CHAPTER 13 BLAST INJURIES

Antonio Pepe, Booker T. King, Alexander Becker, Guy Lin, Tedla Tessema, Mauricio Lynn, Eduard Grass

Blast injury is unique in that it combines the mechanisms of several categories of injury, including blunt, penetrating, and thermal. This results in a wide range of overt and occult injury patterns making the diagnosis and treatment of specific injuries difficult.¹ However, like most problems in medicine, a basic knowledge of and methodical approach to the problem can save lives. The use of explosives can be traced to the use of black powder by the Chinese in the 10th century. In the 1800s other explosive substances were invented, including nitroglycerin, trinitrotoluene (TNT), and dynamite. Explosives have been used in every major conflict by the United States since the American Revolution. Blast injury was first described in World War I and at that time was primarily thought to involve the lung. In World War II, blast injury to the bowel was seen due to an increase in casualties of underwater explosions. The treatment of blast injury advanced during the Korean War. In Vietnam, blast injuries were seen, but the predominant injuries were due to high-velocity gunshot wounds.^2,³

The Israelis had the greatest experience with blast injury during the latter quarter of the 20th century, and have reported extensively on the subject.⁴ Examples of recent domestic terrorist attacks that resulted in significant destruction and casualties include the 1993 bombing of the World Trade Center, the 1995 bombing of the Alfred P. Murrah Federal Building in Oklahoma City, and the bombing of the Centennial Park in Atlanta (1996).^5,⁶ Many casualties of the September 11, 2001 attacks occurred as result of blast effect and structural collapse.⁷

The use of improvised explosive devices (IEDs) by insurgents has become the predominant weapon against coalition troops in Iraq. A recent article reviewed the injuries of wounded soldiers returning to Walter Reed Army Medical Center from March to July 2003. Of 294 casualties seen, 31% sustained blast injuries.⁸ Another study focused on 18 blast-injured patients evaluated at a forward resuscitative surgical hospital. A significant proportion of these casualties presented with penetrating head injuries, severe lung injuries, and multiple open fractures. This study characterizes the lethal effects of blast.¹

MECHANISMS OF INJURY AND INJURY PATTERNS IN EXPLOSIONS

Explosions produce specific injury patterns and the potential to cause life-threatening multisystem or multidimensional injuries. These patterns are the result of the composition and type of bomb, the delivery method, the distance between the victim and the blast, whether the blast occurred in a closed or open space ² and surrounding environmental barriers or hazards. Blast injury is a general term that refers to the biophysical and pathophysiological events and the clinical syndromes that occur when a living body is exposed to blast of any origin. Explosions are caused by a rapid chemical conversion of a solid or liquid into a gas with resultant energy release. Explosives are either high or low order. High-order explosives are designed to detonate quickly, generate heat and loud noise, fill the space with high-pressure gases in 1/1000th second, and produce a supersonic overpressurization shock (the increased pressure above normal atmospheric pressure from a blast) that expands from the point of detonation outward in a pressure pulse. The level of overpressure depends on the following: (1) the energy of the explosion, (2) the distance from the point of detonation, (3) the elapsed time since the explosion, and (4) the measurement technique. Blast strength is described as the ratio of overpressure to ambient pressure. The blast wave (positive wave) moves in all directions away form the explosion, exerting pressures of up to 700 tons (Figure 1). Shock waves possess the quality of brisance (shattering effect). The displaced air then compresses and forms a vacuum returning to the point of detonation (negative wave). The negative phase is not considered to result in blast injury. High-order explosives include TNT, C-4, Semtex, nitroglycerin, dynamite, and ammonium nitrate fuel oil. Low-order explosives produce a subsonic explosion without overpressurization wave. Energy is released slowly and burns by a process of deflagration. Low-order explosives include pipe bombs, gun powder, Molotov cocktails, and pure petroleum-based bombs. Explosives have several effects: the blast pressure wave as described previously, the fragmentation effect, the blast wind, the incendiary thermal effect, secondary blast pressure effects, and ground and water shocks for explosions that occur below ground or water.⁹

Figure 1 Propagation of blast wave over time.

(Data from Jensen JH, Bonding P: Experimental pressure induced rupture of the tympanic membrane in man. Acta Otolaryngol 113:62–67, 1993.)

Fragmentation effect occurs from projectiles included in the container, projectiles produced from the destruction of the container, and from objects surrounding the detonator and target. These projectiles can travel up to 2700 feet per second. The blast wind is created by the motion of air molecules responding to pressure differentials generated by the blast. These winds may be as high as those seen in hurricanes but are not sustained. The incendiary thermal effect is different for high- and low-order explosives. High-order explosives produce higher temperatures for shorter periods of time, usually resulting in a fireball at the time of the detonation. Low-order explosives have a longer thermal effect and cause secondary fires. Secondary blast pressure effects are caused by the blast wave’s reflection off surfaces prolonging and magnifying the effect, particularly in enclosed spaces. Greater transfer of energy to the body occurs. Underground and underwater explosions propagate the shock waves farther and with more force than air.¹⁰

Bombs are weapons and defined as any container filled with explosive material whose explosion is triggered by a clock or other timing device. Terrorist bombs, IEDs, are usually custom-made, may use a number of designs or explosives, and are of two types: conventional (filled with chemical explosives containing the compounds of hydrogen, oxygen, nitrogen, and carbon) or dispersives (filled withchemical or other projectiles such as nails, steel pellets, screws, and nuts) designed to disperse. Nuclear devices rely on nuclear fission or fusion. Explosions can produce unique patterns of injury. They have the potential to inflict multisystem life-threatening injuries on many persons simultaneously. The injury patterns following such events are a product of the composition and amount of the materials involved, the surrounding environment, and the delivery method, the distance between the victim the blast, and any intervening protective barriers or environmental hazards. Because explosions are relatively infrequent, blast-related injuries can present unique triage, diagnostic, and management challenges to providers or emergency care personnel.¹¹

BLAST INJURY: CLINICAL ASPECTS

Blast-related injuries are now very common and have become a threat for populations all over the world. Powerful explosions that result in different tissue and air interactions have the potential to inflict complex and unique injuries. Severely injured patients from explosions often sustain combined blunt, penetrating, and burn injuries.¹² Therefore, knowledge of the mechanisms of blast effect and early recognition of the potential injuries are of paramount importance in the management of blast-injured patients. The injury patterns vary depending on setting (open or closed space), amount of explosive, and chemical properties of the explosive.¹³ Explosions in confined spaces are significantly more deadly and associated with high incidence of primary blast injuries than those in open air. Improvised explosive devices are accompanied by heavy shrapnel that result in various injury patterns involving more body regions and increase severity. This makes management of blast injuries more challenging.⁴ According to their underlying mechanisms, blast injury is classified into four categories: primary, secondary, tertiary, and quaternary (Table 1).¹⁴ Quinary blast injury also has recently been described.

Table 1 Categories of Blast Injury

Type of Blast Injury	Features
Primary	Caused by barotrauma
Primary	Affects gas-filled structures including tympanic membrane, lungs, bowel
Secondary	Caused by flying debris and fragments
	Responsible for most of casualties
	Causes multiple injuries
Tertiary	Caused by collapse and fragmentation of buildings
Tertiary	Causes severe fractures and amputations
Quaternary	Includes all explosion-related injuries
Quaternary	Affected by patient’s premorbidities
Quinary	Hyperinflammatory state
Quinary	Toxins in explosives

Primary Blast Injury

Primary blast injury causes barotrauma. The organs most vulnerable to primary blast injury are the gas-filled, namely the ear, lung, and gastrointestinal tract. The eardrum, the most frequently injured structure, may rupture at pressure as low as 2 psi (pounds/square inch).¹⁵ High overpressure may cause more significant injury to the ear such as dislocation and fracture of the ossicles of the middle ear, cochlear damage, and traumatic disruption of the oval or round window and subsequent permanent hearing loss.

The most common manifestations of ear blast injury are tinnitus, deafness, and vertigo. The fact that tympanic membrane injury occurs at low pressure and much more pressure is needed to damage other structures make tympanic membrane perforation an indicator of blast injury.

The anatomical structure of the lungs is characterized by large surface area with low tensile strength. This makes the lung very susceptible to primary blast injury, and injury to the lung may be the most fatal. The incidence of blast lung injury is unknown. In a study by Brismar and Bergenwald,¹⁶ 8.4% of patients admitted after a blast were diagnosed with lung injury. Hadden et al.¹⁷ in a study from Northern Ireland reported that only 2 of 250 admitted patients (0.8%) suffered from primary blast lung injury; on the other hand, histopathologic evidence consistent with primary blast lung injury was found in 45% of the victims who died at the scene. A high proportion of primary blast lung injury occurs in explosions in enclosed space. In a study of 55 survivors after a terrorist bus bombing, Katz et al.¹⁸ found that 38% of patients had primary blast lung injury. Primary blast lung injury occurs at air pressure of 1100 kpcal (kilopascals) (Figure 2). The pressure differentials disrupt the alveolar walls and the alveolar-capillary membrane, and damage airway epithelium, producing a stripped-epithelium lesion. This results when bronchiolar epithelium is stripped from the basal membrane.¹⁹ As a result of these widespread structural disturbances, hemorrhage, pulmonary contusion, pneumothorax, hemothorax, pneumomediastinum, and subcutaneous emphysema can occur. Intrapulmonary hemorrhage and edema are major factors in the development of initial respiratory insufficiency from primary blast lung injury.²⁰ Some experience apnea, bradycardia, and hypotension as immediate responses to blast injury of the lung. The diagnosis of primary blast lung injury is based on clinical manifestations, such as dyspnea, hypoxia, and hemoptysis. A chest x-ray may show the characteristic bihilar “butterfly” pattern representing underlying pulmonary contusion.^21,²² A tear that may occur between the alveoli and the wall of the venule can create alveolo-venous fistulae, the major prerequisite for another life-threatening condition—arterial air embolism. This is a principal cause of early mortality.¹⁸