Blast Injury

Blast Injury

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)

Blast Lung

Sasser’s article Prehosp Emerg Care 2006;10:165

Correction for Primary Blast Injury Criteria (J Trauma 2006;60:1284)

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