Blast injury

Blast injuries are inflicted on individuals subjected to the effects of the detonation of high-order explosives, explosives that produce a supersonic over-pressurization shock wave, as well as low order explosives which produce a subsonic explosion with no over-pressurization wave. These injuries are compounded when the explosion takes place in a confined space.

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A blast wave generated by an explosion starts with a single pulse of increased air pressure, lasting a few milliseconds. The negative pressure or suction of the blast wave follows immediately after the positive wave. The duration of the blast wave, i.e., the time an object in the path of the shock wave is subjected to the pressure effects, depends on the type of explosive and the distance from the point of detonation. The blast wave progresses from the source of explosion as a sphere of compressed and rapidly expanding gases, which displaces an equal volume of air at a very high velocity. The velocity of the blast wave in air may be extremely high, depending on the type and amount of the explosive used. Indeed, while a hurricane-force wind (approximately 200 km/h) exerts only 0.25 PSI overpressure (i.e. 1.72 kPa), a lethal blast-induced overpressure of 100 PSI (i.e. 690 kPa) travels with a velocity of approximately 1500 mph (i.e. 2414 km/h). An individual in the path of an explosion will be subjected not only to excess barometric pressure, but to pressure from the high-velocity wind traveling directly behind the shock front of the blast wave. The magnitude of damage due the blast wave is dependent on: 1) the peak of the initial positive pressure wave (bearing in mind that an overpressure of 60-80 PSI or 414-552 kPa is considered potentially lethal); 2) the duration of the overpressure; 3) the medium in which it explodes; 4) the distance from the incident blast wave; and 5) the degree of focusing due to a confined area or walls. For example, explosions near or within hard solid surfaces become amplified two to nine times due to shock wave reflection. Moreover, victims located between the blast and a building, generally suffer two to three times the degree of injury compared to an individual in an open space.

Blast injuries are divided into four classes:

• Primary: injuries due to high-order explosive over-pressurization shock wave as it moves through the body targeting gas-containing organs (ear, lungs, and the gastrointestinal tracts)or those containing structures with different specific weights.

In general, primary blast injuries are characterized by the absence of external injuries, thus internal injuries are frequently unrecognized and their severity underestimated. According to the latest experimental results, the extent and types of primary blast-induced injuries depend not only on the peak of the overpressure, but also other parameters such as number of overpressure peaks, time-lag between overpressure peaks, characteristics of the shear fronts between overpressure peaks, frequency resonance, and electromagnetic pulse, among others. There is general agreement that spalling, implosion, inertia, and pressure differentials are the main mechanisms involved in the pathogenesis of primary blast injuries. Thus, the majority of prior research focused on the mechanisms of blast injuries within gas-containing organs/organ systems, while primary blast-induced brain injury has remained underestimated. Moreover, all safety recommendations account for the injurious effects of blast on extra-cerebral body parts/organs and not on hidden brain damage and potential neurological consequences.

There is an outdated dogma that neurological impairments caused by primary blasts are rare because the skull provides excellent protection for the brain. That is, brain injury development is solely a consequence of air-emboli in cerebral blood vessels. Unfortunately, despite recent clinical and experimental findings as well as experience in the current military operations clearly demonstrating significant short- and long-term neurological deficits caused by blast exposure without a direct blow to the head, this old belief prevails in professional literature and clinical practice. Although blast-induced neurotrauma is the most frequent of all in-theater injuries, it is a neglected and under-diagnosed consequence of asymmetric warfare. Its complex clinical syndrome is caused by the combination of all blast effects, i.e., primary, secondary, tertiary and quaternary blast mechanisms. It is noteworthy that blast injuries usually manifest in a form of poly-trauma, i.e. injury involving multiple organs/organ systems. Bleeding from injured organs such as lungs or bowel causes a lack of oxygen in all vital organs, including the brain. Damage of the lungs reduces the surface for oxygen uptake from the air, reducing the amount of the oxygen delivered to the brain. Tissue destructions initiate the synthesis and release of hormones/mediators into the blood which, delivered to the brain, change the brain’s function. Irritation of the nerve endings in injured peripheral tissue and/or organs also significantly contributes to blast-induced neurotrauma.

Individuals exposed to blast frequently manifest loss of memory for events before and after explosion, confusion, headache, impaired sense of reality, and reduced decision-making ability. Patients with brain injuries acquired in explosions often develop sudden, unexpected brain edema and cerebral vasospasm despite continuous monitoring; however, the first symptoms of blast-induced neurotrauma are latent, occurring months or sometimes years after the initial event. The broad variety of symptoms includes weight loss, hormonal disbalance, chronic fatigue and headache, and problems in memory, speech and balance, among others. These changes are often debilitating to the activities of the daily life. Because BINT in blast victims is underestimated, valuable time is often lost for preventive therapy and/or timely rehabilitation.

• Secondary: injuries due to bomb fragments and other objects propelled by the explosion.

These injuries may affect any part of the body and sometimes result in visible hemorrhage. At times the propelled object may become embedded in the body, obstructing the loss of blood to the outside. However, there may be extensive loss of blood within the body cavities. Shrapnel wounds may be lethal and therefore many anti-personnel bombs are designed to generate shrapnel and fragments.

• Tertiary: injuries as a result of the victim becoming a missile and being thrown against other objects. The injuries sustained are then similar to those that are sustained by blunt trauma, including bone fractures and coup/contre-coup injuries.

• Quaternary: all other injuries not included in the first three classes. These include burns, crushing injuries and respiratory injuries.

See also

• Bomb
• Explosive
• Suicide bombings

References

• Explosions and Blast Injuries: A Primer for Clinicians from the CDC

≠ McSwain N. E. & Frame S., 2003, PHTLS Basic and Advanced Prehospital Trauma Life Support, 5th ed., Mosby, St. Louis

Benzinger, T. (1950). Physiological effects of blast in air and water. In German Aviation Medicine, World War II (Vol. 2, pp. 1225-1229). Washington DC: Department of the Air Force.

Cernak, I., Savic, J., Ignjatovic, D., & Jevtic, M. (1999). Blast injury from explosive munitions. J Trauma, 47(1), 96-103; discussion 103-104.

Cernak, I., Savic, J., Zunic, G., Pejnovic, N., Jovanikic, O., & Stepic, V. (1999). Recognizing, scoring, and predicting blast injuries. World J Surg, 23(1), 44-53.

Cernak, I., Savic, V. J., Kotur, J., Prokic, V., Veljovic, M., & Grbovic, D. (2000). Characterization of plasma magnesium concentration and oxidative stress following graded traumatic brain injury in humans. J Neurotrauma, 17(1), 53-68.

Cernak, I., Savic, V. J., Lazarov, A., Joksimovic, M., & Markovic, S. (1999). Neuroendocrine responses following graded traumatic brain injury in male adults. Brain Inj, 13(12), 1005-1015.

Cernak, I., Wang, Z., Jiang, J., Bian, X., & Savic, J. (2001a). Cognitive deficits following blast injury-induced neurotrauma: possible involvement of nitric oxide. Brain Inj, 15(7), 593-612.

Cernak, I., Wang, Z., Jiang, J., Bian, X., & Savic, J. (2001b). Ultrastructural and functional characteristics of blast injury-induced neurotrauma. J Trauma, 50(4), 695-706.

Chiffelle, T. L. (1966). Pathology of direct air-blast injury. In Technical Progress Report DA-49-146-XY-055. Washington DC: Defense Atomic Support Agency, Department of Defense.

Clemedson, C. J. (1956). Blast injury. Physiol. Rev., 36, 336-354.

Dedushkin, V. S., Kosachev, I. D., Tkachenko, S. S., & Shapovalov, V. M. (1992). [Rendering medical care and the volume of the treatment of victims with blast injuries (a review of the literature)]. Voen Med Zh.(1), 13-18.

Owen-Smith, M. S. (1981). Explosive blast injury. Med Bull US Army Eur, 38(7/8), 36-43.

Phillips, Y. Y., & Zajtchuk, J. T. (1989). Blast injuries of the ear in military operations. Ann Otol Rhinol Laryngol Suppl., 140, 3-4.

Rice, D., & Heck, J. (2000). Terrorist bombings: Ballistics, patterns of blast injury and tactical emergency care. The Tactical Edge Journal, Summer, 53-55.

Rossle, R. (1950). Pathology of blast effects. In German Aviation Medicine, World War II (Vol. 2, pp. 1260-1273). Washington DC: Department of the Air Force.

Saljo, A., Bao, F., Haglid, K. G., & Hansson, H. A. (2000). Blast exposure causes redistribution of phosphorylated neurofilament subunits in neurons of the adult rat brain. J Neurotrauma., 17(8), 719-726.