76 TRAUMA AND BLAST INJURIES
D. DANTE YEH, MD • JARONE LEE, MD, MPH
THORACIC TRAUMA Tracheobronchial Injuries
Introduction Diaphragm Injuries
Indications for Resuscitative Thoracotomy BLAST LUNG INJURY
Indications for Urgent Thoracotomy Introduction
Indications for Delayed Thoracotomy Primary Blast Injuries
Thoracic Cage Injuries Secondary Blast Injuries
Lung Parenchyma Injuries Tertiary Blast Injuries
THORACIC TRAUMA
INTRODUCTION
Among trauma victims, thoracic trauma is the second most
common cause of death in the field and the third most
common cause of death in patients who make it to the
hospital. In civilian trauma, the most common mechanism
is blunt trauma and the most frequently encountered inju-
ries (i.e., hemothorax and pneumothorax) are seen in 20%
of patients.1 The majority require only tube thoracos-
tomy for definitive treatment; however, up to 15% of these
patients will require operative intervention,1 whether
immediate (resuscitative), urgent, or delayed. Overall mor-
tality in patients with thoracic trauma is about 10%, with
a low Glasgow Coma Scale score exerting the strongest
influence on mortality.1 Additional predictors of poor out-
comes include increasing age, mechanism of blunt injury,
increasing number of ribs fractured, and concomitant long
bone extremity fractures.1
INDICATIONS FOR RESUSCITATIVE
THORACOTOMY
Patients who arrive without signs of life may benefit from
emergency department thoracotomy (EDT) or “resuscitative”
thoracotomy depending on the amount of time elapsed
since the loss of vital signs (<15 minutes for penetrating
trauma; <10 minutes for blunt trauma).2,3 The goal of this
procedure is to restore spontaneous circulation by rapid
repair of intrathoracic injuries or release of pericardial tam-
ponade, and occlusion of the descending thoracic aorta to
divert perfusion to the brain and heart. Internal cardiac
massage with injection of intracardiac medications may
also be indicated. In cases of bronchovenous air embolism,
clamping of the pulmonary hilum prevents further propa-
gation. Because resuscitative thoracotomy should always
proceed to the operating room for definitive repair, it should
not be attempted without a surgeon immediately available.
Rhee and colleagues reported that the overall survival rate
after EDT is 7.4%, with a survival rate of 15% among all
patients with penetrating injuries and 35% among patients
with penetrating cardiac injuries.4 On the contrary, sur-
vival rates are very low (2%) after blunt traumatic arrest.4
1354
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Quaternary Blast Injuries
Physics of the Blast Wave
Management of Blast Lung Injury
Initial Management and Diagnostic
Approach to the Thoracic Trauma
Patient
It is important to perform an initial cardiac ultrasound,
because EDT can be considered futile if asystole is the pre-
senting rhythm and pericardial tamponade is absent.3 In
patients with appropriate indications, aggressive efforts are
justified, because functional long-term outcomes in survi-
vors are excellent. More than half of survivors are dis-
charged home from the hospital, and more than 75% have
normal cognition, are ambulatory, and have no evidence of
posttraumatic stress disorder.5 However, inappropriate EDT
results in no survival benefit, wasted use of resources, and
exposure of health care workers to needle-stick and bone
fragment injuries.6
INDICATIONS FOR URGENT THORACOTOMY
Commonly accepted indications for urgent thoracotomy
include any of the following: initial chest drain output of
1500 mL; greater than 1500 mL output in the first 24
hours after injury; more than 200 mL bloody output per
hour for 3 consecutive hours; massive air leak (present
during all phases of respiration, associated with inability to
reexpand the lung or affecting ventilation secondary to loss
of tidal volume); or hypotension.7 Rarely, a patient has
sudden cardiovascular collapse or new neurologic symp-
toms, typically after the patient is placed on positive pres-
sure ventilation, that are consistent with air embolism and
require urgent thoracotomy.
INDICATIONS FOR DELAYED THORACOTOMY
Delayed thoracotomy is performed several days after injury
in stable patients, usually for retained hemothorax, trapped
lung, persistent air leak, or rib fixation (discussed later).
THORACIC CAGE INJURIES
Rib Fractures
Rib fractures are seen in 10% of hospitalized trauma
patients.8,9 The morbidity of rib fracture pain is underap-
preciated; one third of patients require hospitalization for
pain control, and pneumonia develops in another third of
these patients.10 The true incidence of rib fractures is likely
higher, in that, a supine chest radiograph is, at best, about

Table 76-1  Chest Wall Trauma Scoring System
Age (years) Number of Rib Fractures
<45 = 1 point <3 = 1 point
45-65 = 2 points 3-5 = 2 points
>65 = 3 points >5 = 3 points
  Score: _____   Score: ______
Pulmonary Contusion Bilateral Rib Fractures
None = 0 points No = 0 points
Mild = 1 point Yes = 2 points
Severe = 2 points   Score: ______
Bilateral = 3 points
  Score: _____
Total Score: _____
From Pressley CM, Fry WR, Philp AS, Berry SD, Smith RS. Predicting outcome
of patients with chest wall injury. Am J Surg 204:910–914, 2012.
50% sensitive for detecting rib fractures. Chest computed
tomography (CT) (eFig. 76-1) is much more sensitive and
can also evaluate for other occult injuries.8 In general, ribs
tend to fracture at their weakest structural point (the pos-
terior angle) or directly at the point of impact.11 They are
rarely the sole injury, and 50% of patients with rib fractures
have other significant injuries.10 In a patient with lower rib
injury (9th through 12th), abdominal solid organ injury
(spleen or liver) should be ruled out.
Pressley and colleagues developed a simple scoring
system based on initial clinical findings (age, number of
fractured ribs, severity of pulmonary contusion [PC], unilat-
eral vs. bilateral rib fractures), to predict the likelihood of
requiring mechanical intubation or intensive care unit (ICU)
admission12 (Table 76-1). The authors found that a patient
with a score of 7 or 8 had a high probability of death, need
for ICU admission, and a need for mechanical ventilation.
Similarly, a score of greater than 5 predicted the need for a
longer hospital stay and prolonged mechanical ventilation.
Other studies found that an increasing number of rib frac-
tures correlates to increasing ICU length of stay (LOS), hos-
pital LOS, and mortality.13,14
Treatment for the vast majority of patients with rib frac-
tures is supportive care, consisting of aggressive pain
control and pulmonary rehabilitation. Deep breathing facil-
itates clearance of secretions to reduce the incidence of
pneumonia. Analgesic options include oral analgesics
(including opioids), intermittent intravenous analgesics,
patient-controlled analgesia, thoracic epidural analgesia
(TEA), intrapleural blocks, intercostal blocks, and thoracic
paravertebral blocks.15 Non-opioid analgesic options include
acetaminophen, nonsteroidal anti-inflammatory drugs
(including ketorolac), anticonvulsants such as gabapentin,
and topical lidocaine patches.16 Numerous small, single-
center trials have reported that pain control with TEA, com-
pared with intravenous opioids, results in superior outcomes
as measured by less pain, improved pulmonary function,
fewer ventilator days, fewer infections, fewer pulmonary
complications, shorter ICU LOS, and shorter hospital
LOS.17-24 Furthermore, TEA may also attenuate the postin-
jury inflammatory response.22,25At present, TEA is the
preferred analgesic modality for pain secondary to blunt
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76  •  Trauma and Blast Injuries 1355
Age 65 Age 65
40
Mortality as percentage of patients
35
30
25
20
15
10
5
0
1–2 3–4 5–6 7
Number of rib fractures
Figure 76-1  Relationship between the number of rib fractures and
mortality. In a retrospective study of patients admitted to trauma centers,
mortality increased with increasing number of rib fractures, an easily quan-
tifiable measure of trauma severity. At each number of rib fractures, mor-
tality for those older than 65 years was greater than that for those younger
than 65. (From Stawicki SPG, Michael D, Hoey, Brian A, et al: Rib fractures in
the elderly: a marker of injury severity. J Am Geriatr Soc 52:805–808, 2004.)
thoracic injury.26 However, TEA is underused, with studies
reporting less than 30% TEA use in eligible patients.27 Epi-
dural analgesia is not without risk, though, and side effects
include hypotension, epidural hematoma, urinary reten-
tion, and epidural abscess.
Interestingly, a recent pooled meta-analysis did not
find any benefit of TEA for duration of mechanical ventila-
tion, ICU LOS, hospital LOS, or mortality.28 For epidural
analgesia to be of benefit, appropriate patient selection is
paramount. Although absolute number of fractured ribs is
predictive of the need for TEA, it is important to examine
the patient carefully to determine whether pain is severe
enough to cause respiratory embarrassment. In fact, one
review reported that epidural analgesia was associated
with increased complications and prolonged LOS in older
patients.29
Another underused analgesic option is the thoracic para-
vertebral block (TPVB) or paravertebral catheterization,
which is easy to learn, has a greater than 90% success rate,
and has a low incidence of side effects.30,31 When successful,
TPVB has been shown to improve pain scores and pulmo-
nary function tests.32 TPVB provides unilateral pain relief
and thus is usually used only for patients with unilateral rib
fractures; however, it is also useful when there are contra-
indications to TEA, such as coagulopathy, spinal fractures,
or altered mental status.
In addition to pain control, a formalized multidisciplinary
pathway that includes aggressive respiratory therapy and
nutritional support has been shown to decrease ventilator
days, LOS, infectious morbidity, and mortality among
patients older than age 45 years with more than four frac-
tured ribs.33
Older patients with rib fractures are at especially high risk
for complications: 15% require intubation, and pneumonia
develops in up to 31%34-36 (Fig. 76-1). In patients older than
age 45 years, morbidity sharply increases when more than
four ribs are fractured.37 Bulger and coworkers reported
that patients older than 65 years with fractured ribs have
double the morbidity and mortality rates compared with
1356 PART 3  •  Clinical Respiratory Medicine
younger patients with similar injuries.27 Bedside vital capac-
ity measurement can predict hospital LOS and identify
those patients requiring discharge to an extended care
facility.38
Nonunion results in a small percentage of rib fractures
and can manifest as chronic pain and discomfort.10 Typi-
cally, follow-up demonstrates that a significant proportion
of patients have chronic persistent pain and impairment of
both work and personal life.39 In one study, patients with rib
fractures had more disabilities at 30 days after injury than
did patients with chronic medical illness. These patients
with rib injuries missed an average of 70 days of work.40
Two months after injury, more than 75% of patients with
rib fractures reported some form of disability.41 Interest-
ingly, the single most important predictive factor for long-
term disability after rib injury was the initial intensity of
pain. The total number of rib fractures and injury on both
sides was not predictive.41
Flail Chest.  A flail chest, also known as “stoved-in” or
“crushed” chest, is the most severe form of blunt thoracic
injury (see Chapter 98). The mortality associated with
flail chest is up to 40%.42 Radiographically, it is defined
as three or more consecutive ribs fractured in at least two
locations. Clinically, a flail chest manifests as paradoxical
incursion (rather than excursion) of the “floating segment”
of chest wall during inspiration (Videos 76-1 and 76-2).
Due to the significant energy transfer required to produce
this injury, flail chest is almost universally accompanied
by PC.
The management of flail chest has evolved over the past
half century. Previously, it was believed that the paradoxical
chest wall movement was the cause of the respiratory
failure and hypoxia. Now, it is understood that the respi-
ratory impairment is due to the underlying pulmonary
parenchymal injury. Historically, efforts were focused on
correcting the paradoxical motion through external stabi-
lization (“sandbagging”), and later, “internal pneumatic
stabilization” (i.e., positive pressure ventilation).43,44 Hence,
in the mid-twentieth century, the predominant treatment
method for all patients with flail chest was mechanical ven-
tilation. Starting in the mid 1970s, some physicians found
that these patients could be adequately managed without
ventilatory support. It was at this time that it was recog-
nized that the underlying PC rather than the chest wall
instability was the driving factor in outcome.45 Currently,
less than half of patients with flail chest require mechanical
ventilation.46 Abnormal gas exchange, not chest wall move-
ment, should drive the decision to mechanically ventilate a
patient with flail chest.47
In the modern management of flail chest, optimal pain
control is paramount. According to the Eastern Association
for the Surgery of Trauma practice management guide-
lines, TEA is the preferred pain treatment modality in the
treatment of flail chest.48 When an epidural catheter is con-
traindicated, TPVB may be considered. If mild to moderate
respiratory compromise is present, a trial of noninvasive
ventilation in conjunction with TEA may be considered
before proceeding to endotracheal intubation. However, in
the absence of respiratory embarrassment, mechanical
ventilation to treat paradoxical chest wall motion is not
recommended.
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Surgical fixation of the “floating” chest wall segment has
been practiced for decades in Europe and Asia, but is under­
used in the United States, likely due to a combination of
relative unfamiliarity with the procedure itself and unfa-
miliarity with the evidence supporting the procedure. In a
survey of trauma surgeons, orthopedic surgeons, and tho-
racic surgeons, only 26% had ever performed or assisted on
the procedure and most were unaware of the published
randomized trials supporting its use.49 European and Asian
studies report clinical benefit, yet the quality of evidence is
poor and consists mainly of small, observational single-
center studies.50-52 To date, three randomized controlled
studies and a meta-analysis evaluating surgical fixation in
patients with flail injury have been published supporting rib
fracture fixation.43 Tanaka and colleagues reported that
patients who underwent internal fixation of their fractured
ribs benefited by less mechanical ventilation, lower inci-
dence of pneumonia, shorter ICU LOS, improved pulmo-
nary function, and quicker return to employment.53
Granetzny and coworkers also reported decreased need for
mechanical ventilation, shorter ICU LOS, and lower inci-
dence of pneumonia in patients randomized to operation.54
Most recently, Marasco and associates demonstrated
decreased ICU LOS and decreased need for tracheostomy in
patients randomized to operative repair of flail chest, with
no difference in duration of invasive mechanical ventila-
tion.46 The optimal time for operative intervention is cur-
rently unknown and no trial has compared surgical fixation
with modern nonoperative management with TEA and
chest physiotherapy. An economic analysis based on
reported incidences of complications and outcomes con-
cluded that, despite the additional cost of surgery, rib fixa-
tion for flail chest remained cost-effective compared with
nonoperative management.55
Numerous techniques are described for rib fracture fixa-
tion, including the use of wire suture, staples, metal or
absorbable plates, and screws.10 A case-control study
reported by de Moya and colleagues concluded that rib frac-
ture fixation significantly decreased the need for analge-
sia.56 Infection of rib fixation hardware is uncommon,
reported to be approximately 2%.10
Rescue therapies such as single lung ventilation and
high-frequency oscillatory ventilation may be considered
when traditional mechanical ventilation fails to improve
oxygenation. However, there is no evidence to support
routine use of these treatment modalities.
The long-term outcome of flail chest managed nonopera-
tively is marked by disability, with 70% of patients reporting
dyspnea and more than 50% reporting chronic chest wall
pain.48,57 Less than half of patients are able to return to
work.58
Sternal Fractures.  The most common cause of sternal
fracture is motor vehicle crash (eFig. 76-2).59 The presence
of sternal fractures has traditionally been considered a
marker of injury severity, especially in previous decades
when seatbelt use was not as widespread. As such, some
advocate for hospital admission and close monitoring to
rule out other serious injuries, such as blunt cardiac injury.
Others report that sternal fracture, ipso facto, is not a sig-
nificant cause of morbidity or mortality, and many believe
that morbidity is mainly attributable to other associated

injuries.59-62 With increasing seatbelt use, the incidence
of sternal fractures has increased while mortality has
decreased.63,64
In the initial workup of a patient with sternal fracture, it
is important to rule out a blunt cardiac injury with a 12-lead
electrocardiogram and serum troponin level. Arrhythmias,
ST changes, heart block, signs of ischemia, and elevated
troponin levels are considered abnormal screening tests and
should be followed by a confirmatory echocardiogram;
normal findings on electrocardiogram and initial troponin
level essentially exclude the diagnosis of blunt cardiac
injury.65 Nuclear medicine studies are not useful in the diag-
nostic workup of blunt cardiac injury. As in rib fractures,
adequate pain control is paramount in the treatment
of sternal fractures. Sternal fracture fixation is rarely
indicated.
Clavicle Fractures.  The clavicle is an S-shaped bone that
acts as a strut between the shoulder and the axial skeleton.
It protects the apex of the lung, brachial plexus, and sub-
clavian vessels. Clavicle fractures follow direct impact to the
extremity or chest, and account for 44% of all fractures to
the shoulder girdle.66
Fractures of the middle third are the most common,
accounting for 69% to 81% of all clavicular fractures.66
Diagnosis of clavicle fractures requires some type of
imaging, usually radiography, although many are only
visualized on CT. Special radiographic views can be ordered
to improve the evaluation for subtle fractures, fracture dis-
placement, or sternoclavicular joint dislocations (eFigs.
76-3 and 76-4). These views include axillary views,
45-degree cephalic tilt, or a serendipity view, which is a
40-degree cephalic tilt.
Treatment generally is nonoperative, with a sling or
figure-of-eight brace, and 2 to 6 weeks of immobilization,
as well as avoidance of heavy lifting and contact sports for
4 to 6 months. Operative treatment is indicated for all open
fractures, skin tenting that will result in an open fracture,
and any neurovascular compromise. A recent Cochrane
meta-analysis of eight trials involving 555 patients exam-
ined the difference between conservative treatment and
surgical fixation among patients with fractures of the
middle third of the clavicle. Unfortunately, due to heteroge-
neity between the studies and overall high risk of bias, no
strong conclusions can be made and the authors concluded
that the decision to operate must be made on a case-by-case
basis.67
LUNG PARENCHYMA INJURIES
Pulmonary Contusion
PC is a common injury, with an incidence of 30% to 75%
in patients suffering blunt thoracic injury48 and up to 17%
of all trauma admissions. PC is most common after a blunt
mechanism of injury, but can also manifest adjacent to a
missile tract through lung parenchyma. At the microscopic
level, the contused lung displays edema, alveolar and intra-
parenchymal hemorrhage, and atelectasis, which results in
intrapulmonary shunting, ventilation-perfusion mismatch,
and decreased lung compliance. This manifests as hypox-
emia, hypercarbia, and increased work of breathing. The
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76  •  Trauma and Blast Injuries 1357
full effects of PC may not be obvious immediately; however,
clinically significant PC becomes apparent within 24 hours.
The natural history of PC is progressive dysfunction over
the first few days and resolution within a week.68
Severe PC can produce systemic effects. Animal studies
demonstrate that after unilateral contusion, there is capil-
lary leak in both ipsilateral and contralateral sides. Both
lungs develop increased edema and accumulation of inflam-
matory cells.69 Inflammatory cytokines are increased both
locally and systemically, and there is evidence of global
immune dysfunction.70-73 Additionally, PC primes the
immune system for an exaggerated response to a subse-
quent second hit, such as infection69,74 (Fig. 76-2). Trauma
patients with PC have twice the rate of ventilator-associated
pneumonia as those without PC.75 At 6 years after injury,
more than half of patients with PC have evidence of lung
fibrosis on CT scan,76 and long-term lung function can be
compromised.39
Because not all PCs are clinically significant, several
authors have attempted to identify factors predictive of
outcome. De Moya and associates developed a simple scoring
system, combining the initial CT findings, Glasgow Coma
Score, and number of fractured ribs, to predict the need for
Lung contusion
Permeability injury to
type I epithelial cells
TLRs
PMN
activation
Alv MØ
↑Chemokines
activation
Surfactant Apoptosis of
dysfunction type II cells
from
Injury to inhibitors
type II cells
?
Activation of
fibroblasts
Figure 76-2  Inflammatory effects following pulmonary contusion. In
the diagram, the potential interactions of the cells and mediators of the
innate inflammatory response to contusion are shown. While this inflam-
matory mechanism may amplify the injury of the contusion, it may also
provide potential targets for therapeutic intervention. TLRs, Toll-like recep-
tors. (From Raghavendran K, Notter RH, Davidson BA, et al: Lung contusion:
inflammatory mechanisms and interaction with other injuries. Shock 32:122–
130, 2009.)
1358 PART 3  •  Clinical Respiratory Medicine

mechanical ventilation. Interestingly, in this study, less than
one third of all PCs were evident on the initial chest radio-
graph (eFig. 76-5).77 Other authors have questioned the
significance of “occult” PC (i.e., apparent only on CT, eFig.
76-6). In a prospective study of 255 patients with PC,
Deunk and colleagues reported that patients with occult
PC fared no worse than those without PC, while those with
PC seen on both chest radiograph and chest CT scan had
significantly worse outcomes.78 Others have attempted to
correlate PC size (as a percentage of total lung volume) with
outcomes. Studies have demonstrated that patients with PC
volume greater than 20% of total lung volume are at
increased risk for requiring mechanical ventilation, devel-
oping pneumonia, and developing acute respiratory distress
syndrome (ARDS).79
At this time there is no well-supported intervention to
treat PC, and management consists mainly of supportive
care and avoidance of iatrogenic injury. Steroids are not
recommended and prophylactic antibiotics are strongly dis-
couraged. Four decades ago, Trinkle and coworkers recog-
nized that crystalloid administration increased PC size
while diuresis decreased PC size.80 Pharmacologic therapies
being investigated include arginine vasopressin and
dexmedetomidine.81A recent animal study reported that
dexmedetomidine infusion in a PC model improved hemo-
dynamic parameters, decreased inflammatory infiltration,
limited the extent of lung damage, and abrogated pulmo-
nary edema.82 In patients with early, severe hypoxemia
(arterial PO2/FIO2 <200), a trial of noninvasive ventilation
may be attempted in order to decrease the need for intuba-
tion; however, the development of pneumothorax must be
carefully monitored.83,84 In animal studies, the application
of positive end-expiratory pressure has been shown to
decrease the size of PCs. Small clinical studies have reported
that recruitment maneuvers are successful in improving
aeration (“open lung” strategy).85 In patients with PC, the
use of airway pressure release ventilation has been reported
to decrease the incidence of ventilator-associated pneumo-
nia; however, experience and evidence is limited.75 For
severe, unilateral PC, lung isolation ventilation may be con-
sidered.86 The use of rescue therapies such as high-frequency
oscillatory ventilation, surfactant administration, prone
positioning, and extracorporeal membrane oxygenation for
the treatment of PC is poorly studied and considered experi-
mental at this time.87-90
In the management of PC, the patient should be resusci-
tated to maintain signs of adequate tissue perfusion. Once
this has been achieved, however, meticulous attention
should be paid to the avoidance of excessive fluid adminis-
tration, to the point of using a pulmonary artery catheter
if necessary to help guide diuretic therapy.48 Aggressive pul-
monary toilet and adequate analgesia are paramount in
preventing pneumonia.
Pulmonary Laceration
Pulmonary laceration reflects tearing of the pulmonary
parenchyma that disrupts the alveolar walls. Pulmonary
lacerations result from several mechanisms, such as alter-
nate compression and decompression of the chest wall or
from a sudden, rapid increase in intrathoracic pressure
with a closed glottis leading to high intra-alveolar pressure
that produces shearing of pulmonary parenchymal tissue.
Alternatively, pulmonary laceration may also result from
direct puncture of lung tissue by a fractured rib, missile, or
stab wound, or from shearing of lung tissue fixed by previ-
ously formed pleural adhesions. The disrupted pulmonary
tissue fills with blood and/or air and manifests on thoracic
imaging as one or more pulmonary parenchymal cavities
(eFig. 76-7), appearing as gas-fluid levels, frequently with
surrounding pulmonary consolidation and ground-glass
opacity related to hemorrhage and atelectasis.
While only a small fraction of patients with thoracic
injury ultimately require urgent thoracotomy, of those
that proceed to surgery, about one third may require lung
resection, usually to remove severely injured lung tissue,
to control hemorrhage, or to remove irreparable proxi-
mal bronchus injuries.91 The extent of resection can
range from simple, nonanatomic “wedge” resection, to
formal anatomic lobectomy, to the extremely morbid pneu-
monectomy. For the majority of penetrating injuries, lung-
sparing techniques such as simple suture or “tractotomy”
are sufficient91-93 (Fig. 76-3). Not surprisingly, there is a

A B
Figure 76-3  Lung-sparing “tractotomy” in which the tract of the penetrating injury is rapidly opened and injured vessels and bronchi ligated.
A, The stapling device is advanced through the orifices of the entry and exit wound and is then closed and fired to staple the lung on either side and to
open the tract (“tractotomy”) for visualization of the injured vessels and bronchi. B, The tractotomy exposes the bleeding vessels, which are then selectively
ligated. The tractotomy approach preserves lung by avoiding wedge resection, lobectomy, or pneumonectomy. (From Asensio JA, Demetriades D, Berne
JD, et al: Stapled pulmonary tractotomy: a rapid way to control hemorrhage in penetrating pulmonary injuries. J Am Coll Surg 185:486–487, 1977.)

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stepwise increase in mortality with increasing extent of
lung resection for trauma: wedge resection (19%), lobec-
tomy (27%), and pneumonectomy (53%).
While most healthy patients can tolerate a wedge resec-
tion or lobectomy, pneumonectomy imposes a tremendous
physiologic burden and patients may succumb to right ven-
tricular failure. Using a porcine model, Cryer and colleagues
demonstrated that pulmonary vascular resistance increases
up to 500% within 4 hours after pneumonectomy.94 Post-
operative complications in survivors are common, and
include pneumonia, bronchopleural fistula, empyema, or
erosion into the pulmonary artery.
Bronchopleural Fistula
A bronchopleural fistula is a direct connection between the
bronchus and atmosphere by way of the pleural space and
tube thoracostomy. While most heal spontaneously, a per-
sistent bronchopleural fistula may seriously impair the
ability to ventilate a patient secondary to loss of tidal volume
through the fistula. It is believed that air flowing through
the fistula impedes healing and therefore medical therapies
are aimed at reducing bronchopleural fistula flow.
Nonsurgical treatments include minimizing airway
pressures (via lower tidal volumes, positive end-expiratory
pressure, and inspiratory time), application of positive intra-
pleural pressure through the chest tube, isolated contralat-
eral lung ventilation, dependent positioning of the side
with the bronchopleural fistula, and use of high-frequency
oscillatory ventilation.95-97 Bronchoscopy is useful to iden-
tify the injury directly (proximal) or the affected bronchial
segment (distal). A balloon is used to occlude the segments
sequentially until a reduction in air leak is noted. Once the
affected bronchus is identified, agents such as silver nitrate,
cyanoacrylate-based agents, gelatin, fibrin, and even fishing
weights have been applied to occlude the bronchial segment
and close the fistula.98-102 Bronchopleural fistula refractory
to medical therapy for more than 7 days may require
pleurodesis or operative intervention.
Miscellaneous
Pneumothorax.  Pneumothorax, air within the pleural
cavity, is present in 40% and 20% of blunt and penetrating
thoracic trauma patients, respectively (see Chapter 81).103
The clinical consequence of pneumothorax ranges from
asymptomatic to the most life-threatening manifestation,
“tension” pneumothorax, whereby progressive air trapping
in the thorax results in a contralateral mediastinal shift,
compression or kinking of the superior vena cava/inferior
vena cava, and a precipitous drop in preload and cardiac
output (Fig. 76-4). Clinically, this form of “obstructive”
shock manifests as hypotension and hypoxia, and should be
treated with immediate thoracic decompression, either
with needle thoracostomy or tube thoracostomy. Current
recommendations from the Advanced Trauma Life Support
program104 are to insert the needle in the mid-clavicular
line at the second intercostal space; however, some authors
have questioned the efficacy of inserting the needle in this
location and recommend instead inserting the needle in
the mid-axillary line at the fifth intercostal space because
of decreased chest wall thickness in this location.105 Addi-
tionally, lateral needle insertion avoids potentially life-
threatening hemorrhagic complications such as laceration
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76  •  Trauma and Blast Injuries 1359
Figure 76-4  Tension pneumothorax. The free air in the left hemithorax
is associated with a shift of the mediastinum into the right chest, depres-
sion of the hemidiaphragm, and widening of the intercostal spaces. Hypo-
tension follows due to impairment of venous return to the right heart, both
by the high intrathoracic pressure and perhaps mechanical compression
or kinking of the superior vena cava. Immediate decompression is required.
of the internal mammary artery, subclavian artery, or pul-
monary artery.106,107 Others recommend inserting a chest
tube at the outset instead of a needle due to frequent failure
rates associated with the latter.108
An open pneumothorax, or “sucking” chest wound, is a
special form of pneumothorax whereby a defect in the chest
wall permits air entry through the wound with diaphrag-
matic movement. If the size of the wound approaches the
size of the trachea, this may significantly hamper ventila-
tion, because air preferentially enters through the wound.109
Before operative repair, the wound should be covered with
a flutter (“Heimlich”) valve or an occlusive dressing with
one side open to allow air egress.
For less severe pneumothorax, the decision to drain the
pleural cavity should be made based on the degree of respi-
ratory compromise and the potential for enlargement to a
tension pneumothorax. Managed without tube thoracos-
tomy, it is estimated that the average pneumothorax absorp-
tion rate is 1.25% per day.110 Clinical significance of a
pneumothorax depends not only upon the absolute size of
the pneumothorax, but also on the preinjury condition of
the patient (e.g., presence of chronic obstructive pulmo-
nary disease) and other associated injuries. Chest tube
insertion is not without risk, and modern series report a
15% to 20% incidence of tube-related complications, with
an additional 15% requiring more chest tubes after subop-
timal placement111,112 (Fig. 76-5). One rare but potentially
fatal complication following pneumothorax drainage is
reexpansion pulmonary edema113 (Fig. 76-6). Prophylactic
antibiotics for the duration of dwell time of the chest tube
are not recommended.114
An “occult” pneumothorax is defined as a pneumothorax
which can only be visualized on chest CT scan; it is not
1360 PART 3  •  Clinical Respiratory Medicine

detectable on chest x-ray nor is it suspected on clinical

Figure 76-5  Tube thoracostomy placement. Diagram showing the
placement of a thoracostomy tube in the mid-axillary line; the tube is
directed anteriorly for drainage of a pneumothorax. (From Van Way CW III,
Buerk CA: Surgical skills in patient care. St. Louis, 1978, CV Mosby.)
examination (Fig. 76-7). “Occult” pneumothorax is present
in up to 12% of seriously injured patients115,116 and, in an
era of liberal CT scanning, comprise more than 50% of all
pneumothoraces diagnosed in injured patients.117 Supine
portable chest radiographs have been consistently shown to
be only 50% sensitive for the detection of pneumothorax.
Ultrasonography has been shown to be more sensitive than
chest radiography for the detection of pneumothorax.118-127
Subtle findings on supine chest radiograph suggestive of
pneumothorax include the “deep sulcus” sign (Fig. 76-8).
The management of “occult” pneumothorax has evolved
over the past 3 decades from mandatory tube thoracostomy
for all “occult” pneumothoraces, progressing to selective
drainage for only those patients undergoing positive pres-
sure ventilation,128 to selective drainage for all patients.115,128
In a large, multicenter observational study involving 569
patients with “occult” pneumothorax across 16 trauma

A B
Figure 76-6  Reexpansion pulmonary edema. A, A pneumothorax can be seen on the right with a subtotal lung collapse. B, The same patient after
expansion of the lung following placement of a thoracostomy tube. Peripheral right upper lobe opacity is now present, consistent with the development
of reexpansion injury and edema in that region of lung. (From Malota M, Kowarik MC, Bechtold B, Kopp R: Reexpansion pulmonary edema following a post-
traumatic pneumothorax: a case report and review of the literature. World J Emerg Surg 6:32, 2011.)

A B
Figure 76-7  Occult pneumothorax. A, Anterosuperior supine chest radiograph of blunt trauma victim. There is no obvious pneumothorax. B, CT scan
reveals a large occult left-sided pneumothorax. (From Ball CG, Hameed SM, Evans D, et al: Occult pneumothorax in the mechanically ventilated trauma patient.
Can J Surg 46:373–379, 2003.)

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Figure 76-8  Deep sulcus sign on chest radiograph. In this supine
patient, a pneumothorax on the left can be recognized by the depth of the
diaphragmatic sulcus on the left compared with the right (arrows). There
is also lucency overlying the left hemidiaphragm, representing air anterior
and lateral to the left hemidiaphragm and seen as an air-tissue interface
(arrowheads).
centers, Moore and colleagues reported that 21% required
immediate tube thoracostomy. Of the remaining patients,
however, only 6% overall failed observation and required
tube thoracostomy for pneumothorax enlargement, respi-
ratory distress, or development of hemothorax. In this
series, 14% of patients on positive pressure ventilation
required tube thoracostomy. Importantly, no patient who
failed observation experienced an adverse event resulting
from delay of chest drainage.129
After drainage, standard management of the chest tube
entails serial chest radiographs to document resolution of
the pneumothorax. A bedside clinical examination should
be performed to rule out an ongoing air leak, which is
usually secondary to persistent alveolar-pleural fistula.130
Air leaks may be graded according to increasing severity:
forced expiratory, expiratory, inspiratory, and continuous.
The vast majority of posttraumatic air leaks in stable
patients are forced expiratory (coughing) or expiratory and
almost all resolve with time and patience.130 Typically, the
chest tube is placed at 20 cm H2O suction and “advanced”
to water seal before removal. It is customary to obtain a
chest radiograph after transitioning to water seal and after
chest tube removal to monitor for pneumothorax reappear-
ance. Pneumothorax recurs after chest tube removal in
11% to 24% of cases; however, if the pneumothorax is
small and stable and the patient is asymptomatic, observa-
tion is frequently successful.131,132 It is common practice to
allow up to 24 hours between changes in chest tube man-
agement, however Schulman and associates reported that
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76  •  Trauma and Blast Injuries 1361
changes may be made at shorter intervals, because clini-
cally significant recurrent pneumothorax appeared within
3 hours.133
Accumulating evidence suggests that smaller 14- to
16-French “pigtail” catheters are equally effective as tradi-
tional large-bore chest tubes (28- to 40-French), require
less dissection, can be placed by the Seldinger technique,
and may be less painful.134,135
Hemothorax.  A hemothorax is blood in the pleural cavity
that can cause a wide range of symptoms from minor dis-
comfort to life-threatening situations (eFig. 76-8). In
general, hemothorax evident on supine chest radiograph
should be drained immediately, because these typically rep-
resent volumes of at least 200 mL. Similar to “occult” pneu-
mothorax, “occult” hemothoraces also exist and the
decision to drain an “occult” hemothorax should take into
consideration the amount of blood present and the morbid-
ity of chest tube insertion.
The initial treatment of hemothorax is tube thoracos-
tomy. Based on the volume of initial output, the next step
may be either urgent thoracotomy or observation. If the
source of bleeding is the pulmonary parenchyma, hemosta-
sis is usually achieved by complete expansion of the lung
because the pulmonary circulation is a low pressure circuit.
Bleeding from lacerated intercostal or internal mammary
arteries is likely to persist and may require urgent thora-
cotomy for definitive hemostasis. Indications for urgent tho-
racotomy include hemodynamic instability, 1500 mL initial
chest tube output, greater than 1500 mL over a 24-hour
period, or greater than 200 mL/hr blood drainage for 3
consecutive hours.136 Hemothorax secondary to major tho-
racic vascular structures (e.g., aorta, pulmonary artery)
almost universally requires emergent thoracotomy for
hemodynamic instability.
Assuming adequate drainage and resolution of the
hemothorax, it is customary to “advance” the chest tube to
water seal before removal, similar to the chest tube manage-
ment for a simple pneumothorax (see earlier). An additional
factor to consider is the daily volume of bloody chest tube
drainage. While there are no standardized guidelines or rec-
ommendations, the majority of trauma surgeons advance
a chest tube once the daily output decreases to between
100 mL and 300 mL per day.
The evacuation of a hemothorax can be incomplete in up
to 20% of cases and can be frustrating to deal with.132,137,138
Untreated, a stagnant hemothorax may evolve into
empyema or fibrothorax (“trapped lung”), two morbid com-
plications.139 Additional chest tube placement is usually
ineffective for clot evacuation.
Early video-assisted thoracic surgery (VATS) (less than 5
days after injury), compared with delayed operation or
additional chest tubes, has been reported to decrease hospi-
tal LOS and decrease conversion to open thoracotomy.140,141
According to the Eastern Association for the Surgery of
Trauma guidelines, there is level 1 evidence that a retained
hemothorax should be treated with early VATS, and not
insertion of a second chest tube. VATS should be considered
within 3 to 7 days of hospitalization because this reduces
the risk for infection and the requirement for thoracotomy
(level 2 evidence). Retained hemothorax less than 300 mL
by chest CT scan may be observed.142 Currently, intrapleural
1362 PART 3  •  Clinical Respiratory Medicine
700
600
500
Suction volume (mL)
400
300
200
100
0 morbidity associated with delayed repair. Death is usually
0 5 10 15 20
Time (min)
Figure 76-9  Comparison of fluid dynamics between two different sizes of
pleural drains. The smaller drain (19-French, blue) is as effective as the
larger one (28-French, brown) in draining fluid. (From Niinami H, Tabata M,
Takeuchi Y, Umezu M: Experimental assessment of the drainage capacity of
small silastic chest drains. Asian Cardiovasc Thorac Ann 14:223–226, 2006.)
thrombolytics are considered second line treatment after
VATS and can be considered in subacute hemothoraces to
improve drainage.143,144
Over the past decade, there has been a trend toward using
smaller chest tubes for evacuating hemothorax.135 When
comparing the standard 36-French to 40-French chest tube
with 28-French to 32-French tubes, Inaba and colleagues
found that the initial drainage volume and total indwelling
time were similar and there were no differences between
groups in tube-related complications or the need for addi-
tional interventions.145 A recent animal study of flow
dynamics provides even further evidence to support that
smaller tube size is equally effective for hemothorax evacu-
ation. Niinami and coworkers reported that a 19-French
fluted silicone drain is capable of draining 11 L/hour146
(Fig. 76-9). Similarly, Kulvatunyou and colleagues reported
that a 14-French “pigtail” catheter seems to drain blood as
effectively as larger bore traditional chest tubes, with a
similar incidence of complications.147
Chylothorax.  Traumatic chylothorax is an uncommon
entity that results from disruption of the thoracic duct. Chy-
lothorax presents as a milky pleural effusion upon resump-
tion of oral intake and the diagnosis is confirmed by finding
triglyceride levels greater than 110 mg/dL with or without
lymphocytes predominating.148 Initial treatment involves
lung reexpansion and parenteral nutrition, with the possi-
ble addition of octreotide. If these measures fail, thoracic
duct embolization or operative intervention is warranted.149
However, the optimal duration of nonoperative manage-
ment is unknown.
Pneumatocele/Intraparenchymal Hematoma.  Also
termed a posttraumatic pulmonary pseudocyst, a pneumato-
cele is an atraumatic cavitary lesion within the parenchyma
following a pulmonary laceration (eFig. 76-9). Asymptom-
atic patients may be managed expectantly and most resolve
within several weeks. For infectious complications, antibiot-
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ics and CT-guided catheter drainage may be attempted.
Operative resection (VATS or thoracotomy) may be neces-
sary if less invasive measures fail.
TRACHEOBRONCHIAL INJURIES
Tracheobronchial injuries present in one of two ways,
depending upon site, size, and communication with the
pleural cavity: they are either immediately apparent, requir-
ing immediate attention (11%), or they are very subtle and
difficult to diagnose.150,151 Two thirds are unrecognized for
more than 24 hours and, in 10%, there is no evidence of
thoracic injury on physical examination or radiographs.150
In this second group of patients, there is no discernible
25 30 not from the tracheobronchial injury itself, but instead from
fatal injuries to adjacent vascular structures.152 Even with
complete transection, the robust peritracheal connective
tissue can splint the tracheal fragments, maintaining
airway continuity. Blunt force likely injures the tracheo-
bronchial tree by one of three mechanisms: rupture from
tracheal compression against the rigid vertebral column,
rupture from increased airway pressures due to compres-
sion of the chest with a closed glottis, or laceration from
shearing forces.153
The majority of tracheobronchial injuries take place
within 2.5 cm of the carina, with main stem bronchial
injuries comprising the majority (86%).150,153 Clinically, the
patient may have dyspnea (the most common symptom),
hoarseness, stridor, hemoptysis, crepitus, or respiratory dis-
tress. Radiographically, the “fallen lung” sign, first described
by Oh and associates in 1969, is a highly specific finding for
this injury. This sign manifests when the patient has a pneu-
mothorax. When pneumothorax is present without tra-
cheobronchial injury, the lung falls toward the hilum
(central displacement), whereas with tracheobronchial
injury, the transected lung falls away from the hilum
(peripheral displacement) (Fig. 76-10). CT scanning may
demonstrate bronchial wall discontinuity (eFig. 76-10 and
Video 76-3) or mediastinal emphysema. A tracheal or prox-
imal bronchus injury should be suspected with pneumome-
diastinum or with a pneumothorax refractory to chest
drainage. Bronchoscopy is the most effective method of
diagnosis.
Although the treatment for large or life-threatening tra-
cheobronchial injuries is immediate repair, selective intuba-
tion beyond the injury alone (or even observation alone)
may be successful in carefully selected patients with small
or partial thickness injuries.7,154
Delayed complications of unrecognized injury include
bronchopleural fistula, atelectasis, bronchiectasis, and
postobstructive pneumonia as well as more serious sequelae
such as mediastinitis or cervical abscess.
DIAPHRAGM INJURIES
Diaphragmatic injury is a rare but morbid injury, present-
ing in less than 1% of blunt trauma and associated with a
21% overall mortality rate.155 More than 90% are seen after
motor vehicle crashes. Two thirds of diaphragm injuries
develop on the left, perhaps because the liver cushions the
impact on the right side. Because of the significant force
 76  •  Trauma and Blast Injuries 1363

required to rupture the diaphragm, these injuries are almost
universally accompanied by other organ injuries, such as
lung (77%), liver (52%), spleen (32%), and stomach
(19%).155
The physical examination is inaccurate for the diagnosis
of diaphragmatic injuries. For most victims of penetrating
injury, there is no sign unique to diaphragmatic injury. For
patients following blunt trauma, dyspnea and pain are
common but nonspecific. Chest radiography is diagnostic in
fewer than half of those with injury to the left hemidia-
phragm (eFig. 76-11) and in only 17% of those with injury
to the right hemidiaphragm156 (Fig. 76-11). CT scan has a
very high sensitivity for blunt diaphragmatic rupture.
Imaging signs of injury include: a nasogastric tube termi-
nating above the diaphragmatic contour, discontinuity of
the hemidiaphragm, herniation of the viscera into the
thorax (eFig. 76-12), diaphragmatic thickening (eFig.
76-13), the “hump sign,” the “band sign,” the “dependent
viscera sign” (eFig. 76-14), the “collar sign” (eFig. 76-15),
and the “dangling sign.”157,158
All acute diaphragmatic injuries should be surgically
repaired. The natural history of traumatic diaphragmatic
hernias is poorly studied, but it is presumed that the ten-
dency is to enlarge over time, with progressive herniation
of abdominal viscera into the chest due to the negative
intrathoracic pressure and positive intra-abdominal pres-
sure. For left-sided penetrating thoracoabdominal wounds,
if there is no immediate indication for operative exploration,
it is recommended to perform a diagnostic laparoscopy,
because 20% will have diaphragm injuries.159,160

BLAST LUNG INJURY

Figure 76-10  “Fallen lung” sign. Chest radiograph obtained 6 hours after
initial presentation of acute dyspnea in an 8-year-old boy. Bilateral pneu-
mothorax, more prominent on the right, is seen. Pneumomediastinum and
soft tissue emphysema are observed. The right lung is seen to be collapsed
inferior to the hilum (fallen lung sign), usually a sign of complete rupture
of the main bronchus. A thoracostomy tube has been inserted on the right,
yet a large right pneumothorax remains. (From Savas R, Alper H: Fallen lung
sign: radiographic findings. Diagn Interv Radiol 14:120–121, 2008.)
INTRODUCTION
An increasing frequency of terrorist bombing attacks
worldwide has resulted in a large number of civilian blast
injuries.161 Blast victims require a standard trauma workup
as recommended by Advanced Trauma Life Support. Addi-
tionally, such victims may also present with a set of pulmo-
nary injuries unique to the blast mechanism.162
Victims of blast injuries manifest different injuries
depending on the type of the bomb, the location of detona-
tion, and whether the targets were military or civilian. Typi-
cally, military victims have different injuries from civilian
victims. Military personnel are young and healthy, and
usually have body armor that protects their thoracic and
abdominal organs, whereas civilian victims range from
children to older adults and are not wearing body protec-
tion. Thus civilian victims present with more thoracic/lung

A B
Figure 76-11  Hemidiaphragmatic injury in the setting of trauma. A, Right hemidiaphragmatic injury. Frontal chest radiograph shows apparent eleva-
tion of the right hemidiaphragm, generally a nonspecific finding. However, in the setting of trauma, diaphragmatic injury with herniation of the liver into
the thorax manifests similarly, as in this example. B, Left hemidiaphragmatic injury. Frontal chest radiograph shows herniation of the stomach into the
left thorax, consistent with a large tear of the left hemidiaphragm.

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1364 PART 3  •  Clinical Respiratory Medicine
and abdominal injuries than military victims. As a general
rule, blast injury victims suffer multiple blunt and penetrat-
ing injuries, including traumatic amputations. Injuries
from blast detonations are classified into the following cat-
egories: (1) primary; (2) secondary; (3) tertiary; and (4)
quaternary.162
PRIMARY BLAST INJURIES
Primary blast injuries result from overpressure effects of the
blast wave (see later). The blast typically injures organs that
have interfaces between different densities, such as air and
tissue, or water and air. Examples include pulmonary baro-
trauma, tympanic membrane ruptures, gastrointestinal
contusions/perforations, and traumatic amputations. Pre-
viously, tympanic membrane rupture was used as a marker
of severity of illness from the blast wave. However, recent
studies show that tympanic membrane rupture is not a
reliable marker of severity, demonstrating poor sensitivity
and specificity.163 Instead, markers of severe blast injury
include the following: (1) >10% total body surface area
burns; (2) skull/facial fractures; (3) penetrating injuries to
the head/torso.163
SECONDARY BLAST INJURIES
Secondary blast injuries result when penetrating injuries
are caused by flying debris, such as bomb fragments
from the explosive device and fragments of bone and teeth
from the bomber and victims. There are case reports
of these biologic fragments transmitting hepatitis B.164,165
Theoretically, transmission of hepatitis C and HIV are also
possible.
TERTIARY BLAST INJURIES
Tertiary blast injuries result when victims are physically
propelled into hard surfaces by the force of the blast wave.
Crush injuries from falling debris also fit into this category.
QUATERNARY BLAST INJURIES
Quaternary blast injuries encompass all other explosion-
related effects such as burns, asphyxia, radiation poisoning,
toxins, psychological trauma, and exacerbation of underly-
ing medical conditions.
PHYSICS OF THE BLAST WAVE
Explosions result when a chemical reaction transforms a
solid or liquid into gas within a very short time period,
resulting in a massive release of energy. The explosion
releases most of its energy as a “blast wave,” a positive pres-
sure front that travels faster than the speed of sound.166 As
a result, victims feel the blast wave before hearing the explo-
sion. In the open-air, the blast wave behaves in a predictable
manner based on the physics of wave motion.167
Detonations within confined spaces or under water cause
blast waves that are accentuated and deadlier.162,164 Under
these conditions, blast waves are reflected back from sur-
faces with a different density, such as walls or air-water
interfaces. The reflected wave superimposes and amplifies
the outgoing blast wave, causing a higher intensity and
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thus much deadlier blast wave. Furthermore, the blast wave
can reflect back from surfaces at an angle greater than 40
degrees, augmenting the incoming wave and creating a
new blast wave. This phenomenon is known as a “mach
stem formation.”168 Studies have shown that explosions
detonated in corners can result in explosions that are up to
eight times deadlier than explosions in the open air.164
Damage to the human body results when the blast wave
transmits energy directly to the body. This energy is trans-
mitted unevenly through body tissues and, as described,
reflects back upon encountering changes in density. As a
result, the majority of damage is done at interfaces of dif-
ferent tissue densities. For example, pulmonary blast inju-
ries result when the blast wave rapidly changes in amplitude
upon entering and exiting the multiple air- and fluid-filled
structures within the lungs. Other air/tissue interfaces
include the gastrointestinal tract, tympanic membranes,
and extremities, where greatly disparate density planes,
such as joints with air, soft tissue, and bones all reside
within a small space. The mechanisms causing these inju-
ries can be classified physiologically into distinct categories:
(1) spalling forces, (2) implosion forces, and (3) inertia
forces.162,167
Spalling Forces
Spalling forces result when the blast wave displaces
and fragments one tissue into another tissue, usually the
higher density tissue into the lower density tissue. For
example, spalling forces cause the forcible movement of
blood from the capillaries into the alveoli, causing alveolar
hemorrhage.
Implosion Forces
Implosion forces result when the highly compressed edge
of the blast wave enters the victim. This results in gas
that rapidly compresses and reexpands causing injury. For
example, implosion forces cause barotrauma by compress-
ing and reexpanding the air in the alveoli. Furthermore,
this rapid change in air density can cause an air embolism
by entering the circulatory system.
Inertia Forces
Inertia forces result when the blast wave causes the differ-
ent tissue densities to absorb different amounts of energy.
This results in the different tissues moving at different veloc-
ities. The resulting shearing of tissue planes causes massive
injuries, typically traumatic avulsions/amputations.
Blast lung injury results from the combination of all the
forces described above. After the initial damage to the
architecture of the alveoli, pulmonary hemorrhage ensues.
The free hemoglobin in the alveoli leads to the formation
of free radicals, worsening edema and an early inflamma-
tory response.169,170 This leukocyte accumulation and
release of inflammatory cytokines leads to further epithe-
lial cell damage over 12 to 24 hours, as well as endothelial
cell damage over 24 to 56 hours. This inflammatory
cascade results in a lung injury syndrome characteristic
of ARDS.
Histologic examination of the lung damaged by blast
injury reveals perivascular edema, extensive alveolar hem-
orrhage during the first 12 hours, and then further epithe-
lial cell damage and detachment from the basement
membrane.169,170

MANAGEMENT OF BLAST LUNG INJURY
Initial management of patients with blast lung injury
should follow standard local trauma protocols and
Advanced Trauma Life Support teaching. Survivors of the
blast wave with primary blast lung injury have a mortality
rate of 11% and represent a group of patients with very
severe injuries.
Clinical features include shortness of breath, cough,
chest pain, hemoptysis, cyanosis, and tachypnea. Hypox-
emia is a typical finding, but may not develop until after
the first few hours following presentation. One case series
found that only 28% of patients had hypoxemia on initial
presentation.170
All patients with suspected blast lung injury should
receive a chest radiograph as soon as possible. Radiographic
findings of blast injury may include not only the classic “bat
wing” appearance on chest radiograph but also subcutane-
ous emphysema; pneumothorax; pulmonary interstitial
emphysema; pneumopericardium; pneumomediastinum;
and pneumoperitoneum.
The general treatment for primary blast lung injury
patients is similar to the treatment for the ARDS patient.
This includes limiting fluid administration to decrease the
chance of pulmonary edema and the use of low-tidal-
volume “lung-protective” ventilation with permissive hyper-
capnia to minimize peak and plateau airway pressures.171
Refractory cases can be considered for rescue treatments for
ARDS, such as inhaled nitric oxide, inhaled prostaglandins,
and open-lung ventilation strategies. However, caution
should be used when considering extracorporeal membrane
oxygenation. The underlying pathophysiology of blast lung
involves alveolar hemorrhage and, as a result, there are
reports that the required anticoagulation for extracorporeal
membrane oxygenation results in catastrophic pulmonary
hemorrhage.172
In the rare case of air embolism from the blast lung
injury, treatment aims to prevent further air emboli. The
patient is placed in the left lateral decubitus position, with
the head down and feet up in an attempt to contain the air
embolism at the apex of the left ventricle. Peak pressures
during positive-pressure ventilation should be minimized
and hyperbaric therapy considered. The diagnosis is a clini-
cal one because CT scans, echocardiography, and observa-
tion of retinal air bubbles on funduscopic exams are
unreliable.162
Patients that survive blast lung injury typically have
excellent long-term pulmonary outcomes. One study found
that, one year after the injury, survivors had normal pulmo-
nary exams, with minimal pulmonary complications.173
INITIAL MANAGEMENT AND DIAGNOSTIC
APPROACH TO THE THORACIC
TRAUMA PATIENT
The assessment of every trauma patient begins with the
time-honored “ABCs”—airway, breathing, and circulation.
In case of suspected tension pneumothorax, pleural decom-
pression should precede intubation. A complete physical
exam should follow the ABCs, with special attention paid
to the presence of decreased breath sounds, distended
neck veins, subcutaneous emphysema, and upper extrem-
ity pulse or neurologic deficits.
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76  •  Trauma and Blast Injuries 1365
If there is a concern for thoracic injury and the patient
has stable vital signs, workup can begin with a chest radio-
graph and thoracic ultrasound. The ultrasound should be
considered as an extension of the physical examination,
and a careful survey of the pericardium and bilateral tho-
racic cavities should be performed on every patient. Large
or clinically significant pneumothoraces or hemothoraces
should be treated immediately with tube thoracostomy
prior to leaving the trauma bay of the emergency depart-
ment. Depending upon the chest radiograph and ultra-
sound findings, a chest CT scan or bronchoscopy may be
required to delineate injury further.
Key Points
■ The majority of patients with pneumothorax and
hemothorax may be adequately managed by tube tho-
racostomy alone.
■ The cornerstone of treatment for rib fractures and flail
chest is pain control.
■ Pulmonary contusion is a major driver of morbidity
and can cause systemic immune dysfunction.
■ Occult pneumothorax may be safely managed with
observation, even in patients on positive pressure
ventilation.
■ Blast lung injury is a unique form of lung injury,
which is most commonly seen in survivors of closed-
space explosions.
■ The diagnosis of blast lung injury is based on clinical
observations and confirmed by plain chest radiograph.
Lung injury is the leading cause of late blast
mortality.
■ Management of blast lung injury is predominantly
supportive and closely approximates the treatment of
acute respiratory distress syndrome.
Complete reference list available at ExpertConsult.
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cal Decisions in Trauma: resuscitative thoracotomy. J Trauma Acute Care
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ment of a high output bronchopleural fistula: a case report. Can J
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Hernandez G, Fernandez R, Lopez-Reina P, et al: Noninvasive ventilation
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 76  •  Trauma and Blast Injuries 1365.e1

eFIGURE IMAGE GALLERY

eFigure 76-1  Blunt thoracic traumatic injury: rib fracture. Axial

enhanced chest CT scan shows displaced right-sided rib fractures (arrows).
(Courtesy Michael Gotway, MD.)

eFigure 76-2  Blunt thoracic traumatic injury: manubrial fracture. Axial

chest CT scan shows a fracture line (arrow) through the manubrium, result-
ing from a motor vehicle collision. (Courtesy Michael Gotway, MD.)

A B
eFigure 76-3  Blunt thoracic traumatic injury: sternoclavicular dislocation. A, Frontal chest radiograph of a patient who fell from height shows subtle
displacement of the medical head of the right clavicle (arrow); compare with the normally positioned left clavicular head. B, Coronal enhanced chest CT
scan displayed in bone windows shows superior dislocation of the medial head of the right clavicle (arrow). (Courtesy Michael Gotway, MD.)

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1365.e2 PART 3  •  Clinical Respiratory Medicine

eFigure 76-4  Blunt thoracic traumatic injury: sternoclavicular dislocation. Axial chest CT scan in a patient following a motor vehicle collision shows
posterior dislocation of the right clavicular head (arrow). Note the normally positioned left clavicular head (arrowhead) and the normal sternoclavicular
joint space (*). (Courtesy Michael Gotway, MD.)

A B
eFigure 76-5  Blunt thoracic traumatic injury: pulmonary contusion on chest radiograph. A, Frontal chest radiograph performed at emergency room
presentation in a patient following a motor vehicle collision shows homogeneous peripheral left lung consolidation (arrow), consistent with contusion.
B, Frontal chest radiograph performed 24 hours following presentation (A) shows significant improvement in the left lung contusion (arrow). (Courtesy
Michael Gotway, MD.)

eFigure 76-6  Blunt thoracic traumatic injury: pulmonary contusion on chest CT scan. Axial chest CT scan performed in a patient following blunt
traumatic thoracic injury shows homogeneous, nonsegmental, peripheral left upper lobe ground-glass opacity and consolidation (arrowheads), typical of
pulmonary contusion. (Courtesy Michael Gotway, MD.)

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 76  •  Trauma and Blast Injuries 1365.e3

A B C D
eFigure 76-7  Blunt thoracic traumatic injury: pulmonary laceration. A, Frontal chest radiograph performed in a patient following a motor vehicle
collision shows right lower lobe consolidation containing an air-fluid level (arrows). B–D, Axial chest CT scan displayed in lung windows shows numerous
right lower lobe areas of cavitation (arrows) associated with surrounding consolidation, consistent with pulmonary laceration. (Courtesy Michael Gotway, MD.)

eFigure 76-8  Blunt thoracic traumatic injury: hemothorax. Axial chest CT scan shows a left pleural effusion containing a masslike area of high attenu-
ation (arrows), representing retracting clot within a hemothorax. (Courtesy Michael Gotway, MD.)

A B
eFigure 76-9  Blunt thoracic traumatic injury: hematoma with pneumatocele development. A, Axial chest CT scan performed in a patient following
blunt traumatic thoracic injury shows a left upper lobe mass (arrows) with surrounding lucency, the latter consistent with cavitation. The material within
the cavity is blood, consistent with hematoma. B, Axial chest CT displayed in lung windows performed 3 weeks following (A) shows evacuation of the
contents of the left upper lobe cavity, revealing a thin-walled cyst (arrows). This lesion spontaneously closed over the ensuing month, consistent with a
pneumatocele. (Courtesy Michael Gotway, MD.)

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1365.e4 PART 3  •  Clinical Respiratory Medicine

eFigure 76-10  Blunt thoracic traumatic injury: tracheobronchial injury. Coronal chest CT displayed in lung windows performed in a patient following
a high-speed motor vehicle collision shows extensive subcutaneous emphysema and pneumomediastinum, both hallmarks of airway injury. The left
mainstem bronchus is fractured (arrows), with gas collecting around the area of airway injury. The associated video (Video 76-3) shows the extensive
pneumomediastinum, subcutaneous emphysema, and medial left apical pneumothorax as well as multifocal lung parenchymal injures. (Courtesy Michael
Gotway, MD.)

A B
eFigure 76-11  Blunt thoracic traumatic injury: diaphragmatic injury on chest radiography. A, Front chest radiograph obtained in a patient after a
motor vehicle collision shows intrathoracic herniation of the stomach (arrows). B, Frontal chest radiograph obtained following chest CT, for which oral
contrast was administered, shows the contrast filling the intrathoracic stomach (arrows). (Courtesy Michael Gotway, MD.)

eFigure 76-12  Blunt thoracic traumatic injury: diaphragmatic injury presenting as intrathoracic visceral herniation. Axial chest CT scan performed
in a patient following blunt traumatic injury shows intrathoracic herniation of the spleen (S) as well as other contents of the left upper quadrant, including
the colon (arrow), consistent with a very large left diaphragmatic tear. (Courtesy Michael Gotway, MD.)

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 76  •  Trauma and Blast Injuries 1365.e5

eFigure 76-13  Blunt thoracic traumatic injury: diaphragmatic injury presenting as diaphragmatic thickening (the “thick crus” sign). Axial chest
CT scan performed in a patient following blunt traumatic injury shows thickening of the right diaphragmatic crus (arrows), due to retraction of this
structure following right diaphragm injury. Compare the right diaphragm crus thickness with the normal left diaphragm crus (arrowhead). (Courtesy Michael
Gotway, MD.)

A B
eFigure 76-14  Blunt thoracic traumatic injury: diaphragmatic injury presenting as the “dependent viscera” sign. A, Normal appearance of the
thoracoabdominal junction. Note the abdominal contents are positioned within the central portion of the image at this level, with the thoracic contents
positioned peripherally. B, Axial chest CT scan performed in a patient following blunt traumatic injury shows that the abdominal viscera (stomach and
left upper quadrant fat, arrows) rests against the posterior chest wall. Normally, as shown in (A), the lung parenchyma and pleura occupy this location.
The positioning of abdominal viscera against the posterior chest wall near the thoracoabdominal junction at chest CT is referred to as the “dependent
viscera” sign and represents intrathoracic visceral herniation, usually due to fairly large diaphragmatic tears. (Courtesy Michael Gotway, MD.)

A B
eFigure 76-15  Blunt thoracic traumatic injury: diaphragmatic injury presenting as the “collar” sign. A, Axial enhanced chest CT scan shows focal
constriction of the stomach (arrowheads) as it enters the thorax through a small left hemidiaphragmatic tear (arrows, left hemidiaphragm). B, Coronal
reformatted CT image shows the focal constriction of the stomach as it passes through the small diaphragmatic defect (arrowheads) to advantage; this
focal constriction is referred to as the “collar” sign (arrow, left hemidiaphragm). (Courtesy Michael Gotway, MD.)

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1366 PART 3  •  Clinical Respiratory Medicine

Marasco SF, Davies AR, Cooper J, et al: Prospective randomized controlled
trial of operative rib fixation in traumatic flail chest. J Am Coll Surg
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Mowery NT, Gunter OL, Collier BR, et al: Practice management guidelines
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Nirula R, Mayberry JC: Rib fracture fixation: controversies and technical
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