Public Health Emergency Preparedness
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Chapter 7. Blast Terrorism
In the short time between January and September 2003, explosive devices were
involved in 73 of 189 terrorist events that occurred worldwide. A 1997 report
by the Department of Justice found an abundance of evidence suggesting that
given intent, the knowledge required to build bombs is readily available in
print and on the Internet. The report cited at least 50 publications in the
Library of Congress; several texts intended for military training, agricultural,
and engineering use; 48 different underground pamphlets and publications; and
countless sources on the World Wide Web. Bomb data from the Federal Bureau of Investigation (FBI) indicate that
from 1987 to 1997, bombing incidents increased approximately 2.5 times, peaking
in 1994 with 3,163 domestic bombing incidents. Of those incidents, 66% involved
explosive devices, and the remaining 24% involved incendiary devices. More
recent bomb data indicate that the number of domestic bombing incidents has
decreased since 1994, with 1,797 incidents in 1999. In most incidents, low-explosive
fillers were used. High-explosive ammonium nitrate mixtures, however, were
used during the first World Trade Center bombing and the Oklahoma City bombing,
highlighting the tremendous destructive power of a significant amount of a
The raw materials for explosive devices are regularly found in areas of farming
or mining activities. Due to the public accessibility of explosives materials
and bomb-building knowledge, a domestic terrorist attack would probably take
the form of a conventional explosive munitions attack. This chapter introduces
the spectrum of injuries caused during an explosion and the differences between
blast trauma and conventional trauma. Both blast trauma and conventional trauma
have aspects of blunt, penetrating, burn, crush, and inhalational injuries.
However, victims of a blast may suffer all of these injuries simultaneously,
with additional injury caused by the blast wave itself, i.e., primary blast
injury. Primary blast injuries are lethal, unique, and often subtle. Although
the vast majority of blast injury victims suffer from conventional injuries,
lack of knowledge about primary blast injuries and failure to recognize a blast's
effect on certain organs can result in additional morbidity and mortality.
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Explosives are solid, liquid, or gaseous substances that, when detonated,
transform rapidly into more stable products in the form of heat, gas, and energy.
Explosives are frequently used in military, demolition, and industrial applications
and are categorized as low explosives or high explosives. Low explosives are
considered propellants and are used chiefly in small arms and munitions. Two
examples are smokeless powder or black powder. High explosives have a greater
potential for destruction due to their higher burning rate and therefore higher
shattering effect. Notable examples of high explosives are TNT (trinitrotoluene),
dynamite, RDX, C-4, ammonium nitrate, ammonium-nitrate fuel oil, HMX, and PETN.
Due to their relative stability, these compounds require another explosive
(e.g., a primer or detonator) to initiate a charge.
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Understanding how an explosion causes tissue damage and injures
victims requires some knowledge of the physics occurring during an explosion.
Detonation of an explosive device causes rapid chemical conversion of an explosive
material with the release of high-pressure gases and energy. These high-pressure
gases expand supersonically, moving air particles, called the blast wind, and
propagating in all directions in the form of a shock wave. The blast wind lasts
milliseconds, and its strength varies with the strength of the explosive device
detonated. Wind velocity can vary from 40 mph from the generation of 1 psi
(pound per square inch) to 1,500 mph from a 100 psi detonation. As it expands,
this shockwave causes compression of the ambient atmosphere and an instantaneous
rise in atmospheric pressure above baseline, known as overpressure. The leading
edge of the expanding blast wave is termed the blast front. As the wave of
overpressure passes through, it subjects tissues in its path to enormous forces
called blast-loading forces (measured in psi). The amount of force capable
of perforating a tympanic membrane is 5 psi, and that considered to be lethal
in 50% of exposures is 80 psi.
Pressure measurements of the blast wave recorded in one place reveal the pressure-time
relationship of the waveform. Key observations include the following:
- Atmospheric pressure rises almost instantaneously to a peak overpressure
as the wave passes through.
- Atmospheric pressure remains supra-atmospheric for some period of time
and then decays to dip below the atmospheric pressure baseline, heralding
the negative pressure phase.
Over time, atmospheric pressure returns to baseline. Due to the expansion
of gases, a state of relative vacuum is created at the detonation site. This
causes the gas flow to reverse during the negative phase—in contrast
to the outward air flow occurring during the positive phase. All of the tissue
injuries described by the blast wave have been due to overpressure. However,
the pathophysiologic effects of underpressure are still under investigation,
there has been some suggestion that underpressure itself can cause injury.
Many believe that the harmful effects on the body caused by a blast
result from the pressure differentials exerted on tissues by the expanding
wave. However, because the peak overpressure decays exponentially, a victim
must be relatively close to the detonation for the blast wave itself to induce
tissue injury. Several factors, including the following, affect the degree
of blast pressure loaded to objects:
- The distance between the object and the detonation.
- The orientation of the object to the incident wave.
- The degree of reflected waves to which the object is subjected.
This latter point is the reason that, given equal peak overpressures, victims
found in corners or in underwater blasts suffer greater injury. In both situations,
the victim is subject to the incident wave in addition to multiple reflected
The three physical properties that cause tissue damage during a blast are
the spalling effect, implosion, and inertia.
When a blast wave travels through tissue of homogenous density, it causes
the tissue to vibrate. However, when a wave passes through air-filled tissue
such as the lungs, intestinal lumen, or the middle ear, it travels from areas
of higher density to the air-filled areas of lower density. The result is tension
at the surface interface, and particles are thrown or spalled into the less
dense medium. This causes micro- and macro-tears in the tissue wall, resulting
in hemorrhage, edema, and the loss of structural integrity.
In implosion, the blast wave is thought to cause compression of tissues (or
organs), resulting in recoil and expansion of the tissue (or organ) as the
wave exits. This causes structural damage to solid tissues principally at
the areas of attachment, e.g., at the hila for solid organs.
Blasts result in a wind with the ability to accelerate people and large stationary
objects. Acceleration and deceleration causes multiple types of injuries,
in particular blunt injuries. Experimental data have suggested that inertia
may act at the level of tissues themselves. In the lungs, due to differing
densities, bronchovascular elements would be expected to accelerate at different
rates than delicate alveolar tissue, resulting in shearing at these sites.
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Many mechanisms of injury are involved in blast injuries.
- Primary blast injury refers to tissue damage by the blast wave itself,
specifically in areas with tissue-gas interfaces such as the lungs, the intestines,
and the tympanic membrane.
- Secondary injury refers to penetrating or blunt injury that results from
the acceleration of shrapnel or debris. Terrorists often add metallic fragments
such as nails to devices to maximize the potential for penetrating injuries.
Secondary injury is the most common type of injury seen, because it does
not require the victim to be near the point of detonation.
- Tertiary injuries result from acceleration-deceleration forces imposed
as the blast wind propels the victim. As the body is tumbled on a rigid surface,
it suffers from blunt injury, in particular closed head injury, as well as
penetrating injuries as it is accelerated over sharp debris.
- A fourth mechanism includes flash and flame burns, inhalational injury,
and crush injuries incurred from fires and structural collapse.
Secondary and tertiary injury overlap significantly, and both are more common
than primary blast injury. However, primary blast injuries are the most severe.
The effects of the blast wave on structural elements and on human tissues
combine to cause complex combinations of injuries in blast victims; injuries
are variable within one event. The principal factor that determines severity
of injury is the distance of the victim from the site of detonation (Table
7.1). Injuries also vary due to the victim's position with respect
to incident waves and the degree of reflected shock waves to which the victim
Primary Blast Injury
Primary blast injuries (PBI) are injuries
caused specifically by exposure of the body to the blast wave. Pulmonary barotrauma,
air embolization, and intestinal perforation are the unique principal causes
of death after a blast. Although most injuries in an explosion are secondary,
tertiary, and miscellaneous (crush, burn, inhalational), a person close enough
to a detonation would be subjected to the effects of the blast on a microscopic
Urban bomb blasts tend to have the following characteristics:
- Most victims sustain minor injuries.
- Most injuries affect the head, neck, and extremities.
- Torso injuries are uncommon yet lethal.
- Primary blast injuries are uncommon because victims tend to die before
arriving at the hospital.
However, because all bomb blast incidents are different, the
types of injuries seen are variable. A blast that occurs in an enclosed space,
such as a bus, is associated with more severe injuries and a higher incidence
of primary blast injuries. The number of casualties would be expected to be
less than in an equipotent detonation in open space. Mortality is also higher
when a blast occurs in an enclosed space, because the shock wave is contained
and reaches a higher overpressure and a longer positive phase. However, containment
of the wave does not affect the generation of propelled debris. Therefore,
secondary and tertiary injuries, including amputations from large objects,
are the same whether the blast occurs in an enclosed space or open air.
The spectrum of PBI reflects involvement of the gas-containing
organs and the pathophysiologic effects of these organs on other systems (Table 7.2). As in conventional trauma, all victims should be managed with careful
attention to the airway, breathing, and circulation; however, in certain patients,
complications may arise with respect to positive-pressure ventilation and fluid
Blast Lung Injury and Air Embolization
The anatomic structure
of the lung makes it susceptible to the effects of blast barotrauma. Alveolar
spaces are engulfed by delicate capillaries in a way that maximizes the surface
area available for gas exchange.
induced by the blast involves the spalling of particles across the tissue-gas
interface (alveolus) with the generation of micro-tears. This fills the air
space with blood, edema, and tissue particles, impairing gas exchange. The
most common lesion of the airway is the stripped-epithelium lesion, in which
the bronchial epithelium and mucociliary apparatus are stripped from the basal
lamina, resulting in ulcerations of the submucosa and impaired clearing of
secretions. Structural tears occur through interfaces of blood vessels and
air spaces, creating direct openings where air bubbles could escape into the
Clinical Findings and Diagnosis
blast lung injury is evidenced by various degrees of the following:
- Chest pain.
- Decreased breath sounds.
- Hypopharyngeal hemorrhage.
- Subcutaneous crepitus.
- Tracheal deviation.
Clinical findings range from contusion and ecchymosis to massive
hemoptysis, severe ventilation/perfusion mismatch, and air leak, leading rapidly
to death. Most blast lung injury develops early in the course of treatment,
within 1-2 hours. Signs and symptoms may progress within 24-48
hours to respiratory failure or acute respiratory distress syndrome (ARDS),
or both. Respiratory failure is often due to secondary additive effects such
as shock, organ failure, or inhalation of smoke and toxic substances.
The most important diagnostic test for blast lung injury is a
chest radiograph. However, in stable patients, computer tomography (CT) scans provide important additional
information. Pulmonary hemorrhage is the most consistent microscopic finding
in blast lung injury, and most survivors of a blast will have infiltrates on
a chest radiograph.
Treatment and Complications
lung injury is not universally fatal, given aggressive and timely management.
Initial management involves maximizing oxygenation and minimizing additional
barotrauma. Most important is maintaining a patent airway, free of blood and
secretions. Victims should be placed on oxygen to prevent hypoxia. Control
of massive hemoptysis involves tracheal intubation and, whenever possible,
selective ventilation of the contralateral lung. The source of bleeding in
massive hemoptysis may be from one or both lungs and is often difficult to
determine. Having a high index of suspicion for pneumothorax or tension pneumothorax
cannot be overstated. The risk is so great that prophylactic tube thoracostomy
has been suggested.
The development of systemic air embolization from injured lung
tissue is a grave complication. The greater the degree of lung injury, the
higher the risk of emboli formation. Although the actual incidence is unknown
and is probably underrecognized, air embolization in blast injury is speculated
to be the main cause of death within the first hour after a blast. Air emboli
in the vascular system carry a high mortality rate because the air bubbles
can potentially cause occlusion of the coronary arteries (myocardial ischemia),
cerebral vessels (stroke), or cardiac outflow tracts (shock). They cause additional
morbidity in the nature of blindness (occlusion of retinal arteries) and ischemia
of end organs. The ultimate clinical result depends on the site of embolization.
Signs and symptoms that suggest arterial air embolization include the following:
- Air bubbles in retinal vessels.
- Chest pain.
- Myocardial ischemia.
- Focal neurologic signs.
- Loss of consciousness.
- Livedo reticularis.
- Tongue blanching.
Air emboli pose a challenge in emergency management of blast victims. Air
emboli are not only difficult to diagnose, but also have a clinical presentation
similar to that of other more familiar clinical entities. For example, myocardial
ischemia, which is usually easily recognized, is most likely to be secondary
to coronary vessel embolization (versus the traditional mechanisms of ischemia)
in victims with blast lung injury. Management of these patients should focus
on halting the passage of air. However, in patients exhibiting a change in
their mental status, more common traumatic causes (e.g., intracranial hemorrhage
from blunt head injury) should be addressed first, before focusing on embolization.
Air emboli can be confirmed by direct visualization of air bubbles
or disrupted air passages via echocardiography, transcranial Doppler, CT scan,
or bronchoscopy. Unfortunately, there are no data on the sensitivity of these
techniques in detecting emboli in blast victims. Transesophageal echocardiography
can detect gas bubbles as small as 2 µm, but its availability is
limited. Sudden circulatory or neurologic collapse, especially if positive-pressure ventilation (PPV) has been
started, combined with a high index of suspicion, is enough to make the diagnosis
of air embolization until proved otherwise. Other suggestive clinical findings
include possible evidence of bubbles in retinal vessels, aspiration of air
from arterial lines, or marbling of the skin or tongue.
In conventional penetrating and blunt lung injuries, management
of massive air embolization involves thoracotomy on the affected side to stop
the passage of air. Based on this experience, management of air embolization
in blast lung injury has also been primarily surgical. However, in blast lung
injury, identifying the source of emboli may be difficult, since both lungs
or multiple sites may be involved. Temporarily placing patients in specific
positions to trap air bubbles anatomically (to prevent them from entering the
circulation) has been suggested. However, there is no single maneuver that
prevents air from entering both the arterial and venous circulation simultaneously.
Despite the lack of data, placing the patient in a modified left decubitus
position (more toward prone) or prone position is thought to be the most anatomically
logical alternative. These positions place the coronary ostia in the lowest
position in the body and the left atrium in the highest position. Because of
the practical limitations of having patients in these positions, placing the
patient with the injured lung down, or in the dependent position, to minimize
embolization by increasing venous pressures on that side, has also been suggested.
Hyperbaric oxygen therapy has been successfully used to treat
cerebral air emboli from diving decompression injuries by actually causing
bubble volume to decrease. Again, recommendations for management of blast-induced
air embolization are largely based on conventional trauma experience. Stopping
the passage of air bubbles into the circulation is paramount; however, doing
so by surgically clamping the hilum when the injury is not clearly unilateral
may not be necessary. Knowledge of lung isolation techniques is important for
Positive-pressure ventilation (PPV) is a last resort for blast
victims; it is reserved for cases of severe respiratory failure or massive
hemoptysis, or for patients requiring emergency surgery for other reasons.
Cardiovascular, respiratory, or neurologic collapse within minutes of PPV being
instituted has been reported. In addition, PPV is thought to contribute to
the generation of air emboli due to the high airway pressures it causes, and
it has been implicated in the later reopening of fistulas.
In the spontaneously breathing patient, pulmonary venous pressures
are higher than airway pressure, which prevents the passage of emboli into
the venous system. During PPV or when pulmonary vascular pressures are low
(e.g., with hypovolemia), airway pressures are higher, and the gradient is
reversed, facilitating the passage of air and debris into the vascular system.
Techniques based on experience in ventilating patients with pulmonary contusion
and ARDS have been proposed for ventilating victims of blast lung injury who
must be intubated. These techniques include low peak inspiratory pressures
(<35-40 cm H2O), low tidal volumes, high peak end-expiratory pressures,
permissive hypercapnea, high-frequency jet ventilation, pressure-controlled
inverse-ratio ventilation, and nitric oxide inhalation. As a last heroic attempt,
extracorporeal membrane oxygenation has been suggested.
Gastrointestinal Blast Injury
After lung injury, gastrointestinal (GI) injury is the second most lethal injury
after a blast. Abdominal injuries secondary to open-air blasts are less common
than blast lung injury; however, they are much more common in underwater blasts.
of GI injury is similar to that of blast lung injury, and abdominal injuries
are a significant cause of delayed mortality. As the wave impacts the abdominal
cavity, it compresses and distorts the internal tissues, resulting in hemorrhage
and/or rupture of solid organs. As the blast wave passes through tissues with
a gas interface, it causes spalling of particles into the intestinal lumen.
The terminal ileum and colon are predisposed to injury because they contain
the greatest amount of air, while the small intestine is relatively spared.
The resultant wall tears, intramural hematomas, and hemorrhage may predispose
the intestine to perforation. In severe blasts, the direct force of the wave
itself may also cause perforation, although it is unknown whether the perforation
is immediate or delayed.
Clinical Findings and Diagnosis
The signs and symptoms of
GI injury may be nonspecific and change over time. They include the following:
- Lack of bowel sounds.
- Involuntary guarding.
- Rebound tenderness.
- Abdominal pain.
- Nausea and vomiting.
- Orthostasis or syncope.
- Testicular pain.
Evaluation of the abdomen begins with a physical examination, standard trauma
screening laboratory tests, and a high index of suspicion for injury. Making
the diagnosis of perforation in an area of trauma is challenging for many reasons.
First, the findings can be subtle and masked by other, more critical injuries.
Second, the patient may be unconscious, making the value of serial examinations
limited. Third, diagnostic examinations, although useful for detecting hemorrhage,
may be misleading or insensitive in the early stages of perforation.
The goals of management are
to identify and control internal bleeding and to identify and repair any perforated
viscus. In stable patients in whom injury is suspected, the abdominal radiograph
has largely been replaced by CT scan, ultrasonography, and diagnostic peritoneal
lavage. CT scan provides useful information regarding intra-abdominal hemorrhage,
organ injury, free intraperitoneal air, and intramural hematoma; however, it
has a low sensitivity for identifying a hollow viscus perforation. In hemodynamically
stable patients with blast lung injury too severe to be surgical candidates,
exploratory abdominal procedures may be delayed. In these patients, broad-spectrum
antibiotics are recommended pending confirmation of an intact bowel. Exploratory
laparotomy may be necessary in hemodynamically unstable patients in whom internal
bleeding is suspected. Because surgical outcomes in blast victims are poor,
surgery, like intubation, is a last resort and should be weighed against the
risk associated with missing a perforation.
Blast Auditory Injury
The auditory system is the system most frequently injured during a blast.
Auditory injury is more common than lung or GI injury because the overpressure
necessary to perforate tympanic membranes (5 psi) is well below that expected
to cause lung or GI injury. Hearing loss either with or without a ruptured
tympanic membrane is quite common. It can be debilitating and make communication
with the victim difficult. Although some sensorineural hearing deficits improve
over the first few hours, deficits are permanent in approximately 30% of
Normally, sound pressure
waves are transmitted from the tympanic membrane through the ossicular bones
in the middle ear, where they are converted into mechanical vibrations. These
mechanical vibrations, through the involvement of perilymph in the membranous
labyrinth, are converted again into nerve impulses at the organ of Corti in
the cochlea. The blast wave overwhelms this intricate and delicate system and
is then amplified down the conductive and sensory neural pathways. The result
can be injury to any of part of the auditory system, including perforation
of the tympanic membrane, disruption of the ossicular chain, or damage to the
organ of Corti.
In addition to the damage caused by amplification of the shock wave within
the auditory system, the instantaneous rise in overpressure inflicts additional
damage. The ability to equilibrate middle ear pressure via the eustachian tube
is overwhelmed. The resulting expansion of the cavity and distortion of tissue
causes additional mechanical injury.
Tympanic Membrane Rupture
Tympanic membrane rupture from most
causes heals spontaneously, with 10% of the eardrum expected to heal per month.
Spontaneous healing has been observed in perforations involving <80% of
the membrane. Complications include failure to heal (10-20%), infection, and
Despite the long-held belief that tympanic membrane perforation is a marker
for delayed onset of pulmonary and GI blast injuries, this does not appear
to be the case based on outcomes of 142 survivors of suicide bombings. Of the
survivors who had perforated tympanic membranes, none developed delayed presentations
of other primary blast injuries. Those with pulmonary blast injury were acutely
ill early in their course, and none had a delay in presentation of respiratory
symptoms. Notably, 18% of those with blast lung injury did not have perforated
tympanic membranes. Therefore, isolated tympanic membrane rupture does not
seem to be a marker for delayed onset of other primary blast injuries. Regardless,
due to the paucity of data, and in particular the lack of pediatric data, it
would seem prudent to delay the implementation of official clinical guidelines
regarding the management of pediatric victims of auditory blast injury. Evaluation
and management should be done on a case-by-case basis.
Ossicular Chain and Cochlear Injury
Ossicular bones attach
to the tympanic membrane and transmit its vibrations to the cochlea, where
the vibrations are converted into neural impulses via tiny hair cells. The
overpressure can cause distortion and fracture of the ossicular bones, but
this is rare, and blasts causing inner-ear damage, yet sparing the ossicular
bones have been reported. The relative resilience of the ossicular bones is
not shared with the cochlea at the organ of Corti. This delicate system is
overwhelmed by the amplification of waves, causing loss of structural integrity
with damage of the inner and outer hair cells. The result is the development
of conductive and/or sensorineural hearing loss.
Victims may be initially
unaware of acoustic injury or may complain of tinnitus, hearing loss, or ear
pain. The spectrum of clinical findings in auditory blast injury includes the
- Tympanic perforation.
- Ossicular chain disruption.
- Ossicular chain fracture.
- Labyrinthine fistula.
- Perilymphatic fistula.
- Loss of hair cell integrity.
- Conductive hearing loss.
- Sensory hearing loss.
- Basilar membrane rupture.
In general, emergency management
of auditory injuries involves clearing the ear canal of debris, minimizing
exposure to loud noises or water, and taking precautions against infection.
Otolaryngology followup for a complete evaluation and to watch for future complications
(e.g., cholesteatoma formation) is recommended. Prophylactic use of antibiotics
is not recommended.
The heart and blood vessels can be directly or indirectly
injured by a blast wave. Cardiac involvement during a blast usually manifests
as coronary vessel embolization and ischemia. Blood vessels within certain
organs have a propensity for injury and may contribute to the generation of
microthrombi, which results in disseminated intravascular coagulation. Cardiac
blast injury that manifests as hemorrhage in the epicardium, myocardium, or
papillary muscles is quite rare.
Hypotension in blast victims often has multiple causes. It can involve blood
loss from major musculoskeletal or abdominal injury or from a blast-related,
vagally mediated reflex. This reflex, which is seen immediately after a significant
blast exposure, causes hypotension without vasoconstriction and bradycardia.
It is the most common effect on the cardiovascular system by the blast wave
itself. The hypotension can be profound and self-limiting, and there may be
no external signs of injury.
Traditionally, aggressive volume replacement to support circulation is required
in trauma victims with cardiovascular collapse. However, excessive volume replacement
is detrimental to patients with lung injury. Research in animals has suggested
that fluid replacement actually impairs cardiovascular performance in the setting
of a blast. However, inadequate pulmonary vascular pressure has been suggested
to promote the passage of air into the pulmonary venous system. Therefore,
administration of fluids in increments of 5 mL/kg, titrated to clinical response,
has been recommended. Either too much or too little fluid can be harmful, and
the judicious use of fluids to maintain euvolemia is probably the best approach.
As in all trauma patients, colloids should be used to replace massive hemorrhage,
improve oxygenation, and minimize oncotic fluid shifts. Monitoring of central
venous pressure and/or pulmonary pressures is a useful adjunct to fluid management.
Sentinel injuries are subtle injuries that can increase the risk of having
or developing serious blast injury. These patients should be monitored closely,
no matter how clinically well they appear. Sentinel injuries include the
- Traumatic amputations.
- Hypopharyngeal contusion.
- Subcutaneous emphysema.
- Hearing loss.
- Ruptured tympanic membrane.
Traumatic amputations frequently result from a blast. However, they are rarely
found among survivors because the overpressure needed to cause such injury
more often than not causes death at the scene. The mechanism for traumatic
amputations has been hypothesized to be a combination of the blast wave itself,
the effect of propelled fragments on tissues, and the added force of the blast
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Incendiary devices are fire-bombs used to cause maximal fire damage to flammable
objects including people, buildings, and equipment. The massive fire caused
by these devices effectively and easily causes mass panic, and the relative
ease of obtaining materials to fabricate some devices makes them a potential
vehicle for terrorist attacks. Incendiary devices range from simple Molotov
cocktails, which are gasoline-filled bottles ignited with a rag, to military
bombs that contain flammable materials such as napalm. Modern incendiary devices
are complex bombs with flammable substances (e.g., kerosene) that can be ignited
by either a fuse or a primary explosive.
Napalm was originally made by mixing an aluminum soap of naphthalene and palmitate
with gasoline. The result was a sticky flammable substance that, in contrast
to liquid flammables, would stick to the intended target and burn longer. Napalm
was later modified to contain mixtures of benzene, gasoline, and polystyrene.
Napalm stores were eventually destroyed; however, incendiary devices containing
napalm have allegedly been used in the 1990s in northern Iraq and Croatia.
Incendiary devices containing mixtures of kerosene still have military applications.
The principal incendiary agents are thermite, magnesium, white phosphorus,
and hydrocarbons. Based on FBI data for 1999, most of the devices involved
in incendiary bombing incidents (223 actual bombings and 114 attempts) in the
United States used gasoline as the flammable agent.
Emergency management of victims of incendiary devices involves identifying
and treating the following:
- Severe burns (second- and third-degree).
- Respiratory compromise.
- Carbon monoxide poisoning.
These burn victims should be managed as any other burn victim, with special
attention to identifying blast injuries and removing the incendiary agent from
the skin. Carbon monoxide poisoning is of particular concern in napalm exposure,
because carbon monoxide is a byproduct of napalm combustion. Due to the radiant
heat emitted from the combustion of these materials, prolonged exposure may
lead to severe dehydration.
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The Aviation and Transportation Security Act, signed into law on November
19, 2002, instituted several measures with the goal of making flying safer,
including the following:
- Creating the Transportation Security Administration (TSA).
- Screening of all baggage for explosive materials.
- Fortifying of cockpit doors.
- Increasing the number of sky marshals aboard planes.
- Training flight crews on management of hijacking incidents.
According to TSA data, 100% of baggage is now screened (compared with 5% prior
to September 11, 2001). By August 2003, the TSA had intercepted 2.4 million
knives, nearly 1,500 firearms, and more than 51,000 box cutters.
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