|Classification and external resources|
A blast injury is a complex type of physical trauma resulting from direct or indirect exposure to an explosion. Blast injuries occur with the detonation of high-order explosives as well as the deflagration of low order explosives. These injuries are compounded when the explosion occurs in a confined space.
Blast injuries are divided into four classes: primary, secondary, tertiary, and quaternary.
Primary injuries are caused by blast overpressure waves, or shock waves. These are especially likely when a person is close to an exploding munition, such as a land mine. The ears are most often affected by the overpressure, followed by the lungs and the hollow organs of the gastrointestinal tract. Gastrointestinal injuries may present after a delay of hours or even days. Injury from blast overpressure is a pressure and time dependent function. By increasing the pressure or its duration, the severity of injury will also increase.
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 such as the lungs, while primary blast-induced traumatic brain injury has remained underestimated. Blast lung refers to severe pulmonary contusion, bleeding or swelling with damage to alveoli and blood vessels, or a combination of these. It is the most common cause of death among people who initially survive an explosion.
Secondary injuries are caused by fragmentation and other objects propelled by the explosion. These injuries may affect any part of the body and sometimes result in penetrating trauma with visible bleeding. At times the propelled object may become embedded in the body, obstructing the loss of blood to the outside. However, there may be extensive blood loss within the body cavities. Fragmentation wounds may be lethal and therefore many anti-personnel bombs are designed to generate fragments.
Most casualties are caused by secondary injuries. Some explosives, such as nail bombs, are deliberately designed to increase the likelihood of secondary injuries. In other instances, the target provides the raw material for the objects thrown into people, e.g., shattered glass from a blasted-out window or the glass facade of a building.
Displacement of air by the explosion creates a blast wind that can throw victims against solid objects. Injuries resulting from this type of traumatic impact are referred to as tertiary blast injuries. Tertiary injuries may present as some combination of blunt and penetrating trauma, including bone fractures and coup contre-coup injuries.
Young children, because they weigh less than adults, are at particular risk of tertiary injury.
Traumatic amputations quickly result in death, and are thus rare in survivors, and are often accompanied by significant other injuries. The rate of eye injury may depend on the type of blast. Psychiatric injury, some of which may be caused by neurological damage incurred during the blast, is the most common quaternary injury, and post-traumatic stress disorder may affect people who are otherwise completely uninjured.
High-order explosives produce a supersonic overpressure shock wave, while low order explosives deflagrate (subsonic combustion) and do not produce an overpressure wave. A blast wave generated by an explosion starts with a single pulse of increased air pressure, lasting a few milliseconds. The negative pressure (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 material 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. As a result, individuals between the blast and a building generally suffer two to three times the degree of injury compared to those in open spaces.
Blast injuries can cause hidden brain damage and potential neurological consequences. 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 polytrauma, i.e. injury involving multiple organs or 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 destruction initiates the synthesis and release of hormones or mediators into the blood which, when delivered to the brain, change its function. Irritation of the nerve endings in injured peripheral tissue or organs also contributes significantly 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 swelling and cerebral vasospasm despite continuous monitoring. However, the first symptoms of blast-induced neurotrauma (BINT) may occur months or even years after the initial event, and are therefore categorized as secondary brain injuries. The broad variety of symptoms includes weight loss, hormone imbalance, chronic fatigue, headache, and problems in memory, speech and balance. These changes are often debilitating, interfering with daily activities. Because BINT in blast victims is underestimated, valuable time is often lost for preventive therapy and/or timely rehabilitation.
Casualty estimates and triage
Explosions in confined spaces or which cause structural collapse usually produce more deaths and injuries. Confined spaces include mines, buildings and large vehicles. For a rough estimate of the total casualties from an event, double the number that present in the first hour. Less injured patients often arrive first, as they take themselves to the nearest hospital. The most severely injured arrive later, via Emergency Services ("upside-down" triage). If there is a structural collapse, there will be more serious injuries that arrive more slowly.
- Editorial Board, Army Medical Department Center & School, ed. (2004). Emergency War Surgery (3rd ed.). Washington, DC: Borden Institute. Retrieved 2010-11-01.
- Blast Injury Translating Research Into Operational Medicine. James H. Stuhmiller, PhD. Edited by William R. Santee, PhD Karl E. Friedl, PhD, Colonel, US Army. Borden institute (2010)
- Chapter 1: Weapons Effects and Parachute Injuries, pp. 1–15 in Emergency War Surgery (2004)
- Sasser SM, Sattin RW, Hunt RC, Krohmer J (2006). "Blast lung injury". Prehosp Emerg Care 10 (2): 165–72. doi:10.1080/10903120500540912. PMID 16531371.
- Born CT (2005). "Blast trauma: The fourth weapon of mass destruction". Scandinavian Journal of Surgery 94 (4): 279–85. PMID 16425623.
- Keyes, Daniel C. (2005). "Medical response to terrorism: preparedness and clinical practice". Lippincott Williams & Wilkins. pp. 201–202. ISBN 978-0-7817-4986-2
- Marks, ME (2002). The Emergency Responder's Guide to Terrorism. Red Hat Publishing Co., Inc. pp. 30–2. ISBN 1-932235-00-0.
- Cernak, I., and L. J. Noble-Haeusslein. 2010. Traumatic brain injury: An overview of pathobiology with emphasis on military populations. J Cereb Blood Flow Metab 30(2):255-266.
- "Explosions and Blast Injuries: A Primer for Clinicians" (PDF). CDC. Retrieved 2013-12-29.. Occasionally updated.
- Chaloner E (2005). "Blast injury in enclosed spaces: All doctors should know the basic management of patients injured by explosive blast" (PDF). BMJ 331 (7509): 119–20. doi:10.1136/bmj.331.7509.119. PMC 558684. PMID 16009670.
- McSwain NE, 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 VJ, Ignjatovic D, Jevtic M (1999). Blast injury from explosive munitions. J Trauma, 47(1), 96-103; discussion 103-104.
- Cernak I, Savic VJ, 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 VJ, 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 VJ, 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 TL (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 CJ (1956). Blast injury. Physiol. Rev., 36, 336-354.
- Dedushkin VS, Kosachev ID, Tkachenko SS, Shapovalov, VM (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, MS (1981). Explosive blast injury. Med Bull US Army Eur, 38(7/8), 36-43.
- Phillips Y, Zajtchuk, JT (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 KG, Hansson HA (2000). Blast exposure causes redistribution of phosphorylated neurofilament subunits in neurons of the adult rat brain. J Neurotrauma., 17(8), 719-726.