Trauma caused by explosions traditionally has been divided into the injury caused by the direct effect of the blast wave (primary injuries); the effects caused by other objects that are accelerated by the explosive wave, (secondary injuries); the effects caused by movement of the victim (tertiary injuries); and miscellaneous effects caused by the explosion or explosives.
High-Order Explosives. High-order explosives are chemical materials that have
an extremely high reaction rate. This reaction often is called a detonation.
Examples of high-order explosives include nitroglycerin, dynamite, C-4, picric
acid, Semtex, ammonium nitrate fuel oil mixture (ANFO), trinitrotoluene (TNT),
and pentaeruthrotetranitrate (PETN).
When an HE detonates, it is converted almost instantaneously into a gas at very
high pressure and temperature. For example, the major ingredient in Composition
C-4 (Cyclotrimethylenetrinitramine or RDX [Royal Demolition eXplosive]) can
generate an initial pressure of more than 4 million pounds per square inch
(4x10E6 PSI).13 These high pressure gases rapidly expand from the original
volume and generate a marked pressure wave—the blast wave that moves outward in
all directions. The result is a sudden shattering blow to the immediate
surroundings.
HEs further are categorized as primary and secondary high explosives. The
primary HE is very sensitive, can be detonated very easily, and generally is
used only in primary and electrical detonators. Secondary HEs are less
sensitive, require a high energy shock wave to achieve detonation, and generally
are safer to handle.
The blast wave refers to an intense rise in pressure—often called over
pressure—that is created by the detonation of a high explosive
This increase in pressure can be so abrupt that it can shatter materials—also
known as a shock wave. This effect is termed brisance and varies from one HE to
another. Because the explosive gases continue to expand outward, the pressure
wave rapidly deteriorates into an acoustic wave. Until the wave deteriorates
enough to completely engulf the body simultaneously, tissue damage will depend
on both the magnitude of the pressure spike and the duration of the force
(represented by the area under the curve).
A blast wave that would cause only modest injury in the open can be lethal if
the victim is in a confined area or near a reflecting surface such as a solid
wall or a building.9 If the pressure wave is near a solid barrier, the pressure
exerted at the reflecting surface may be many times that of the incident blast
wave.
Low-Order Explosives. LEs are designed to burn and subsequently release energy
relatively slowly. These explosives often are called propellants because the
most common use is to propel a projectile through a barrel. The principal
military uses for LEs are as propellants and in fuses. Typical improvised LEs
include pipe bombs, gunpowder, black powder, and petroleum-based bombs such as
Molotov cocktails or gasoline tankers. Since LEs do not form shock waves, they
do not have the quality of brisance.
Three Possible Mechanisms of Injury of Primary Blast Injury. The first mechanism
of injury usually described as the etiology of primary blast injury is the
implosion of gas-filled spaces as the high pressure blast wave compresses
them.18,19 This theory states that the organs that are most vulnerable to blast
injury are those containing air because the air readily is compressed. Hollow
organs are compressed and disrupted by the rapid external pressure increase. The
resulting force causes shearing of vascular beds, ear damage, pulmonary
contusions, pneumothorax, and gastrointestinal (GI) hemorrhage. In some cases,
the force of a pressure wave can be significant enough that it forces air into a
blood vessel, creating air emboli. There isn’t enough time during the passage of
the overpressure phase of the blast wave for gas to transfer from the lungs to
the outside world through the trachea.20
The second possible major mechanism of primary blast injury often is termed
spalling. This is thought to occur when a blast wave moves from a dense medium
such as water to a less dense medium such as air. This often is compared to the
effect of striking the outside of a rusty bucket with a hammer and watching the
flakes of rust fly off the inside of the bucket. In human tissues, the transfer
of reflected blast injury through the dense substrates such as muscle and liver
into the less dense material of the GI tract and lungs may cause spalling.
Spalling also is believed to occur when the blast wave transits from the rib
cage into the lung.
The third possible mechanism of primary blast injury is the inertial effect
related to the differences in tissue density and speed of the blast wave through
the tissues of different densities. This may be the most important effect of the
blast injury and currently is thought to be the major cause of primary blast
injuries. The differences in speed of movement result in shearing and tearing
forces expressed as a stress wave propagated into the underlying tissues.21,22
The resulting forces exceed the tensile strength of the material and cause
shearing of vascular beds, pulmonary contusions, and GI hemorrhages.23
The true mechanism of primary blast injury likely is some combination of these
theoretical mechanisms. Of these, the shearing and tearing forces appear to fit
best. Primary blast injury is common in the ear, the respiratory tract, and the
GI tract.
Ear Damage. Of the three organ systems, the ear is the most easily damaged, but
it also is the easiest to protect. The structures of the ear are designed to
collect and magnify sounds, so that the tympanic membrane moves with the sounds.
Unfortunately, the ear’s structures also collect and magnify pressure waves. At
a pressure of about 35 kilopascals (5 PSI), the human eardrum may rupture. With
an overpressure of 100 kPa (14 PSI) almost all eardrums rupture. The eardrum
most frequently ruptures into the inferior pars tensa. At lesser pressures, the
overpressure may cause hemorrhage into the drum without a rupture. With
extremely high pressures, the drum may be destroyed and the ossicles dislocated
or fractured.
Rupture of the eardrum will cause pain, hearing loss, and may cause tinnitus.
Eardrum perforations, hearing loss, and dizziness may interfere with daily
activities and may affect the individual’s quality of life.24
Physical examination may reveal blood in the external canal. Examination of the
tympanic membrane with an otoscope may show evidence of the perforation.
It often is held as gospel that rupture of the tympanic membrane is a marker for
serious gastrointestinal or pulmonary injury. If the patient has ear protection,
this may not be the case. Likewise, if the patient is in the water with his head
out of the water, the tympanic membranes may not be exposed to an underwater
blast wave. Isolated eardrum rupture does not appear to be a good marker of
either concealed pulmonary blast injury or poor prognosis.25
Auditory barotrauma is quite common in blast injuries. In the Oklahoma City
bombing, the incidence of auditory injury was 35%.1,13 This does not count those
patients with partial, temporary hearing loss or those who complained of
tinnitus for an extended period of time.24
Pulmonary Damage. The lungs have been considered to be the non-auditory organs
most at risk for suffering primary blast injury. Blast lung is a direct
consequence of the supersonic pressure wave generated by an HE.26 (See Figure
4.) It is the most common fatal injury caused by the primary blast injury among
the initial survivors of the explosion. These lung injuries may not be apparent
externally or immediately, but may lead to death if not diagnosed and treated
promptly. An overpressure of about 40 PSI causes lung injuries.
Damage to the lungs can include pulmonary contusions with or without a
laceration, and/or pulmonary barotrauma such as pneumothorax, pulmonary
interstitial emphysema, pneumomediastinum, or subcutaneous emphysema.
It is best to assume that if a patient is wheezing after a blast injury, that
the wheezing is due to a pulmonary contusion. Other causes of wheezing may be
pulmonary edema from myocardial contusion or infarction, or exacerbation of
underlying disorders such as asthma or chronic obstructive pulmonary disease
(COPD).
The most common lung injury associated with a blast wave is a pulmonary
contusion. This may take the form of micro-hemorrhages with perivascular/peribronchial
disruption. It appears to be more common on the side closest to the explosion,
but this may be influenced by the geometry of the surrounding area and reflected
energy.27-29 The alveolar wall may be torn, causing a blood-filled emphysematous
change to the lung. Pulmonary contusions may develop with or without a pulmonary
laceration.
Pulmonary contusions impair gas exchange at the alveolar level. The changes seen
on microscopic examination closely resemble the pulmonary contusions seen in
non-penetrating blunt chest trauma.
Parallel thoracic ecchymoses, once thought to be along the ribs, may be seen
with larger blast loads.20,28 These ecchymoses parallel the intercostal spaces.
Rib fractures may occur due to blast injury, but are much more likely to be due
to secondary or tertiary blast injury mechanisms, at least in survivors.29,30
The patient may have minimal or no symptoms initially. The patient also may
complain of chest pain or respiratory distress. Signs of blast lung usually are
present at the time of the initial evaluation, but have been reported as late as
48 hours after the explosion occurs.
The overpressure may cause pulmonary barotrauma, including pneumothorax or
pneumomediastinum. The patient may develop pulmonary interstitial emphysema,
subcutaneous emphysema, and systemic air embolism with larger blast
loads.20,22,23 Significant bronchopleural fistulae may lead to air embolism. Air
emboli may present in a variety of ways, including shock, myocardial infarction,
spinal infarction, or cerebrovascular accident.
Blast lung is characterized clinically by the triad of apnea, bradycardia, and
hypotension. The clinician should suspect blast lung in any victim who presents
with dyspnea, cough, hemoptysis, or chest pain following blast exposure.
A simple frontal chest x-ray is diagnostic for most cases of pulmonary
barotrauma from blast. Blast lung produces a characteristic butterfly pattern on
chest x-ray. The pulmonary injuries found may range from scattered isolated
petechiae to confluent pulmonary hemorrhages. The radiographic evidence of
pulmonary injury usually begins within hours of the explosion and begins to
resolve within one week.31
Gastrointestinal Damage. GI injuries may not be apparent externally. They have a
great potential to cause death and may be much more difficult to protect
against.
GI injuries once were thought to occur with the same frequency as lung injury. A
recent large Israeli case series found that abdominal injuries were seen only
with massive trauma.32 In this series, all patients were injured from open air
explosions. The patient may have a greater risk for GI injury when exposed to an
underwater explosion.33
The GI injury of primary blast injury is inconsistent in presentation. It may
consist of hemorrhage beneath the visceral peritoneum or may extend into the
mesentery, colon, and cecum.27,28 Contused bowel may necrose and perforate
several days after the initial trauma. The perforated bowel may be apparent
immediately, or may perforate only after a delay of up to 48 hours.34,35
Pneumoperitoneum is a relatively rare complication of GI barotrauma.36 This
complication has a wide differential diagnosis ranging from perforated viscus to
simple dissection of air through the retroperitoneum.
The colon is the most common site of both hemorrhage and perforation.33 This is
thought to be because the colon has the most bowel gas accumulation in the GI
tract.
Solid organ laceration and testicular rupture also are seen due to primary blast
injury, but are less frequent and often are associated with large blast loads.37
The most common solid organ lesions reported were subcapsular hematomas in the
liver, spleen, and kidneys.31 Mesenteric, scrotal, and retroperitoneal
hemorrhages have been reported.28
These lesions can lead to the clinical signs of absent bowel sounds, bright red
blood per rectum, guarding, and rebound tenderness. The clinical symptoms can
include abdominal pain, nausea, vomiting, diarrhea, and tenesmus. Blast injury
to the GI tract should be suspected in anyone exposed to an explosion who has
abdominal pain, nausea, vomiting, hematemesis, rectal pain, testicular pain,
unexplained hypovolemia, or any finding compatible with an acute abdomen.
The clinician should be aware that the abundant high-velocity fragments
associated with recent suicide bombs also may cause intra-abdominal injuries.
These injuries certainly can include penetrating bowel injuries.38 Initial
symptoms of penetration are the same as outlined above.
Brain Injury. Primary blast injury can cause concussion or traumatic brain
injury, although this finding is difficult to differentiate from the concussion
due to impact with another object. The clinician should be quick to consider
computed tomography (CT) or magnetic resonance imaging (MRI) in these patients.
Cardiac Injury. Myocardial contusion may occur with arrhythmia or hypotension.39
Secondary Blast Injury. Secondary blast injury is caused by the bomb fragments
and other debris that are propelled by the intense energy release of the
explosion. (These fragments often erroneously are referred to as “shrapnel.”
Shrapnel is the name for an artillery round containing multiple round lead balls
that was designed during World War I by then-Lt. Shrapnel. This round
essentially functions as a very large shotgun with several hundred half-inch
lead balls.) (See Figures 5-7.) Conventional military explosives may create
multiple fragments with initial velocities of up to 2500 m/second (8202
feet/second).40 (In contrast, the very fast moving M-16 round has a muzzle
velocity of 2800 feet [853 meters] per second.)41
Glass causes many of the secondary blast injuries (up to 50% of all blast
injuries). Victims who are peppered with glass often are difficult to
distinguish from victims who are peppered with glass and have penetrating
injuries.42
Secondary blast injuries may not be obvious initially. A seemingly small
abrasion or wound may mask the entrance wound for a substantial fragment.
Up to 10% of blast survivors have significant eye injuries.43 (See Figure 8.)
These injuries may be perforations from high-velocity projectiles. Glass is
notorious for causing these ocular injuries. Window fragments often don’t kill,
but they can cause blindness and ruptured globes. At the speed that explosively
propelled fragments of glass travel, there is no time for the blink reflex to
operate. These injuries may occur with minimal initial discomfort and may
present days after the event. Symptoms include eye pain and irritation, foreign
body sensation, alterations of vision, periorbital swelling, or periocular
contusions. Signs can include loss of vision, decreased visual acuity, globe
perforation or rupture, lid lacerations, and subconjunctival hemorrhage around
the point of entry.
Tertiary Blast Injuries. Tertiary blast injuries are caused when the victim’s
body is propelled into another object by the blast winds.20,44 Tertiary effects
result from the bulk flow of gas away from the explosion. Blast winds can
generate a body acceleration of more than 15 gs. They most often occur when the
victim is quite close to the explosion.
This displacement of the victim can take place relatively far from the point of
detonation if the victim is positioned in the path gases must take to vent from
a structure, such as a doorway, window, or hatch. Likewise, if the patient is in
an alley, magnification of the blast wind may occur due to the configuration of
the buildings.
The deceleration caused by impact into a rigid structure causes the majority of
injuries. A person who is flung into a fortified immovable object with a
velocity greater than 26 feet/second (7.92 meters/second) has a mortality rate
of about 50%.45 The most common injuries are fractures and closed head injuries.
Isolated body parts may be broken, dislocated, or even amputated. Injuries from
this mechanism also depend on what the victim hits in the environment and can
range from simple contusions to impalement. Victims may tumble along the ground,
sustaining abrasions, contusions, and “road rash.”
Miscellaneous Blast Effects (Quaternary Blast Injuries). This category of injury
includes burns from fire or radiation, crush injury associated with structural
collapse, poisoning from carbon monoxide or other toxic products of the
explosion, and inhalation of dust or chemicals from the explosion.
The unprotected human body can survive a blast with a peak overpressure of 30
PSI (206 kPa), but buildings and other structures collapse with the stress of
only a few pounds per square inch. This means that people may survive the
effects of the blast only to be injured by collapsing buildings.
The blast may be a vector for chemical and biological warfare agents. The
effects of these agents on the body may well overshadow any part of the
explosive energy.
Patients who have been exposed to a blast in an enclosed area should have
carboxyhemoglobin levels obtained. Inhalation of irritant gases or dusts also
may trigger wheezing in these patients.
Immediate Death. Fatal injuries may occur due to blast effects involving the
head, chest, and abdomen and often are seen in victims who are close to the
detonation.46 Indeed, in some of these victims close to the site of the blast,
parts of the victim (or perpetrator) may become missiles that kill or wound
other victims.47 Immediate death may occur from massive pulmonary bleeding with
rapid suffocation despite good care. The patient may develop a massive air
embolism or may sustain a significant brain injury. The patient may suffer a
traumatic amputation and exsanguinate before help arrives. Finally, the patient
may have a crush injury or impalement injury that causes rapid death before
extrication can occur.
The field physician or paramedic should consider a patient dead in the field
when:
there is an amputated body part without signs of life;
there are no effective respirations;
there is no palpable pulse; and
there are dilated pupils.
Persons with immediate, severe respiratory insufficiency that is caused by a
blast effect have far less chance of survival.
Cardiopulmonary resuscitation (CPR) at the scene never is indicated. There will
be too many injured, not enough medical providers, and no significant chance of
successful resuscitation in this blunt trauma patient.
Evaluation and Management
Expect that the most severely injured patients will arrive after the less
injured. The less injured often skip EMS and proceed directly to the closest
hospitals. For a rough prediction of the number of “first wave” of casualties,
double the first hour’s casualty count. Remember that a secondary device may be
employed that can cause substantial additional casualties, which may include
EMS, fire, police, and media.
Most of the injuries seen after a conventional explosive detonates are blunt,
penetrating, and thermal trauma that is well known to prehospital providers,
emergency physicians, and trauma surgeons.48 Much of this trauma includes
soft-tissue, orthopedic, or head injuries.11,49,50 The approach to the casualty
with blast-related injury, therefore, is the same as for any other trauma
victim.
The first and most important step of management is assessment of life support
needs and ensuring that the patient has an adequate airway, appropriate
ventilation, and adequate circulation. A thorough physical examination then
should be performed. The clinician should look for sentinel signs of potentially
significant blast exposure. (See Tables 2 and 3.) Unfortunately, when the health
care provider is faced with dramatic injuries such as amputations, fragment
injuries, and multiple critically ill patients, it is altogether too easy to
miss the subtle signs of blast injury. If the clinician does not consider the
possibility of primary blast injury, the patient’s care may be complicated
further.
Pulmonary. Blast lung is treated by correcting the effects of barotrauma if any
is found. Gas exchange is supported. The provider should be aware that positive
pressure ventilation may exacerbate pneumothorax and cause air embolism in the
presence of bronchopleural fistula. The patient’s body should be positioned to
ensure that the effects of air embolism are minimized.
In victims with mild respiratory distress, supplemental oxygen by nasal cannula
is appropriate. Those patients with significant respiratory distress or
hemoptysis should have an endotracheal tube placed. This is not without hazard,
however.
Positive pressure ventilation markedly increases the possibility of both air
embolism and pulmonary barotrauma. The provider should take the least invasive
measure that still provides appropriate airway support in these patients.51
Avoid peak end-expiratory pressure (PEEP) and high ventilation pressures.
In one study using thoracic CT scans of patients with pulmonary contusion (not
blast injury), patients with less than 18% contusion did not require intubation
or ventilation.52 Patients with more than 28% contusion always required
ventilation.
Because the combination of positive pressure ventilation and blast lung injury
poses such a high risk for tension pneumothorax, some authors suggest bilateral
prophylactic chest tubes after intubation. If the patient needs air evacuation,
this becomes more desirable. If a patient with a blast lung injury abruptly
decompensates, the clinician should presume that the patient has a tension
pneumothorax and treat accordingly.
If the patient survives the blast lung and other trauma, there is a good chance
that he will regain lung function within a year.53
Hypotension. Hypotension in blast injury victims can be due to several
mechanisms:
blood loss due to wounds (otherwise not related to the cardiovascular system);
blood loss due to gastrointestinal hemorrhage;
blood loss due to intra-abdominal solid organ rupture;
hypotension from compression of vessels and heart by pneumothorax;
hypotension due to the cardiovascular effects of an air embolism; and
hypotension due to vagal reflexes.
The patient’s fluid volume should be supported without excessive fluid
replacement. Often, blood products or colloid solutions should be used rather
than crystalloid. Too much fluid replacement of course can cause increased
respiratory distress as either congestive heart failure or acute respiratory
distress syndrome.
Gastrointestinal. Blast injury of the GI tract can be managed in much the same
way as blunt trauma of the abdomen. If the patient has an obvious penetrating
wound of the abdomen, then urgent surgical management is indicated. If the
patient is unconscious but hemodynamically stable or is conscious with abdominal
complaints and is hemodynamically unstable, then fluid resuscitation should be
undertaken. If the patient’s blood pressure stabilizes and remains stable, then
a CT scan of the abdomen is appropriate. If the blood pressure does not improve,
then urgent surgical management is indicated.
If the patient is conscious with abdominal findings and is hemodynamically
stable, then an abdominal CT scan should be obtained. If the patient is stable,
then an abdominal CT scan with oral and intravenous contrast is a reasonable
screening procedure.
While abdominal CT scan is appropriately specific, it may not be sufficiently
sensitive to identify hollow viscus injury.31 If patients who have been scanned
continue to have signs of abdominal pathology, then a diagnostic peritoneal
lavage is appropriate. If the effluent contains significant red blood cells,
bacteria, bile, or fecal matter, then urgent laparotomy is indicated. CT must
precede peritoneal lavage or false positive air and fluid will be introduced.
In the context of a mass casualty incident, there should be a low threshold for
laparotomy when a hollow viscus injury is suspected. Close observation may not
be available because of the number of casualties. Clinical signs and symptoms of
early bowel injury, particularly in children, may be so subtle as to be easily
missed in the patient with multiple injuries.54
Wound Management. For lacerations and fragment wounds, avoid primary closure and
consider the use of delayed primary closure in these wounds. There is about an
80% rate of infection when fragment wounds are sutured. All debris that is flung
by the explosion is not radiopaque, and the wise provider carefully should
explore injuries and consider CT, ultrasound, or MRI of wounds to evaluate for
radiolucent foreign bodies. Update the tetanus status as appropriate.
Air Embolism. Air embolism should be treated as soon as the diagnosis is
considered. The first step should be to place the patient on high flow oxygen.
Next, the patient should be positioned properly. The usual recommended
positioning is the left lateral decubitus position with the head down. If only
one lung is injured, the injured lung should be placed in the dependent position
(which may override the left side down position described above.) By placing the
injured lung down, the alveolar oxygen pressure is lower with a subsequent
decreased risk of air entering the lungs. It should be noted that a recent
review article about gas embolism opined that a flat position would be more
appropriate.55 The review article also discusses use of increased fluids,
heparin, and corticosteroids as treatments for gas embolism. This review article
does not cite any work about blast injury in its bibliography and does not
mention blast lung injury as an etiology of gas embolism. The author feels that
there isn’t enough evidence specific to blast lung as an etiology of gas
embolism to make a more specific recommendation.
The definitive treatment for air embolism is hyperbaric oxygenation, which often
is not available in a timely fashion. Hyperbaric oxygenation will reduce the
bubble size (by Boyle’s gas law), increase tissue oxygenation, and increase the
solubility of the gas. The United States Navy protocols for gas embolism and
decompression sickness would be an appropriate reference.
Disposition
The disposition of these patients depends on the injury sustained by each
victim. Those who were close to the center of the explosion should be considered
for observation for at least 24 hours.
(EM Reports Feb 2004)
Sasser's article Prehosp Emerg Care 2006;10:165
Correction for Primary Blast Injury Criteria (J Trauma 2006;60:1284)