The hallmark of primary blast injury is damage to the respiratory system, or “blast lung,” and is manifested by varying degrees of pulmonary contusion and barotrauma. The extent of pulmonary pathology is directly proportional to the velocity of chest-wall displacement by the incoming blast wave (16), which in turn is dictated by the size of the explosive charge, distance from blast epicenter, orientation of the thorax in relation to the blast wave, and geography of nearby reflecting surfaces. Injury tends to be worse on the side of approach of blast waves in open air but is usually bilateral or diffuse when the victim is located in a confined space (17).

As a blast wave propagates through the chest, enormous pressure differentials are generated at interfaces between media of different densities (8,13) resulting in alveolar tears and vascular disruption. There is also evidence from rat lung models that subtle biochemical changes and free-radical-mediated oxidative stresses contribute to blast-induced injury (18,19). Pleural or subpleural petechiae are the mildest pathological findings (17,20). Higher energy stress waves conducted deeper into the lung can cause subpleural hemorrhage where the blast front first contacted the chest wall, as well as near the diaphragm and mediastinum, where reflections and summations of stress waves occur (7,21). Even more powerful blast impulses cause large parenchymal tears and stripping of small airway epithelium (22). Communication between the airways and the pleural space can lead to simple or tension pneumothorax, hemothorax, traumatic emphysema, and alveolo-venous fistulae, which, in the already compromised lung, will precipitate even more rapid respiratory failure. Unfortunately, the need for early positive-pressure ventilation to treat such patients with rapidly progressing respiratory failure can aggravate the situation, increasing the risk for both tension pneumothorax and air embolism (3).

Clinically, blast lung injury can appear very similar to a pulmonary contusion from blunt chest trauma but without associated rib fractures or chest wall injury (13,23). This is rarely seen in the absence of other secondary or tertiary explosion injuries. Like blunt pulmonary contusion, gas exchange is impaired at the alveolar level, and the degree of respiratory insufficiency depends on the extent of hemorrhage. Signs and symptoms of primary pulmonary blast injury may include dyspnea, difficulty completing sentences in one breath, rapid shallow respirations, poor chest wall expansion, cough, hemoptysis, decreased breath sounds, and wheezes.

A dreaded complication of primary pulmonary blast injury is the development of arterial air embolism, thought to be responsible for most of the sudden deaths that occur within the first hour after blast exposure (24). The true incidence of systemic air embolism is unknown. Only those with clinical evidence of blast lung injury seem to be at risk, with a greater incidence following explosions in confined spaces (25).

Large blast impulses passing through the lung can cause hemopneumothoraces, traumatic emphysema, and vascular disruption (6). Air emboli result from the direct communication created between the traumatized pulmonary airspace and vasculature. Such communication can develop at any time after a blast injury, either directly from the blast or as a
complication of therapy for respiratory failure (24). Normally, in a patient with spontaneous respirations, the airway pressure remains lower than the pulmonary venous pressure. After blast trauma, states of low pulmonary venous pressure (hypovolemia) or high airway pressure (positive-pressure ventilation, coughing, or tension pneumothorax) may cause the pressure gradient to reverse, allowing air to enter the pulmonary circulation (26,27,28) and to be systemically disseminated. One of the first animal studies linking air embolism with blast lung injury subjected a dog to a near-lethal air blast. Showers of carotid air emboli were detected for 30 minutes after injury (29). Animal experiments have also demonstrated coronary air emboli in rats dying immediately following a blast (9).

Obstruction from air bubbles may occur in any vascular bed. The passage of air bubbles causes a transient precapillary block and arterial spasm, dilatation, stasis, and ischemia (9). Air emboli to the heart or brain are thought to be the most common cause of rapid death solely caused by blast injury in immediate survivors (30,31,32). The introduction of as little as 2 milliliters of air into the cerebral circulation can be fatal (33,34). Likewise, as little as 0.5 to 1 milliliter of air injected into a pulmonary vein can cause cardiac arrest from coronary air embolism (35).

Clinical manifestations of systemic air embolism depend on the location of embolic occlusion and on the degree of resultant ischemia. Air embolism is often heralded by a rapid decompensation immediately following intubation and positive-pressure ventilation (36); such collapse is usually unresponsive to conventional resuscitation (37). Hemoptysis, suggesting communication between pulmonary blood vessels and the airway, was seen in 22% of cases of systemic air embolism in one large series (38). Other symptoms include blindness due to air in retinal vessels, focal neurological deficit or loss of consciousness following cerebral obstruction, and chest pain from coronary obstruction and myocardial ischemia. Air emboli to the skin may produce a reddish-blue mottling discoloration called livido reticularis. Tongue blanching and pharyngeal petechiae may be seen. An arterial blood gas sample may appear frothy with air bubbles, and EKG may reveal arrhythmias or ischemia (39). In those with lung trauma, the combination of hemoptysis and circulatory or CNS dysfunction immediately after initiation of positive-pressure ventilation is sufficient to make the provisional diagnosis of systemic air embolism (27).

Gas-containing abdominal structures are injured in a similar manner as the lungs (17), but such injuries are frequently occult and overshadowed by the more immediately life-threatening manifestations of pulmonary blast injury (24). Military studies have found that in open-air bombings, GI injury occurs with the same frequency as lung injury (40) and at lower pressures following blasts in enclosed spaces (41). Victims of underwater explosions seem to be at a much greater risk for GI injury, especially if treading water or partially submerged (39).

Blast injury tends to affect the colon more often than the small bowel, owing to the greater amount of air in the former. Damage may range from edema to hemorrhage to frank rupture. Rupture is commonly delayed 24 to 48 hours, after stretching and ischemia have weakened the bowel wall (42). Tangential shear waves affecting the liver, spleen, and kidneys have been described, causing subcapsular petechiae, contusions, lacerations, or rupture (39,43). However, nonbowel or solid organ injuries seen following explosions are far more likely to occur from the effects of secondary or tertiary blast injury (8). Signs and symptoms of GI blast injury are nonspecific and include abdominal pain, nausea, vomiting, diarrhea, tenesmus, absent or decreased bowel sounds, rebound tenderness, guarding, or frank rectal bleeding.

The ear is designed to amplify ambient sound waves, and the thin tympanic membrane is directly exposed to the surrounding air. It is not surprising that blast injury to the auditory system occurs much more commonly and at much lower overpressures than do pulmonary or GI blast injury. As a frame of reference, extremely loud acoustic waves, such as those generated at a concert, are generally less than 0.04 psi. Overpressures of at least 1 to 8 psi are needed to cause tympanic membrane rupture (44,45), whereas the threshold for lung injury is typically upward of 50 to 100 psi.

Blast waves are known to cause conductive, sensorineural, and mixed hearing defects. Conductive loss is usually caused by rupture of the tympanic membrane, although ossicular chain disruption may also be seen (24). Such defects are rarely found in isolation, however; most casualties will invariably suffer some degree of concomitant sensorineural hearing loss (46). Blast-related inner ear damage due to transient cochlear dysfunction can cause acute sensorineural hearing loss, often accompanied by tinnitus, which can be quite incapacitating in the moments following an explosion (24). Vertigo and balance disorders have also been described but are thought to be more likely secondary to blunt head injury than primary auditory damage (47).

Although tympanic membrane rupture is objective evidence of significant exposure to blast overpressure and was once thought to be an effective marker for occult pulmonary or GI blast injury, a recent Israeli study demonstrated no significant correlation. In fact, no patients with isolated tympanic membrane rupture later developed evidence of lung or GI pathology (48).

Secondary blast injury, caused by shrapnel and displaced debris, is responsible for the majority of casualties resulting from an explosive event, partly because victims do not have to be close to the blast epicenter to be injured. In fact, blast winds channeled by an alleyway or corridor can be magnified substantially (49), causing significant secondary blast injury to those distant from the epicenter. Shrapnel injuries have been reported in 20% to 40% of blast victims, with an increased incidence in enclosed spaces (50). Injuries from all types of missiles have been described, although in the urban setting, glass has been the most common
hazard (9). Terrorists often deliberately pack small metal objects such as nails, bolts, and screws around an explosive charge in an attempt to increase shrapnel injuries; military shell casings are specifically designed to fragment to achieve a similar goal. These irregularly shaped missiles are generally of high mass and therefore high kinetic energy. The kinetic energy is dissipated rapidly along wound tracts to produce severe tissue destruction (51). Such wounds are usually heavily contaminated. At missile speeds of 15 meters per second (m/s), skin may be lacerated; at speeds of 120 m/s and above, body penetration and significant tissue damage can occur (9). A detonation causing a peak overpressure of 5 psi, just strong enough to rupture half of exposed tympanic membranes, may generate a blast wind of up to 70 m/s (156 mph) (6), a speed that, although not sustained, can exceed that of most hurricanes (52). A blast wind sufficient to cause primary lung injury in a significant number of casualties may exceed 400 m/s (895 mph) (6). Most conventional military explosives can propel fragments with initial velocities reaching 1,500 m/s (53). Secondary blast injuries were a significant cause of morbidity in the Oklahoma City bombing; the Murrah Building’s glass facade shattered and was propelled over an area of many city blocks. Similarly, in the 1998 U.S. embassy bombing in Nairobi, flying glass wounded people up to 2 km away (52).

Tertiary blast injury is a feature of high-energy explosions and occurs when the individual becomes the missile. A high explosive blast wind may propel a 75 kilogram adult with an acceleration of close to 15 G’s. Typical patterns of blunt trauma and deceleration injury are seen when casualties are thrown against a solid object or the ground. Blunt head injury is a leading cause of death in blast victims. Tertiary blast injury accounted for most of the pediatric casualties in the Oklahoma City bombing because children are lighter and more easily displaced by blast wind. There was a high incidence of skull fractures, closed head injuries, and long-bone fractures.

A variety of other blast-related injuries have been described. Ocular injuries from flying debris are very common after explosions. Injury can be extensive and can involve all tissues of the eye, the ocular adnexa, and the orbit, including simple corneal abrasions, lid lacerations, global rupture, retinal detachment, intraocular foreign bodies, and orbital fractures. Retinal air embolism is also a potential cause of visual disturbance. A review of ocular injuries sustained by survivors of the 1995 Oklahoma City bombing found an 8% overall incidence of ocular injury, with 71% of injuries occurring within 300 feet of the point of detonation. The Murrah Building’s glass facade, shattered by the blast, accounted for two-thirds of all ocular injuries (54).