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 high explosive.
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.
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.
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 shock wavecauses 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:
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:
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 waves.
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.
Many mechanisms of injury are involved in blast injuries.
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 is exposed.
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 level.
Urban bomb blasts tend to have the following characteristics:
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 resuscitation management.
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.
The pathophysiology 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 circulation.
Clinically, blast lung injury is evidenced by various degrees of the following:
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.
Blast 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 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 patient management.
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.
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.
The pathophysiology 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.
The signs and symptoms of GI injury may be nonspecific and change over time. They include the following:
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.
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 victims.
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 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 cholesteatoma formation.
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 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 following:
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 following:
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 wind.
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:
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.
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:
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.