest during sports activities. N Engl J Med 1995;333:
337-42.
328. Link MS, Ginsburg SH, Wang PJ, Kirchhoffer JB, Berul CI, Estes NA 3rd, et al.
Commotio cordis: cardiovascular manifestations of a rare survivor. Chest 1998;
114:326-8.
329. Link MS, Wang PJ, Pandian NG, Bharati S, Udelson JE, Lee MY, et al. An
experimental model of sudden death due to low-energy chest-wall impact (com-
motio cordis). N Engl J Med 1998;338:1805-11.
330. Maron BJ, Gohman TE, Kyle SB, Estes NA 3rd, Link MS. Clinical prole and
spectrum of commotio cordis. JAMA 2002;287:1142-6.
331. Pediatrics AAO. Risk of injury from baseball and softball in children. Pediatrics
2001;107:782-4.
332. Mattox KL. Red River anthology. J Trauma 1997;42:353-68.
333. Mattox KL, Wall MJ Jr. Historical review of blunt injury to the thoracic aorta.
Chest Surg Clin North Am 2000;10:167-82, x.
334. Lee RB, Stahlman GC, Sharp KW. Treatment priorities in patients with traumatic
rupture of the thoracic aorta. Am Surg 1992;58:37-43.
335. Smith RS, Chang FC. Traumatic rupture of the aorta: still a lethal injury. Am J Surg
1986;152:660-3.
336. Burkhart HM, Gomez GA, Jacobson LE, Pless JE, Broadie TA. Fatal blunt aortic
injuries: a review of 242 autopsy cases. J Trauma 2001;50:113-5.
337. Cohen AM, Crass JR, Thomas HA, Fisher RG, Jacobs DG. CT evidence for the
osseous pinch mechanism of traumatic aortic injury. Am J Roentgenol 1992;159:
271-4.
338. Horton TG, Cohn SM, Heid MP, Augenstein JS, Bowen JC, McKenney MG, et al.
Identication of trauma patients at risk of thoracic aortic tear by mechanism of
injury. J Trauma 2000;48:1008-13; discussion 1013-4.
339. Ben-Menachem Y. Rupture of the thoracic aorta by broadside impacts in road
trafc and other collisions: further angiographic observations and preliminary
autopsy ndings. J Trauma 1993;35:363-7.
340. Nagy K, Fabian T, Rodman G, Fulda G, Rodriguez A, Mirvis S. Guidelines for the
370 Curr Probl Surg, March 2004
diagnosis and management of blunt aortic injury: an EAST Practice Management
Guidelines Work Group. J Trauma 2000;48:1128-43.
341. Feliciano DV. Trauma to the aorta and major vessels. Chest Surg Clin North Am
1997;7:305-23.
342. Feczko JD, Lynch L, Pless JE, Clark MA, McClain J, Hawley DA. An autopsy case
review of 142 nonpenetrating (blunt) injuries of the aorta. J Trauma 1992;33:846-9.
343. Hattori Y, Sugimura S, Watanabe K, Iriyama T, Negi K, Yamashita M, et al. Acute
traumatic dissection and blunt rupture of the thoracic descending aorta: a case
report. Ann Thorac Cardiovasc Surg 1999;5:198-201.
344. Bourgeois M, Duperret S, Vedrinne JM, Bui-Xuan B, Allaouchiche B, Motin J.
Post-traumatic dissection of the aortic isthmus with favorable outcome without
surgical treatment: value of transesophageal echocardiography. Ann Fr Anesth
Reanim 1995;14:218-21.
345. Kram HB, Appel PL, Wohlmuth DA, Shoemaker WC. Diagnosis of traumatic
thoracic aortic rupture: a 10-year retrospective analysis. Ann Thorac Surg 1989;
47:282-6.
346. Sturm JT, Luxenberg MG, Moudry BM, Perry JF. Does sternal fracture increase the
risk for aortic rupture? Ann Thorac Surg 1989;48:697-8.
347. Clark DE, Zeiger MA, Wallace KL, Packard AB, Nowicki ER. Blunt aortic trauma:
signs of high risk. J Trauma 1990;30:701-5.
348. Richardson RL, Khandekar A, Moseley PW. Traumatic rupture of the thoracic
aorta. South Med J 1979;72:300-1.
349. Shackford SR, Virgilio RW, Smith DE, Rice CL, Weinstein ME. The signicance
of chest wall injury in the diagnosis of traumatic aneurysms of the thoracic aorta.
J Trauma 1978;18:493-7.
350. Trachiotis GD, Sell JE, Pearson GD, Martin GR, Midgley FM. Traumatic thoracic
aortic rupture in the pediatric patient. Ann Thorac Surg 1996;62:724-31 ; discussion
731-2.
351. Marnocha KE, Maglinte DD. Plain-lm criteria for excluding aortic rupture in blunt
chest trauma. Am J Roentgenol 1985;144:19-21.
352. Mirvis SE, Bidwell JK, Buddemeyer EU, Diaconis JN, Pais SO, Whitley JE, et al.
Value of chest radiography in excluding traumatic aortic rupture. Radiology
1987;163:487-93.
353. Ayella RJ, Hankins JR, Turney SZ, Cowley RA. Ruptured thoracic aorta due to
blunt trauma. J Trauma 1977;17:199-205.
354. Gundry SR, Williams S, Burney RE, Cho KJ, Mackenzie JR. Indications for
aortography in blunt thoracic trauma: a reassessment. J Trauma 1982;22:664-71.
355. Gundry SR, Burney RE, Mackenzie JR, Wilton GP, Whitehouse WM, Wu SC, et
al. Assessment of mediastinal widening associated with traumatic rupture of the
aorta. J Trauma 1983;23:293-9.
356. Woodring JH, King JG. Determination of normal transverse mediastinal width and
mediastinal-width to chest-width (M/C) ratio in control subjects: implications for
subjects with aortic or brachiocephalic arterial injury. J Trauma 1989;29:1268-72.
357. Burney RE, Gundry SR, Mackenzie JR, Wilton GP, Whitehouse WM, Wu SC.
Comparison of mediastinal width, mediastinal-thoracic and -cardiac ratios, and
mediastinal widening in detection of traumatic aortic rupture. Ann Emerg Med
1983;12:668-71.
358. Demetriades D, Gomez H, Velmahos GC, Asensio JA, Murray J, Cornwell EE 3rd,
Curr Probl Surg, March 2004 371
et al. Routine helical computed tomographic evaluation of the mediastinum in
high-risk blunt trauma patients. Arch Surg 1998;133:1084-8.
359. Vloeberghs M, Duinslaeger M, Van den Brande P, Cham B, Welch W. Posttrau-
matic rupture of the thoracic aorta. Acta Chir Belg 1988;88:33-8.
360. Dyer DS, Moore EE, Ilke DN, McIntyre RC, Bernstein SM, Durham JD, et al.
Thoracic aortic injury: how predictive is mechanism and is chest computed
tomography a reliable screening tool? a prospective study of 1,561 patients.
J Trauma 2000;48:673-82; discussion 682-3.
361. Sturm JT, Hankins DG, Young G. Thoracic aortography following blunt chest
trauma. Am J Emerg Med 1990;8:92-6.
362. Mirvis SE, Shanmuganathan K, Buell J, Rodriguez A. Use of spiral computed
tomography for the assessment of blunt trauma patients with potential aortic injury.
J Trauma 1998;45:922-30.
363. Curry JD, Recine CA, Snavely E, Orr M, Fildes JJ. Periaortic hematoma on
abdominal computed tomographic scanning as an indicator of thoracic aortic
rupture in blunt trauma. J Trauma 2002;52:699-702.
364. Hills MW, Thomas SG, McDougall PA, Hewitt-Falls EA, Graham JC, Deane SA.
Traumatic thoracic aortic rupture: investigation determines outcome. Aust N Z
J Surg 1994;64:312-8.
365. Munoz A, Moreno R, Martin V, Iniguez A, Alvarez J. Aortography delays surgery
of CT proven acute traumatic rupture of the thoracic aorta: case report. Acta Radiol
1991;32:386-8.
366. Chen MY, Regan JD, DAmore MJ, Routh WD, Meredith JW, Dyer RB. Role of
angiography in the detection of aortic branch vessel injury after blunt thoracic
trauma. J Trauma 2001;51:1166-71; discussion 1172.
367. Ahrar K, Smith DC, Bansal RC, Razzouk A, Catalano RD. Angiography in blunt
thoracic aortic injury. J Trauma 1997;42:665-9.
368. Downing SW, Sperling JS, Mirvis SE, Cardarelli MG, Gilbert TB, Scalea TM, et
al. Experience with spiral computed tomography as the sole diagnostic method for
traumatic aortic rupture. Ann Thorac Surg 2001;72:495-501 ; discussion 501-2.
369. Fabian TC, Davis KA, Gavant ML, Croce MA, Melton SM, Patton JH, et al.
Prospective study of blunt aortic injury: helical CT is diagnostic and antihyperten-
sive therapy reduces rupture. Ann Surg 1998;227:666-76 ; discussion 676-7.
370. Holmes J, Bloch R, Karmy-Jones R. Natural history of non-operative management
of aortic injury. Australian Trauma Association/Trauma Association of Canada -
Combined Annual Meeting, Sydney, Australia; March 2, 2001.
371. Smith MD, Cassidy JM, Souther S, Morris EJ, Sapin PM, Johnson SB, et al.
Transesophageal echocardiography in the diagnosis of traumatic rupture of the
aorta. N Engl J Med 1995;332:356-62.
372. Mollod M, Felner JM. Transesophageal echocardiography in the evaluation of
cardiothoracic trauma. Am Heart J 1996;132:841-9.
373. Brathwaite CE, Cilley JM, OConnor WH, Ross SE, Weiss RL. The pivotal role of
transesophageal echocardiography in the management of traumatic thoracic aortic
rupture with associated intra-abdominal hemorrhage. Chest 1994;105:1899-901.
374. Kepros J, Angood P, Jaffe CC, Rabinovici R. Aortic intimal injuries from blunt
trauma: resolution prole in nonoperative management. J Trauma 2002;52:475-8.
375. Malhotra AK, Fabian TC, Croce MA, Weiman DS, Gavant ML, Pate JW. Minimal
372 Curr Probl Surg, March 2004
aortic injury: a lesion associated with advancing diagnostic techniques. J Trauma
2001;51:1042-8.
376. Shapiro MJ, Yanofsky SD, Trapp J, Durham RM, Labovitz A, Sear JE, et al.
Cardiovascular evaluation in blunt thoracic trauma using transesophageal echocar-
diography (TEE). J Trauma 1991;31:835-9; discussion 839-40.
377. Vignon P, Gueret P, Vedrinne JM, Lagrange P, Cornu E, Abrieu O, et al. Role of
transesophageal echocardiography in the diagnosis and management of traumatic
aortic disruption. Circulation 1995;92:2959-68.
378. Katyal D, McLellan BA, Brenneman FD, Boulanger BR, Sharkey PW, Waddell JP.
Lateral impact motor vehicle collisions: signicant cause of blunt traumatic rupture
of the thoracic aorta. J Trauma 1997;42:769-72.
379. Ochsner MG Jr, Champion HR, Chambers RJ, Harviel JD. Pelvic fracture as an
indicator of increased risk of thoracic aortic rupture. J Trauma 1989;29:1376-9.
380. Mirvis SE, Bidwell JK, Buddemeyer EU, Diaconis JN, Pais SO, Whitley JE.
Imaging diagnosis of traumatic aortic rupture: a review and experience at a major
trauma center. Invest Radiol 1987;22:187-96.
381. Hunink MGM, Bos JJ. Triage of patients to angiography for detection of aortic
rupture after blunt chest trauma: cost-effectiveness analysis of using CT. Am J
Roentgenol 1995;165:27-36.
382. Blackmore CC, Zweibel A, Mann FA. Determining risk of traumatic aortic injury:
how to optimize imaging strategy. Am J Roentgenol 2000;174:343-7.
383. Kirsh MM, Behrendt DM, Orringer MB, Gago O, Gray LA Jr, Mills LJ, et al. The
treatment of acute traumatic rupture of the aorta: a 10-year experience. Ann Surg
1976;184:308-16.
384. Karmy-Jones R, Carter YM, Nathens A, Brundage S, Meissner MH, Borsa J, et al.
Impact of presenting physiology and associated injuries on outcome following
traumatic rupture of the thoracic aorta. Am Surg 2001;67:61-6.
385. Simon BJ, Leslie C. Factors predicting early in-hospital death in blunt thoracic
aortic injury. J Trauma 2001;51:906-10 ; discussion 911.
386. Hudson HM 2nd, Woodson J, Hirsch E. The management of traumatic aortic tear
in the multiply-injured patient. Ann Vasc Surg 1991;5:445-8.
387. Borman KR, Aurbakken CM, Weigelt JA. Treatment priorities in combined blunt
abdominal and aortic trauma. Am J Surg 1982;144:728-32.
388. Langanay T, Verhoye JP, Corbineau H, Agnino A, Derieux T, Menestret P, et al.
Surgical treatment of acute traumatic rupture of the thoracic aorta: a timing
reappraisal? Eur J Cardiothorac Surg 2002;21:282-7.
389. Pretre R, Murith N, Faidutti B. Increased association of cardiac and thoracic
vascular lesions after closed trauma of the thorax. Ann Chir 1995;49:854-7.
390. Lemermeyer G, Talwar MK, Mullen JC, Klassen N. Traumatic rupture of the
thoracic aorta during the second trimester of pregnancy. Ann Thorac Surg
1996;61:1541-3.
391. Pate JW, Gavant ML, Weiman DS, Fabian TC. Traumatic rupture of the aortic
isthmus: program of selective management. World J Surg 1999;23:59-63.
392. Pate JW. Is traumatic rupture of the aorta misunderstood? Ann Thorac Surg
1994;57:530-1.
393. Akins CW, Buckley MJ, Daggett W, McIlduff JB, Austen WG. Acute traumatic
disruption of the thoracic aorta: a ten-year experience. Ann Thorac Surg 1981;31:
305-9.
Curr Probl Surg, March 2004 373
394. Maggisano R, Nathens A, Alexandrova NA, Cina C, Boulanger B, McKenzie R, et
al. Traumatic rupture of the thoracic aorta: should one always operate immediately?
Ann Vasc Surg 1995;9:44-52.
395. Warren RL, Akins CW, Conn AK, Hilgenberg AD, McCabe CJ. Acute traumatic
disruption of the thoracic aorta: emergency department management. Ann Emerg
Med 1992;21:391-6.
396. Pierangeli A, Turinetto B, Galli R, Caldarera l, Fattori R, Gavelli G. Delayed
treatment of isthmic aortic rupture. Cardiovasc Surg 2000;8:280-3.
397. Orringer MB, Kirsh MM. Primary repair of acute traumatic aortic disruption. Ann
Thorac Surg 1983;35:672-5.
398. Schmidt CA, Wood MN, Razzouk AJ, Killeen JD, Gan KA. Primary repair of
traumatic aortic rupture: a preferred approach. J Trauma 1992;32:588-92.
399. McBride LR, Tidik S, Stothert JC, Barner HB, Kaiser GC, Willman VL, et al.
Primary repair of traumatic aortic disruption. Ann Thorac Surg 1987;43:65-7.
400. Razzouk AJ, Gundry SR, Wang N, del Rio MJ, Varnell D, Bailey LL. Repair of
traumatic aortic rupture: a 25-year experience. Arch Surg 2000;135:913-8 ;
discussion 919.
401. Jahromi AS, Kazemi K, Safar HA, Doobay B, Cina CS. Traumatic rupture of the
thoracic aorta: cohort study and systematic review. J Vasc Surg 2001;34:1029-34.
402. Tatou E, Steinmetz E, Jazayeri S, Benhamiche B, Brenot R, David M. Surgical
outcome of traumatic rupture of the thoracic aorta. Ann Thorac Surg 2000;69:70-3.
403. Galloway AC, Schwartz DS, Culliford AT, Ribakove GH, Grossi EA, Esposito RA,
et al. Selective approach to descending thoracic aortic aneurysm repair: a ten-year
experience. Ann Thorac Surg 1996;62:1152-7.
404. Pate JW, Fabian TC, Walker WA. Acute traumatic rupture of the aortic isthmus:
repair with cardiopulmonary bypass. Ann Thorac Surg 1995;59:90-8 ; discussion
98-9.
405. Tiraboschi R, Terzi A, Merlo M, Giordano D, Procopio AM, Sonzogni V, et al.
Traumatic rupture of the aortic isthmus: our experience with 23 cases. Ital Heart J
2000;1(suppl):1047-51.
406. Bouchart F, Bessou JP, Tabley A, Litzler PY, Haas-Hubscher C, Redonnet M, et al.
Acute traumatic rupture of the thoracic aorta and its branches: results of surgical
management. Ann Chir 2001;126:201-11.
407. Leach WR, Sundt TM 3rd, Moon MR. Oxygenator support for partial left-heart
bypass. Ann Thorac Surg 2001;72:1770-1.
408. Karmy-Jones R, Carter Y, Meissner M, Mulligan MS. Choice of venous cannula-
tion for bypass during repair of traumatic rupture of the aorta. Ann Thorac Surg
2001;71:39-41; discussion 41-2.
409. Westaby S. Hypothermic thoracic and thoracoabdominal aneurysm operation: a
central cannulation technique. Ann Thorac Surg 1992;54:253-8.
410. Kouchoukos NT, Wareing TH, Izumoto H, Klausing W, Abboud N. Elective
hypothermic cardiopulmonary bypass and circulatory arrest for spinal cord protec-
tion during operations on the thoracoabdominal aorta. J Thorac Cardiovasc Surg
1990;99:659-64.
411. von Oppell UO, Dunne TT, De Groot MK, Zilla P. Traumatic aortic rupture:
twenty-year meta-analysis of mortality and risk of paraplegia. Ann Thorac Surg
1994;58:585-93.
412. Hoffman JW Jr, Gilbert TB, Cardarelli MG, Downing SW. Nonheparinized partial
374 Curr Probl Surg, March 2004
cardiopulmonary bypass for repair of traumatic aortic rupture. J Extra Corpor
Technol 2002;34:172-4.
413. Forbes AD, Ashbaugh DG. Mechanical circulatory support during repair of
thoracic aortic injuries improves morbidity and prevents spinal cord injury. Arch
Surg 1994;129:494-7; discussion 497-8.
414. Cowley RA, Turney SZ, Hankins JR, Rodriguez A, Attar S, Shankar BS. Rupture
of thoracic aorta caused by blunt trauma: a fteen-year experience. J Thorac
Cardiovasc Surg 1990;100:652-60 ; discussion 660-1.
415. Wahl WL, Michaels AJ, Wang SC, Dries DJ, Taheri PA. Blunt thoracic aortic
injury: delayed or early repair? J Trauma 1999;47:254-9 ; discussion 259-60.
416. Schmid FX, Philipp A, Link J, Zimmermann M, Birnbaum DE. Hybrid manage-
ment of aortic rupture and lung failure: pumpless extracorporeal lung assist and
endovascular stent-graft. Ann Thorac Surg 2002;73:1618-20.
417. Dake MD, Miller DC, Semba CP, Mitchell RS, Walker PJ, Liddell RP. Translu-
minal placement of endovascular stent-grafts for the treatment of descending
thoracic aortic aneurysms. N Engl J Med 1994;331:1729-34.
418. Kato N, Hirano T, Ishida M, Shimono T, Cheng SH, Yada I, et al. Acute and
contained rupture of the descending thoracic aorta: treatment with endovascular
stent grafts. J Vasc Surg 2003;37:100-5.
419. Lachat M, Pfammatter T, Witzke H, Bernard E, Wolfensberger U, Kunzli A, et al.
Acute traumatic aortic rupture: early stent-graft repair. Eur J Cardiothorac Surg
2002;21:959-63.
420. Fujikawa T, Yukioka T, Ishimaru S, Kanai M, Muraoka A, Sasaki H, et al.
Endovascular stent grafting for the treatment of blunt thoracic aortic injury.
J Trauma 2001;50:223-9.
421. Orford VP, Atkinson NR, Thompson K, Milne PY, Campbell WA, Roberts A, et al.
Blunt traumatic aortic transection: the endovascular experience. Ann Thorac Surg
2003;75:106-12.
422. Borsa JJ, Hoffer EK, Karmy-Jones R, Fontaine AB, Bloch RD, Yoon JK, et al.
Angiographic description of blunt traumatic injuries to the thoracic aorta with
specic relevance to endograft repair. J Endovasc Ther 2002;9(suppl 2):II-84-91.
423. Mattison R, Hamilton IN Jr, Ciraulo DL, Richart CM. Stent-graft repair of acute
traumatic thoracic aortic transection with intentional occlusion of the left subcla-
vian artery: case report. J Trauma 2001;51:326-8.
424. Fattori R, Napoli G, Lovato L, Russo V, Pacini D, Pierangeli A, et al. Indications
for, timing of, and results of catheter-based treatment of traumatic injury to the
aorta. Am J Roentgenol 2002;179:603-9.
425. Rousseau H, Soula P, Perreault P, Bui B, Janne dOthee B, Massabuau P, et al.
Delayed treatment of traumatic rupture of the thoracic aorta with endoluminal
covered stent. Circulation 1999;99:498-504.
426. Hoffer EK, Karmy-Jones R, Bloch RD, Meissner MH, Borsa JJ, Nicholls SC, et al.
Treatment of acute thoracic aortic injury with commercially available abdominal
aortic stent-grafts. J Vasc Intervent Radiol 2002;13:1037-41.
427. Thompson CS, Rodriguez JA, Ramaiah VG, DiMugno L, Shaque S, Olsen D, et
al. Acute traumatic rupture of the thoracic aorta treated with endoluminal stent
grafts. J Trauma 2002;52:1173-7.
428. Lowe LH, Bulas DI, Eichelberger MD, Martin GR. Traumatic aortic injuries in
children: radiologic evaluation. Am J Roentgenol 1998;170:39-42.
Curr Probl Surg, March 2004 375
429. Spouge AR, Burrows PE, Armstrong D, Daneman A. Traumatic aortic rupture in
the pediatric population: role of plain lm, CT and angiography in the diagnosis.
Pediatr Radiol 1991;21:324-8.
430. Hormuth D, Cefali D, Rouse T, Cutshaw J, Turner W Jr, Rodman G Jr. Traumatic
disruption of the thoracic aorta in children. Arch Surg 1999;134:759-63.
431. Striffeler H, Leupi F, Kaiser G, Althaus U. Traumatic rupture of the thoracic aorta
in childhood with special reference to the therapeutic strategy. Eur J Pediatr Surg
1993;3:50-3.
432. Patel K, Allen K, Hinrichs C, Jihayel A, Donahoo JS. Traumatic aortic arch injury.
Ann Thorac Surg 2002;73:666.
433. Carter YM, Karmy-Jones R, Aldea GS. Delayed surgical management of a
traumatic aortic arch injury. Ann Thorac Surg 2002;73:294-6.
434. Verbeke SJ, De Waele JJ, Hesse UJ, Vermassen FE, De Roose J. Severe
complications after nonoperative treatment of traumatic aortic rupture. J Trauma
2002;53:784-6.
435. Mull DH, Jessen ME. Alternate surgical approach for posttraumatic thoracic aortic
pseudoaneurysm. J Trauma 1997;42:546-8.
436. Graham JM, Feliciano DV, Mattox KL, Beall AC Jr. Innominate vascular injury.
J Trauma 1982;22:647-55.
437. Dosios TJ, Salemis N, Angouras D, Nonas E. Blunt and penetrating trauma of the
thoracic aorta and aortic arch branches: an autopsy study. J Trauma 2000;49:696-703.
438. Mattox KL, Feliciano DV, Burch J, Beall AC Jr, Jordan GL Jr, De Bakey ME. Five
thousand seven hundred sixty cardiovascular injuries in 4459 patients: epidemio-
logic evolution 1958 to 1987. Ann Surg 1989;209:698-705 ; discussion 706-7.
439. Rosenberg JM, Bredenberg CE, Marvasti MA, Bucknam C, Conti C, Parker FB Jr.
Blunt injuries to the aortic arch vessels. Ann Thorac Surg 1989;48:508-13.
440. Pretre R, Murith N, Faidutti B. Lesions of the supra-aortic arterial trunks by closed
trauma. Ann Chir 1994;48:836-44.
441. Hemmila MR, Hirschl RB, Teitelbaum DH, Austin E, Geiger JD. Tracheobronchial
avulsion and associated innominate artery injury in blunt trauma: case report and
literature review. J Trauma 1999;46:505-12.
442. Letsou G, Gertler JP, Baker CC, Hammond GL. Blunt innominate injury: a report
of three cases. J Trauma 1989;29:104-8.
443. Weiman DS, McCoy DW, Haan CK, Pate JW, Fabian TC. Blunt injuries of the
brachiocephalic artery. Am Surg 1998;64:383-7.
444. Natali J, Maraval M, Kieffer E, Petrovic P. Fractures of the clavicle and injuries of
the subclavian artery. J Cardiovasc Surg (Torino) 1975;16:541-7.
445. Stover S, Holtzman RB, Lottenberg L, Bass TL. Blunt innominate artery injury.
Am Surg 2001;67:757-9.
446. Kendall KM, Burton JH, Cushing B. Fatal subclavian artery transection from
isolated clavicle fracture. J Trauma 2000;48:316-8.
447. Rozycki GS, Tremblay L, Feliciano DV, Tchorz K, Hattaway A, Fountain J, et al.
A prospective study for the detection of vascular injury in adult and pediatric
patients with cervicothoracic seat belt signs. J Trauma 2002;52:618-23 ; discussion
623-4.
448. Miller FB, Richardson JD, Thomas HA, Cryer HM, Willing JJ. Role of CT in
diagnosis of major arterial injury after blunt thoracic trauma. Surgery 1989;106:
596-603.
376 Curr Probl Surg, March 2004
449. Gavant ML, Menke PG, Fabian T, Flick PA, Graney MJ, Gold RE. Blunt traumatic
aortic rupture: detection with helical CT of the chest. Radiology 1995;197:125-33.
450. Nicholls SC. Management of great vessel injury. In: Karmy-Jones R, Nathens A,
Stern E, editors. Thoracic Trauma and Critical Care. Boston, Mass: Kluwer
Academic Publishers; 2002. 303-13.
451. Becker GJ, Benenati JF, Zemel G, et al. Percutaneous placement of a balloon-
expandable intraluminal graft for life-threatening subclavian arterial hemorrhage. J
Vasc Intervent Radiol 1991;2:225-9.
452. Desai M, Baxter AB, Karmy-Jones R, Borsa JJ. Potentially life-saving role for
temporary endovascular balloon occlusion in atypical mediastinal hematoma. Am J
Roentgenol 2002;178:1180.
453. May J, White G, Waugh R, Yu W, Harris JH. Transluminal placement of a
prosthetic graft-stent device for treatment of a subclavian artery aneurysm. J Vasc
Surg 1993;18:1056-9.
454. Madoff DC, Brathwaite CE, Manzione JV, Bilaniuk JW, Giron F, Char D, et al.
Coexistent rupture of the proximal right subclavian and internal mammary arteries
after blunt chest trauma. J Trauma 2000;48:521-4.
455. McCoy DW, Weiman DS, Pate JW, Fabian TC, Walker WA. Subclavian artery
injuries. Am Surg 1997;63:761-4.
456. Keene JJ, Edwards FH. Cardiopulmonary support for emergent innominate artery
repair complicating tracheal surgery. J Extra Corpor Technol 2001;33:114-6.
457. Shah PM, Ivatury RR, Babu SC, Nallathambi MN, Clauss RH, Stahl WM. Is limb
loss avoidable in civilian vascular injuries? Am J Surg 1987;154:202-5.
458. Kelly JP, Webb WR, Moulder PV, Moustouakas NM, Lirtzman M. Management of
airway trauma, II: combined injuries of the trachea and esophagus. Ann Thorac
Surg 1987;43:160-3.
459. Snelleman JA, Tadros T, van der Lugt A, Bogers AJ. Traumatic rupture of the
innominate and left common carotid artery: case report. J Trauma 2002;52:571-2.
460. Wernly JA, Campbell CD, Replogle RL. Traumatic avulsion of the innominate and
left carotid arteries: successful repair. J Thorac Cardiovasc Surg 1982;84:392-7.
461. Cordova J, Scott WJ. Repair of combined traumatic rupture of the brachiocephalic
trunk and left common carotid artery by using hypothermic circulatory arrest.
J Trauma 1999;47:790-2.
462. Ruebben A, Merlo M, Verri A, Rossato D, Savio D, Muratore P, et al. Combined
surgical and endovascular treatment of a traumatic pseudo-aneurysm of the
brachiocephalic trunk with anatomical anomaly. J Cardiovasc Surg (Torino)
1997;38:173-6.
463. Berguer R, Kline RA. Methods for reconstruction of proximal subclavian artery
lesions: transposition and bypass. Semin Vasc Surg 1996;9:98-104.
464. Edwards JD, Sapienza P, Lefkowitz DM, Thorpe PE, McGregor PE, Agrawal DK,
et al. Posttraumatic innominate artery aneurysm with occlusion of the common
carotid artery at its origin by an intimal ap. Ann Vasc Surg 1993;7:368-73.
465. Richardson JD, Smith JM, Grover FL, Arom KV, Trinkle JK. Management of
subclavian and innominate artery injuries. Am J Surg 1977;134:780-4.
466. Mohlala ML, Vanker EA, Ballaram RS. Internal mammary artery haematoma. S
Afr J Surg 1989;27:136-8.
467. Cheng SG, Glickerman DJ, Karmy-Jones R, Borsa JJ. Traumatic sternomanubrial
Curr Probl Surg, March 2004 377
dislocation with associated bilateral internal mammary artery occlusion. Am J
Roentgenol 2003;180:810.
468. Bowles BJ, Teruya T, Belzberg H, Rivkind AI. Blunt traumatic azygous vein injury
diagnosed by computed tomography: case report and review of the literature.
J Trauma 2000;49:776-9.
469. Snyder CL, Eyer SD. Blunt chest trauma with transection of the azygous vein: case
report. J Trauma 1989;29:889-90.
470. Thurman RT, Roettger R. Intrapleural rupture of the azygous vein. Ann Thorac
Surg 1992;53:697-9.
471. Mills SA, Johnston FR, Hudspeth AS, Breyer RH, Myers RT, Cordell AR. Clinical
spectrum of blunt tracheobronchial disruption illustrated by seven cases. J Thorac
Cardiovasc Surg 1982;84:49-58.
472. Kinsella TJ, Johnsrud LW. Traumatic rupture of the bronchus. J Thorac Surg
1947;16:571.
473. Baumgartner F, Sheppard B, de Virgilio C, Esrig B, Harrier D, Nelson RJ, et al.
Tracheal and main bronchial disruptions after blunt chest trauma: presentation and
management. Ann Thorac Surg 1990;50:569-74.
474. Marty-Ane CH, Picard E, Jonquet O, Mary H. Membranous tracheal rupture after
endotracheal intubation. Ann Thorac Surg 1995;60:1367-71.
475. Kiser AC, OBrien SM, Detterbeck FC. Blunt tracheobronchial injuries: treatment
and outcomes. Ann Thorac Surg 2001;71:2059-65.
476. Lee RB. Traumatic injury of the cervicothoracic trachea and major bronchi. Chest
Surg Clin North Am 1997;7:285-304.
477. Velly JF, Martigne C, Moreau JM, Dubrez J, Kerdi S, Couraud L. Post traumatic
tracheobronchial lesions: a follow-up study of 47 cases. Eur J Cardiothorac Surg
1991;5:352-5.
478. Taskinen SO, Salo JA, Halttunen PE, Sovijarvi AR. Tracheobronchial rupture due
to blunt chest trauma: a follow-up study. Ann Thorac Surg 1989;48:846-9.
479. Martin de Nicolas JL, Gamez AP, Cruz F, Diaz-Hellin V, Marron M, Martinez JI,
et al. Long tracheobronchial and esophageal rupture after blunt chest trauma: injury
by airway bursting. Ann Thorac Surg 1996;62:269-72.
480. Kirsh MM, Orringer MB, Behrendt DM, Sloan H. Management of tracheobronchial
disruption secondary to nonpenetrating trauma. Ann Thorac Surg 1976;22:93-101.
481. Grover FL, Ellestad C, Arom KV, Root HD, Cruz AB, Trinkle JK. Diagnosis and
management of major tracheobronchial injuries. Ann Thorac Surg 1979;28:384-91.
482. Wood D. Tracheobronchial trauma. In: Karmy-Joes R, Nathens A, Stern E, editors.
Thoracic Trauma and Critical Care. Boston, Mass: Kluwer Academic Publishers;
2002. 109-22.
483. Wintermark M, Schnyder P, Wicky S. Blunt traumatic rupture of a mainstem
bronchus: spiral CT demonstration of the fallen lung sign. Eur Radiol 2001;11:
409-11.
484. Nishiumi N, Maitani F, Yamada S, Kaga K, Iwasaki M, Inokuchi S, et al. Chest
radiographic assessment of tracheobronchial disruption associated with blunt chest
trauma. J Trauma 2002;53:372-7.
485. Ferretti GR, Thony F, Bosson JL, Pison C, Arbib F, Coulomb M. Benign
abnormalities and carcinoid tumors of the central airways: diagnostic impact of CT
bronchography. Am J Roentgenol 2000;174:1307-13.
486. Kawamoto S, Yuasa M, Tsukuda S, Heshiki A. Bronchial atresia: three-dimen-
378 Curr Probl Surg, March 2004
sional CT bronchography using volume rendering technique. Radiat Med 2001;19:
107-10.
487. Regel G, Seekamp A, Aebert H, Wegener G, Sturm JA. Bronchoscopy in severe
blunt chest trauma. Surg Endosc 1990;4:31-5.
488. Karlikaya C, Ucan E, Oto O, Akkoclu A, Cimrin A, Akpinar O. Successful brin
glue repair of iatrogenic bronchial rupture. Respir Med 1993;87:397-8.
489. Rossbach MM, Johnson SB, Gomez MA, Sako EY, Miller OL, Calhoon JH.
Management of major tracheobronchial injuries: a 28-year experience. Ann Thorac
Surg 1998;65:182-6.
490. Beal SL, Pottmeyer EW, Spisso JM. Esophageal perforation following external
blunt trauma. J Trauma 1988;28:1425-32.
491. Kemmerer DL, Hilgenkamp KH. Patterns of injury during motor vehicle accidents.
Neb Med J 1988;73:3-9.
492. Niezgoda JA, McMenamin P, Graeber GM. Pharyngoesophageal perforation after
blunt neck trauma. Ann Thorac Surg 1990;50:615-7.
493. Steinman E, Utiyama EM, Pires PW, Birolini D. Traumatic wounds of the
esophagus. Rev Hosp Clin Fac Med Sao Paulo 1990;45:127-31.
494. Ayabe H, Tsuji H, Akamine S, Tagawa Y, Kawahara K, Tomita M. Combined
transection of the trachea and esophagus following cervical blunt trauma. Thorac
Cardiovasc Surg 1993;41:193-5.
495. Wilson RF. Esophagus. In: Maull KI, Rodriguez A, Wiles III CE, editors.
Complications in Trauma and Critical Care. Philadelphia, Pa: WB Saunders; 1996.
347-58.
496. Sartorelli KH, McBride WJ, Vane DW. Perforation of the intrathoracic esophagus
from blunt trauma in a child: case report and review of the literature. J Pediatr Surg
1999;34:495-7.
497. Micon L, Geis L, Siderys H, Stevens L, Rodman GH Jr. Rupture of the distal
thoracic esophagus following blunt trauma: case report. J Trauma 1990;30:214-7.
498. Komborozos VA, Belenis I, Malagari C, Yannopoulos P. Delayed traumatic rupture
of the thoracic aorta into the esophagus. Dis Esophagus 1998;11:66-7.
499. Weigelt JA, Thal ER, Snyder WH 3rd, Fry RE, Meier DE, Kilman WJ. Diagnosis
of penetrating cervical esophageal injuries. Am J Surg 1987;154:619-22.
500. Glatterer MS Jr, Toon RS, Ellestad C, McFee AS, Rogers W, Mack JW, et al.
Management of blunt and penetrating external esophageal trauma. J Trauma
1985;25:784-92.
501. Flowers JL, Graham SM, Ugarte MA, Sartor WM, Rodriquez A, Gens DR, et al.
Flexible endoscopy for the diagnosis of esophageal trauma. J Trauma 1996;40:
261-5 ; discussion 265-6.
502. Nesbitt JC, Sawyers JL. Surgical management of esophageal perforation. Am Surg
1987;53:183-91.
503. Karmy-Jones R, Wagner JW, Lewis JW Jr. Esophageal injury. In: Trunkey DD,
Lewis FR, editors. Current Therapy of Trauma, 4th ed. St. Louis, Mo: Mosby;
1999. 209-16.
504. Karmy-Jones R. Thoracic trauma. In: Corson JD, Williamson RCN, editors.
Surgery. London, England: Mosby; 2001. 2-8 1-2:8.14.
505. Braun RA, Goldware RR, Flores LM. Cervical tracheal transsection with esopha-
geal stula. Arch Otolaryngol 1972;96:67-71.
Curr Probl Surg, March 2004 379
506. Chapman ND, Braun RA. The management of traumatic tracheo-esophageal stula
caused by blunt chest trauma. Arch Surg 1970;100:681-4.
507. Reed WJ, Doyle SE, Aprahamian C. Tracheoesophageal stula after blunt chest
trauma. Ann Thorac Surg 1995;59:1251-6.
508. Sorensen VJ. Diaphragmatic Injuries. In: Karmy-Jones R, Nathens A, Stern E,
editors. Thoracic Trauma and Critical Care. Boston, Mass: Kluwer Academic
Publishers; 2002. 261-6.
509. Mansour KA. Trauma to the diaphragm. Chest Surg Clin North Am 1997;7:373-83.
510. Sharma OP. Pericardio-diaphragmatic rupture: ve new cases and literature review.
J Emerg Med 1999;17:963-8.
511. Sharma OP. Traumatic diaphragmatic rupture: not an uncommon entity: personal
experience with collective review of the 1980s. J Trauma 1989;29:678-82.
512. Shah R, Sabanathan S, Mearns AJ, Choudhury AK. Traumatic rupture of dia-
phragm. Ann Thorac Surg 1995;60:1444-9.
513. Karmy-Jones R, Carter Y, Stern E. The impact of positive pressure ventilation on
the diagnosis of traumatic diaphragmatic injury. Am Surg 2002;68:167-72.
514. Villavicencio RT, Aucar JA, Wall MJ Jr. Analysis of thoracoscopy in trauma. Surg
Endosc 1999;13:3-9.
515. Lindsey I, Woods SD, Nottle PD. Laparoscopic management of blunt diaphrag-
matic injury. Aust N Z J Surg 1997;67:619-21.
516. Ochsner MG, Rozycki GS, Lucente F, Wherry DC, Champion HR. Prospective
evaluation of thoracoscopy for diagnosing diaphragmatic injury in thoracoabdomi-
nal trauma: a preliminary report. J Trauma 1993;34:704-9; discussion 709-10.
517. Maekawa T, Yabuki K, Satou K, Mishima G, Tamasaki Y, Watabe S, et al. A
patient with a traumatic right diaphragmatic hernia occurring 4 years after
sustaining injury: statistical observations of a delayed diaphragmatic hernia caused
by uncomplicated injury in Japan. Nippon Geka Hokan 1997;66:116-25.
518. Hegarty MM, Bryer JV, Angorn IB, Baker LW. Delayed presentation of traumatic
diaphragmatic hernia. Ann Surg 1978;188:229-33.
519. Reber PU, Schmied B, Seiler CA, Baer HU, Patel AG, Buchler MW. Missed
diaphragmatic injuries and their long-term sequelae. J Trauma 1998;44:183-8.
520. Sattler S, Canty TG Jr, Mulligan MS, Wood DE, Scully JM, Vallieres E, et al.
Chronic traumatic and congenital diaphragmatic hernias: presentation and surgical
management. Can Respir J 2002;9:135-9.
521. Menezes SL, Chagas PS, Macedo-Neto AV, Santos VC, Rocco PR, Zin WA.
Suture or prosthetic reconstruction of experimental diaphragmatic defects. Chest
2000;117:1443-8.
522. Skerrit SJ. The diagnosis of ventilator-associated pneumonia. In: Karmy-Jones R,
Nathens A, Stern E, editors. Thoracic Trauma and Critical Care. Boston, Mass:
Kluwer Academic Publishers; 2002. 397-402.
523. Shammas NW, Kaul S, Stuhlmuller JE, Ferguson DW. Traumatic mitral insuf-
ciency complicating blunt chest trauma treated medically: a case report and review.
Crit Care Med 1992;20:1064-8.
380 Curr Probl Surg, March 2004

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