Blast injury: A case study

International Emergency Nursing (2012) 20, 173–178

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CASE STUDY

Blast injury: A case study Steven Housden MSc BSc (Hons) BN (Hons) RN (A) Queen Alexandra’s Royal Army Nursing Corps (QARANC), United Kingdom Received 26 May 2011; received in revised form 5 September 2011; accepted 6 September 2011

Introduction Blast injuries can occur in the civilian setting, but are typically seen in both military and civilian casualties on operations (Hodgetts et al., 2006; Elliott, 2010). However, there is now a greater potential to witness the effects of explosions in the UK due to terrorism and the increased use of Improvised Explosive Devices (IEDs). The use of IEDs are synonymous with Iraq and Afghanistan (Ramasamy et al., 2009), however, IEDs have been utilised by terrorists with devastating results in Bali (2002, 2005), Madrid (2004), and in the UK and Northern Ireland when the Irish Republican Army (IRA) were active, including the Omagh bombing in 1998. The more recent bombings in London (July 2005), showed how civilian authorities have had to manage extensive blast injuries (Shirley, 2006). Explosions can cause considerable injuries through several mechanisms; by the blast wave, blast wind, fragmentation, blunt force trauma, thermal and chemical burns, yet having carried out an extensive search there is little literature in UK nursing journals pertaining to blast injuries. As emergency nurses are in a key position to treat casualties presenting with these injuries, it is essential to understand the phenomenon that is blast, and the wound patterns it can cause.

Case study The case report is focused on an Afghan male, approximately 50 years of age, who had been involved in an exploE-mail address: [email protected]

sion caused by an IED in the Helmand province. The casualty was flown to the base’s medical facility by the Medical Emergency Response Team (MERT) helicopter for resuscitation. On arrival the patient was given high flow oxygen via a non-rebreath mask, and observations of pulse, blood pressure, oxygen saturation and respiratory rate were monitored, and the primary survey carried out. In the civilian approach to emergency care, the ABCD paradigm has always been used, however, the military approach is ÆCæABCD, where ÆCæ denotes catastrophic haemorrhage. This approach has been adopted because the evidence shows external peripheral haemorrhage to be the leading cause of death in combat casualties (Hodgetts et al., 2006). The military has also introduced Battlefield Advanced Trauma Life Support (Joint Services Publication 570, 2008), which closely follows Advanced Trauma Life Support and utilises the ÆCæABCDE approach to treat blast and ballistic injuries which are immediately life threatening (Hodgetts et al., 2006). The chest examination was carried out using the pneumonic RISE N FALL, as taught in the Battlefield Advanced Trauma Life Support (BATLS) guidelines (Joint Services Publication 570, 2008).

Assessment – Primary survey ÆCæ – CATASTROPHIC HAEMORRHAGE: No catastrophic haemorrhage had occurred (i.e.: no traumatic amputation, no external haemorrhage due to the severing of major blood vessels). A – AIRWAY: Was intact and patent; no stridor, no obstruction on inspection, therefore no requirement for an airway adjunct.

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174 B – BREATHING: (Chest assessment using the pneumonic ‘RISE N FALL’).  R – Rate: Rapid, greater than 30 breaths per minute.  I – Injuries: None seen on exposure; no fragmentation injury, no burns.  S – Symmetry: Unable to fully assess chest movement.  E – Effort: Considerable effort to breathe, accessory muscles used; casualty was in severe respiratory distress.  N – Neck signs:  T – Trachea: Unable to tell ascertain any central deviation.  W – Wounds: None present to neck.  E – Emphysema: No surgical emphysema felt on examination.  L – Larynx: Visibly intact.  V – Veins: None visibly distended  E – Every time (to check every time).  F – Feel: No wounds or crepitus felt.  A – Assess resonance: Hyper-resonance heard over the left side of chest when percussed, indicating a tension pneumothorax.  L – Listen: Auscultation was difficult to establish air entry due to background noise.  L – Look: Looking at the casualty’s back showed no entry or exit wounds. C – CIRCULATION: The casualty had a palpable radial pulse, indicating a systolic blood pressure 80–90 mm Hg. The casualty’s abdomen was soft, non-tender. The casualty was cannulated, but due to a radial pulse present no fluid was infused, following hypotensive resuscitation guidelines as set in BATLS (Joint Services Publication 570, 2008). D – DISABILITY: The casualty scored A on the AVPU scale. GCS could not be ascertained due to language barriers, even with an interpreter present. E – EXPOSURE: Showed no other obvious life threatening injuries, no obvious limb fractures or other injuries due to fragmentation or burns. No catastrophic haemorrhage had occurred, but the assessment during the primary survey identified a left sided tension-pneumothorax, which is caused when air enters the intrapleural space and cannot escape resulting in a progressive increase in trapped air. This leads to a mediastinal shift, which causes the displacement of the, trachea, heart and vena cava, resulting in decreased cardiac output (Ursic and Curtis, 2010). The adjacent lung is also compressed, preventing lung expansion and ventilation, leading to respiratory distress.

Treatment The resultant tension pneumothorax required decompression of the chest (Ursic and Curtis, 2010) using needle thoracocentesis, by placing a large bore cannula into the second intercostal space, midclavicular line (Cullinane et al., 2001), followed shortly by the insertion of a chest drain (Davis et al., 2005). Haemodynamic instability requires fluid resuscitation, and the aim was for hypotensive resuscitation until the casualty could be treated at the Italian emergency hospital.

S. Housden Therefore following BATLS guidelines for hypotensive resuscitation, fluid replacement was not started immediately because of a palpable radial pulse (Joint Services Publication 570, 2008). However, the evidence shows that hypotensive resuscitation can only be maintained for an hour, as prolonged hypotensive resuscitation has a poor clinical outcome (Garner et al., 2010). The casualty was given IV morphine for pain control, and once stabilised, he was transferred to an Italian led trauma hospital in Bost, several miles from Lashkar Gah. It can be seen from the primary survey that the casualty had sustained no external injuries such as traumatic amputation of limbs, fragmentation (shrapnel) injuries or burns. Indeed it is possible that a casualty can have little or no obvious external injuries, as supported by Kluger (2003) where clear data has been generated from the Israeli–Palestinian conflict. Kirkman and Watts (2011) states observations from the First World War pertaining to casualties who developed shock despite no obvious external injuries. Therefore the rationale for including this particular casualty as a case study is despite a left sided tension pneumothorax, he had not sustained any external injury. This is an important message to convey in treating casualties, who can rapidly deteriorate due to severe injuries in the absence of obvious external injuries.

The nature of blast Blast is produced by an explosion caused by the rapid conversion of a solid or liquid to a gas, due to an intense exothermic reaction (Horrocks, 2001). When a high-explosive detonates (such as gelignite, trinitrotoluene, C4 or Semtex), an increase in air pressure is created, known as an overpressure or blast wave, which travels supersonically up to 8000 m/s (Cullis, 2001). This overpressure attains its peak pressure in the first few milliseconds following the blast (Owers et al., 2010), and can reach pressures of 20–30 kbar, where 1 kbar is 1000 times atmospheric pressure (Kocsis and Tessler, 2009). As the blast wave expands, the energy of the blast wave dissipates and the pressure decreases. If the distance from the explosion is doubled, the peak overpressure will be decreased to one eighth of its original pressure. Following the blast wave is rapidly moving air known as the blast wind, and as the gas expands, the air pressure drops causing a relative vacuum referred to as an underpressure causing reversal in the direction of the blast wind (Wolf et al., 2009). Fig. 1 shows the relationship between the blast overpressure/air pressure against time. Blast waves can be sub-divided into stress waves and shear waves. Stress waves are longitudinal waves like sound waves, but travel at or slightly faster than sound waves, but differ in their high amplitude and velocity. Shock waves are a special type of stress wave, and cause primary blast injury (PBI) of the lung and small bowel. Shear waves are transverse waves, characterised by long duration, low velocity and cause compression of visceral structures (Horrocks, 2001). In the abdomen, stress waves cause damage at the microscopic level, whereas the shear wave causes tearing of the tissues due to gross body wall and visceral motion. Laceration of solid abdominal viscera is related to very high blast loading (Owers et al., 2010).

Blast injury: A case study

175

Pressure

Peak air pressure

Positive air pressure Atmospheric air pressure

injuries caused by explosive devices were classified as such. What is valid about the article is the main causes of injury are identified for the first time, and the evidence generated regarding blast injury to the lungs is of great significance. The Centre for Disease Control and Prevention (CDC, 2006) states the same model, but no reference to its origin, and only DeWitte and Tract (2005) references the CDC for this classification. See Table 1 for a classification of injuries.

Negative air pressure

Primary blast injuries (PBIs) Time (m/secs)

Fig. 1

Air pressure vs. time.

The proximity to the centre of the blast is an important consideration; the closer to the centre of the blast, the greater the effects of the over pressure/blast wave will be (Wolf et al., 2009). A PBI is more likely to occur if the detonation occurs in confined spaces such as a building or a bus, and is due the amplification of the blast wave by solid surfaces that reflect it, increasing its force. A blast wave is also transmitted quicker through water than through the air (Wolf et al., 2009). Pure blast injury can in result in little evidence of external trauma, however, the detonation of IEDs usually result in fragmentation injury (Horrocks, 2001).

Blast injuries An extensive search of the literature relating to blast and blast injury has continually shown four types of injury based upon the mechanism that caused them: primary, secondary, tertiary and quaternary, (Hicks et al., 2010; Bridges, 2006; Cernak et al., 2011; Rosenfeld and Ford, 2010; Belanger et al., 2005). Many authors including Horrocks (2001), Kirkman and Watts (2011), Wolf et al. (2009), Cernak et al. (2011), Owers et al. (2010) and Chaloner (2005) relate this classification of blast injuries to research carried out by Zuckerman (1940). Zuckerman’s research was centred around the effects of explosions on mice, rats, guinea pigs, rabbits, cats, monkeys and pigeons. In his paper based on this research, Zuckerman (1940) stated the main mechanisms in which an explosion may kill (blast wave, fragmentation) and linked the blast wave to the cause of Blast Lung. However, in his paper, Zuckerman does not actually classify these injuries into primary, secondary, tertiary and quaternary injuries. From a review of the literature since 1940, it is not possible to ascertain exactly when the

Table 1

A primary blast injury (PBI) is caused when the pressure wave passes through media of different density such as air to tissue, causing acceleration and deceleration as it passes through the tissues, and also results in the implosion and then expansion of gas bubbles present. The process is known as spalling and when it affects the lungs it can result in a condition known as Blast Lung, and is the most common cause of PBI death. Blast Lung is characterised by the rupture of alveoli capillaries and the subsequent influx of blood and development of pulmonary oedema, which leads to a reduction in pulmonary gas exchange with subsequent hypoxia and hypercarbia (Kirkman and Watts, 2011; Bridges, 2006; Rosenfeld and Ford, 2010). Blast Lung leads to the development of acute respiratory failure and can occur within minutes (Bridges, 2006), but a late presentation can also occur 24–48 h later (Chaloner, 2005). The term Blast Syndrome is used to characterise the signs and symptoms of acute respiratory failure caused by Blast Lung and includes dyspnoea, hypoxia and coughing. Where suspected, casualties should have a chest X-ray, but not if it delays the treatment of acute respiratory failure (Bridges, 2006). With regards to fluid resuscitation, excess crystalloid fluid replacement can lead to pulmonary oedema in primary blast injury (Wolf et al., 2009). It is believed that 17–47% of blast victims who die have evidence of Blast Lung (Wolf et al., 2009), and much of the data originates from Northern Ireland and Israel (Bridges, 2006). The gastrointestinal tract is also susceptible to the pressure wave like the lungs are due to its air content (Horrocks, 2001). Cho et al. (2010) conducted a study of 133 combat casualties with colonic injuries, and found 71% acquired injuries through the blast wave and fragmentation, reflecting the use of IEDs. However, abdominal injury is less common than lung injury (Owers et al., 2010), and not as common as extremity wounds (Barker, 2001). Blast-induced neurotrauma, also known as traumatic brain injury (TBI) is a major medical concern, and is a well

Classification of blast injuries.

Injury classification

Type of injury sustained

Primary

Blast Lung, haemothoracies, haemothorax, pneumothorax, tension pneumothorax, acute arterial gas embolism, gastrointestinal perforation, blast-induced neurotrauma, eye rupture, tympanic membrane perforation Fragmentation/penetrative injuries Traumatic amputation, fractures, head injuries, blunt trauma Burns, crush injuries, angina, hypertension, closed and open brain injury, toxic inhalation, psychological problems

Secondary Tertiary Quaternary

176 documented injury (Cernak et al., 2011; Walker et al., 2010; Hicks et al., 2010; Kocsis and Tessler, 2009; Bell et al., 2009; Desmoulin and Dionne, 2009). Dougherty et al. (2011) carried out a retrospective cohort study of 2254 American personnel injured by explosions, and found that 37% of them had experienced some degree of TBI. Symptoms can vary from mild injuries such as blast injury headache (Walker et al., 2010) to fatal injuries including sub-arachnoid haemorrhage, subdural haematoma, and hyperaemia of the brain and meninges (Rosenfeld and Ford, 2010). However, the exact mechanism of how blast causes TBI is not understood (Kocsis and Tessler, 2009; Yilmaz and Pekdemir, 2006). The tympanic membrane (TM) is the anatomical structure most susceptible to increases in pressure (Breeze et al., 2011), and was traditionally used as a predictive marker of blast injury; no perforation would mean minimal exposure to blast (Wolf et al., 2009; Harrison et al., 2009). However, in a study by Harrison et al. (2009), only 16% of 167 American servicemen injured by blast exhibited TM, and was uncommon in casualties with PBI. Tympanic membrane perforation is now considered a poor indicator of blast injury (Wolf et al., 2009; Horrocks, 2001; Kluger, 2003; Harrison et al., 2009).

Secondary blast injuries Secondary injuries are caused by the blast wind, which is the rapid movement of air behind the blast wave. The blast wind accelerates fragments from the explosive device and surrounding materials causing fragmentation injuries. Indeed, fragmentation injuries are the greatest cause of injuries from exploding ordinance such as artillery shells (Hill et al., 2001). Fragments are described as primary or secondary, where primary fragments are integral to the device such as bomb casing, and secondary fragments come from the environment such as wood and debris (Joint Services Publication 570, 2008). Fragments may possess enough energy to pass through many sections of the bowel, resulting in entry and exit wounds, leading to peritonitis due to bowel contents contaminating the abdominal cavity (Hill et al., 2001). Individuals close enough to the detonation to suffer PBI usually have overwhelming secondary blast injuries (Horrocks, 2001) including ocular and maxillofacial trauma (Bridges, 2006), but those wearing body armour can be protected by injury from fragmentation (Desmoulin and Dionne, 2009), and may survive to exhibit PBI (Owers et al., 2010) as body armour will not protect from the blast wave (Dougherty et al., 2011). The literature supports the theory that body armour has allowed for increased survival rates from decreased thoracic wounds (Rosenfeld and Ford, 2010; Dougherty et al., 2011), however, Propper et al. (2010) states that insufficient evidence exists to support this theory.

Tertiary blast injury Tertiary injury is caused by the displacement of the body or its parts, resulting in blunt trauma caused by being thrown

S. Housden through the air by the blast wind, and impacting with the ground or other objects (DeWitte and Tract, 2005; Hicks et al., 2010). Traumatic amputation is the partial or total avulsion of a limb, with approximately 1–7% of blast casualties sustaining traumatic amputations, (Bridges, 2006; Wolf et al., 2009; Stansbury et al., 2008). However, the literature is divided as to its classification as a tertiary injury. DeWitte and Tract (2005), Cullinane et al. (2001), and the CDC (2006) classify traumatic amputations as a tertiary injury. However, Bridges (2006), Belanger et al. (2005) consider them as PBIs. Wolf et al. (2009) provides an excellent argument for tertiary over primary mechanisms, however, Horrocks (2001) and Harrison et al. (2007) explains in considerable detail a combination of primary and tertiary mechanisms; the blast wave fracturing the shaft of the long bones while the blast wind causes the disruption of the soft tissues leading to partial or total avulsion of the limb. Death occurring in individuals who have sustained traumatic amputations is mainly due to severe secondary and tertiary injuries such as decapitation, evisceration or open chest wounds, but also Blast Lung or catastrophic haemorrhage (Horrocks, 2001). Overall, it is believed 10% of battlefield deaths are caused by significant wounds to the extremities and can be caused by primary, secondary and tertiary mechanisms (Hodgetts et al., 2006). Secondary and tertiary injuries usually outnumber primary injuries, and remain responsible for the greatest number of battlefield injuries and deaths (Desmoulin and Dionne, 2009).

Quaternary blast injury The presence of flash burns indicates close proximity to the detonation, although the number presenting is small, but those who have been critically injured by the blast may have significant burns (Bridges, 2006). Quaternary blast injuries also include toxic substance exposure such as radiation, carbon monoxide, and psychological trauma. According to Wolf et al. (2009), a quinary pattern of injury may exist, having cited a study by Kluger et al. (2007), which was based on the clinical observations of patients admitted to the Tel Aviv Medical Centre following a terrorist bombing. A total of 27 patients were injured, with three dying. Four patients in close proximity to the explosion developed a hyperinflammatory state manifested as low central venous pressure, positive fluid balance, sweating and hyperpyrexia, possibly caused by unconventional materials used to make the bomb. However, this appears to be the only evidence to suggest a quinary mode of blast injury, and is not yet acknowledged in the literature or by the medical authorities as a true mechanism of injury.

Conclusion Injuries from explosive devices can be caused by the actual blast wave, the blast wind, fragmentation, burns and blunt trauma (Horrocks, 2001). However, the effects of explosions can severely injure a casualty without leaving any obvious external injuries, either through the direct effect of the blast wave causing PBI, or by the blast wind throwing the casualty causing tertiary injury (Kluger, 2003). The

Blast injury: A case study casualty in the case study had sustained a tension pneumothorax in the absence of fragmentation injury, which required needle thoracocentesis and insertion of a chest drain. It was unclear if the tension pneumothorax was a primary or tertiary injury, as it was difficult to ascertain the exact cause due to language barriers, even with the interpreter present. Furthermore, it was not possible to follow his progress after evacuation from the base. However, the lack of obvious injuries is an important factor to bear in mind when dealing with a blast casualty, as there may be an underlying life threatening injury.

Acknowledgement Thanks to Rebecca Hoskins, Consultant Nurse & Senior Lecturer in emergency care at the University of the West of England, Bristol.

References Barker, P., 2001. Penetrating wounds of the torso. Journal of the Royal Army Medical Corps 147, 62–72. Belanger, H.G., Scott, S.G., Scholten, J., Curtiss, G., Vanderploeg, R.D., 2005. Utility of mechanism-of-injury-based assessment and treatment: blast injury case illustration. Journal of Rehabilitation Research and Development 42, 403–412. Bell, R.S., Vo, A.H., Neal, C.J., Tigno, J., Roberts, R., Mossop, C., Dunne, J.R., Armonda, R.A., 2009. Military traumatic brain and spinal column injury: a 5 year study of the impact blast and other military grade weaponry on the central nervous system. Journal of Trauma, s104–s111. Breeze, J., Pearson, C.R., Henney, S., Reid, A., 2011. Ear injuries sustained by British service personnel subjected to blast trauma. The Journal of Laryngology & Otology 125, 13–17. Bridges, E.J., 2006. Blast injuries: from triage to critical care. Critical Care Nursing Clinics of North America 18, 333–348. Centers for Disease Control & Prevention (CDC), 2006. Explosions and blast injuries: a primer for clinicians. . Cernak, I., Merkle, A., Koliatsos, V.E., Bilik, J., Luong, Q.T., Mahota, T.M., Xu, L., Slack, Windle, D., Ahmed, F.A., 2011. The pathology of blast injuries and blast-induced neurotrauma as identified using a new experimental model of injury in mice. Neurobiology of Disease 41, 538–551. Chaloner, E., 2005. Blast injury in enclosed spaces. British Medical Journal 331, 119–120. Cho, S.D., Kiraly, L.N., Flaherty, S.F., Herzig, D.O., Lu, K.C., Schreiber, M.A., 2010. Management of colonic injuries in the combat theatre. Diseases of the Colon and Rectum 53 (5), 728– 734. Cullinane, D.C., Morris, J.A., Bass, J.G., Rutherford, E.J., 2001. Needle thoracostomy may not be indicated in the trauma patient. Injury, International Journal of the Care of the Injured 32, 749–752. Cullis, I.G., 2001. Blast waves and how they interact with structures. Journal of the Royal Army Medical Corps 147, 16–26. Davis, D.P., Pettit, K., Rom, C.D., 2005. The safety and efficacy of pre-hospital needle and tube thoracostomy by aeromedical personnel. Pre-hospital Emergency Care 2, 191–197. Desmoulin, G.T., Dionne, J., 2009. Blast-induced neurotrauma: surrogate use, loading mechanisms and cellular responses. Journal of Trauma 67 (5), 1113–1122. DeWitte, M., Tract, E., 2005. Challenges of blast injury. Topics in Emergency Medicine 27 (3), 176–179.

177 Dougherty, A.L., Macgregor, A.J., Han, P.P., Heltemes, K.J., Galarneau, M.R., 2011. Visual dysfunction following blastrelated traumatic brain injury from the battlefield. Brain Injury 25 (1), 8–13. Elliott, C., 2010. The use of silver-impregnated dressings in blast injury. British Journal of Nursing 19 (13), 835–839. Garner, J., Watts, S., Parry, C., Bird, J., Cooper, G., Kirkman, E., 2010. Prolonged permissive hypotensive resuscitation is associated with poor outcome in primary blast injury with controlled haemorrhage. Annals of Surgery 251 (6), 1131–1138. Harrison, S.E., Kirkman, E., Mahoney, P., 2007. Lessons learnt from explosive attacks. Journal of the Royal Army Medical Corps 153 (4), 278–282. Harrison, C.D., Berbarta, V.S., Grant, G.A., 2009. Tympanic membrane perforation after combat blast exposure in Iraq: a poor biomarker of primary blast injury. Journal of Trauma 67 (1), 210–211. Hicks, R.R., Fertig, S.J., Desrocher, R.E., Koroshetz, W.J., Pancrazion, J.J., 2010. Neurological effects of blast injury. Journal of Trauma 68 (5), 1257–1263. Hill, P.F., Edwards, D.P., Bowyer, G.W., 2001. Small fragment wounds: biophysics, pathophysiology and principles of management. Journal of the Royal Army Medical Corps 147, 41– 51. Hodgetts, T.J., Mahoney, P.F., Russell, M.Q., Byers, M., 2006. ABC to ÆCæABC: redefining the military trauma paradigm. Emergency Medicine Journal 23, 74. Horrocks, C.L., 2001. Blast injuries: biophysics, pathophysiology and management principles. Journal of the Royal Army Medical Corps 147, 28–40. Joint Services Publication 570, 2008. Battlefield Advanced Trauma Life Support (BATLS), fourth ed. Royal Centre for Defence Medicine. Kirkman, E., Watts, S., 2011. Characterisation of the response to primary blast injury. Philosophical Transactions of the Royal Society of London 336, 286–290. Kluger, Y., 2003. Bomb explosions in acts of terrorism-detonation, wound ballistics, triage and medical concerns. Israel Medical Association Journal 5, 235–340. Kluger, Y., Nimrod, A., Biderman, P., Mayo, A., Sorkin, P., 2007. The quinary pattern of blast injury. American Journal of Disaster Medicine 2 (1), 21–25. Kocsis, J.D., Tessler, A., 2009. Pathology of blast-related brain injury. Journal of Rehabilitation Research and Development 46 (6), 667–672. Owers, C., Morgan, J.L., Garner, J.P., 2010. Abdominal trauma in primary blast injury. British Journal of Surgery 98, 168–179. Propper, B.W., Gilford, S.M., Calhoon, J.H., McNeil, J.D., 2010. Wartime thoracic injury: perspectives in modern welfare. Annals of Thoracic Surgery 89, 1032–1036. Ramasamy, A., Hill, A.M., Clasper, J.C., 2009. Improvised explosive devices: pathophysiology, injury profiles and current medical management. Journal of the Royal Army Medical Corps 155 (4), 265–272. Rosenfeld, J., Ford, N.L., 2010. Bomb blast, mild traumatic brain and psychiatric morbidity: a review. Injury 41, 437–443. Shirley, P.J., 2006. Critical care delivery: the experience of a civilian terrorist attack. Journal of the Royal Army Medical Corps 152, 17–21. Stansbury, L.G., Lalliss, S.J., Branstetter, J.G., Bagg, M.R., Holcomb, J.B., 2008. Amputations in US military personnel in the current conflicts in Afghanistan and Iraq. Journal of Orthopaedic Trauma 22 (1), 43–46. Ursic, C., Curtis, K., 2010. Thoracic and neck trauma. Part two. International Emergency Nursing 18, 99–108. Walker, R.L., Clark, M.E., Nampiaparampil, D.E., Mcllvried, Gold, M.S., Okonkwo, R., Kerns, R.D., 2010. The hazards of war: blast injury headache. The Journal of Pain 11 (4), 297–302.

178 Wolf, S.J., Bebarta, V.S., Bonnett, C.J., Pons, P.T., Cantrill, S.V., 2009. Blast injuries. The Lancet 374, 405–415. Yilmaz, S., Pekdemir, 2006. An unusual primary blast injury: traumatic brain injury due to primary blast injury. American Journal of Emergency Medicine, 97–98.

S. Housden Zuckerman, S., 1940. Experimental study of blast injuries to the lungs. Lancet 2, 219–224.