Author: Alison Tompkins / Editor: Adrian Boyle / Reviewer: Mohamed Elwakil / Codes: HAP11 / Published: 20/11/2017 / Review Date: 20/11/2020
Barotrauma refers to physical damage to body tissues by changes in ambient pressure. This may be the result of many mechanisms but this module concentrates on the epidemiology, pathophysiology, pattern of injury and management of primary blast injuries. These are the direct result of exposure to the significant atmospheric pressure changes generated from detonation of explosive devices. Barotrauma resulting from underwater diving and pulmonary barotrauma from mechanical ventilation will not be discussed. Blast injuries can cause multisystem and life-threatening injuries, which require complex triage, diagnostic, and management challenges for the health care provider.
Epidemiology of Blast Injuries
The incidence of explosions and resultant blast injuries increased in number throughout the twentieth century. Although some of these events are attributable to increasing industrialisation, they are predominantly the result of attacks using explosive weapons1. Bombs are the primary weapon of terrorist groups2;3. Between 1990 and 1995, the FBI reported 355 deaths and 3176 injuries resulting from 15,700 criminal bombing incidents1. Emergency physicians need to understand the pathophysiology, recognition and management of blast injuries.
Physics and pathophysiology of barotrauma
On detonation of an explosive device, a blast wave is generated by the rapid transformation of the explosive material from a solid (or liquid) to a gas4;5. Almost instantaneously, the explosive increases in volume up to 100000 times and results in a well-demarcated expanding shock wave of extremely high pressure. This blast wave dissipates rapidly and is followed by the recoil of the surrounding air and a slightly longer period of low (sub-atmospheric) pressure4
Types of blast Injury
Primary blast injuries result directly from the effects of the abnormal ambient pressure generated during the blast wave. The magnitude of the peak overpressure and the duration of the blast wave correlates with the risk of primary blast injury5.
The air around the blast is displaced by the wave of overpressure resulting in high-velocity blast winds. Loose objects are displaced and form projectiles that have the potential to cause both blunt and penetrating injuries. These secondary blast injuries form the most common type of injury following an explosion4. Middle ear, lungs, and gastro intestinal tract are most susceptible to primary blast injuries.
Tertiary blast injuries are the result of the impact of people themselves against other structures when displaced by the blast wave or winds. They are usually blunt injuries but may include impalement.
The quaternary (or miscellaneous) blast injuries include those injuries not attributable directly to the blast itself but which result from the effects of the blast. They may include burns, inhalational injury and crush injury following building collapse.
Recognising Primary Blast Injury
Primary blast injuries are rare. Secondary and tertiary injuries affecting the musculoskeletal system and the head predominate following an explosion6;7. Table 1 demonstrates factors relating to the event that should alert the emergency physician to a greater likelihood of primary blast injury in addition to these more immediately-obvious injuries. Some of these features may be sought from the patient, some from emergency personnel attending the scene of the incident and some may remain unknown until long-after the last casualties are attended to.
Larger explosive devices generate higher and more sustained overpressures.
Usually detonated in close proximity to large groups of people; the close proximity increases the risk of primary blast injury.
Enhance blast munitions
Includes fuel-air explosives. Designed to result in increased primary blast injury.
Blast wave reflects off and reverberates within fixed structures resulting in complex and multiple waves of overpressure augmenting blast effects.
Sustained propagation of blast wave results in primary blast injury even at distance from the detonation centre.
The closer to the detonated device, the higher the overpressure to which a victim is exposed.
Personal Protective Equipment
Does not protect from primary blast injury. The protection from secondary and some tertiary blast injury results in increased risk of primary blast in survivors.
Flash burns occur in patients who were in close proximity to the detonation centre and thus at higher risk of primary blasts injuries.
Table 1: Explosion and patient factors increasing risk of primary blast injury. Adapted from text1;5;11.
Effect on Tissues
Two types of pressure waves are generated by the interaction of the blast wave with the body12.
Stress waves are longitudinal forces moving at supersonic speeds which create spalling effects at tissue-gas interfaces1;13. This is where the shock wave travelling through a tissue reaches an interface with a tissue of lower density (such as gas) and creates a negative reflection at that interface causing fragmentation of the surface of the higher density tissue. This results in microvascular damage5. Stress waves also cause implosion of gas-containing structures such as bowel or alveoli by the higher-pressure tissues surrounding them. Blood, is forced into the gas-filled compartments by the pressure differential across these interfaces5.
Shear waves are longer duration and lower velocity transverse pressure waves that result from differences between the rates of acceleration and deceleration of tissues with different densities in response to the blast waves. These shear forces result in tearing of tissues and organs and may result in injury to their attachments1.
Key steps in evaluating a patient with barotrauma and the initial ED-based management of barotrauma
Patients attending the Emergency Department following a blast are more likely to be critically ill with higher injury severity scores and more body areas injured than in other forms of multi-trauma14. Initial management should be given in accordance with standard trauma management 13;15.
Most injuries following explosions are due to secondary and tertiary blast injuries. Primary blast injury remains, however, a significant cause of morbidity and mortality and consideration to its effects should be given in the emergency department. In order to adequately assess a patient at risk of primary blast injury (who is likely to have other forms of blast injury), one must have an awareness of the types of injury likely to have been sustained during an explosion and actively seek their symptoms and signs.
The initial management of a blast victim is the same as for any multi-trauma patient
The ear is designed to efficiently transmit pressure waves and is the organ most likely to sustain primary blast injury. It is essential therefore that every patient involved in a blast, when appropriate and taking into consideration other injuries, be assessed otologically in the course of their hospital assessment16.
Many victims will suffer a short-lived but profound period of sensorineural deafness and tinnitus that resolves within hours 1;17. Persisting deafness and tinnitus results from tympanic membrane rupture that may occur at pressures as low as 5psi5 and this usually occurs at the pars tense6. Although intact tympanic membranes were once relied upon as a reliable marker of absence of exposure to significant overpressures, significant primary blast injuries may occur in its absence16 and in one study, 36.7% of patients with blast lung injury had intact tympanic membranes18.
Disruption of the ossicular chain, most often at the incudomalleolar joint17, and distortion or destruction of the oval or round windows are rarer primary blast injuries but cause significant morbidity2. Vertigo is relatively rare following blast injury and although perilymph fistulae should be excluded in patients with unresolving vertigo at two weeks, it is usually attributable to concussional syndromes following head injury17.
In the ED, little treatment is required for tympanic membrane rupture17. ED medics must ensure that otological examination is performed and recorded18;19 and all patients, whether conscious of deafness or not should undergo audiometric follow-up1;17. Simple advice can be given to patients regarding the avoidance of submersion in water, probing the ear canal, and seeking early antibiotics in the event of infection.
A normal otological examination does not exclude serious blast injury to other organs.
Second-most susceptible to blast injury are the lungs9 and pulmonary barotrauma, or blast lung, is the commonest cause of critical illness in patients with primary blast-injuries2. It is found on autopsy in a high proportion of immediate fatalities9;15 and body armour is not protective against injury2;15. Blast forces are propagated through lung parenchyma, causing widespread disruption at the capillary-alveolar membrane and tearing of alveolar septa9. Systemic air embolism may also result from loss of integrity of the tissue-gas interface in the lungs and in turn causes a plethora of symptoms depending on the site of embolism:
- Focal or diffuse neurological deficit from embolism to brain or spinal cord
- Myocardial infarction from coronary artery embolisation
- Ischaemia and infarction of the GI tract
- Limb ischaemia or infarction
- Visual field defects from retinal artery embolism15
N Engl J Med 2013; 368:1045 March 14, 2013 DOI: 10.1056/NEJMicm1203842
Chest radiography (Panel A) and computed tomography (Panel B) revealed typical appearances of blast lung (pulmonary barotrauma), with interstitial and alveolar filling defects and prominent air bronchograms in a butterfly pattern.
Patients may show no signs of external trauma but usually have clinical and radiological evidence of blast lung at the time of presentation to hospital2;9;11;15. They may however be asymptomatic in early stages1;10;11. It is vital to measure pulse oximetry in all patients and decrease in peripheral oxygen saturation may be the earliest sign of the development of blast lung2. Other symptoms include breathlessness, chest pain, wheeze and cough with haemoptysis. On examination, there may be tachypnoea, dyspnoea, increased work of breathing, cyanosis and on auscultation there may be absent or reduced breath sounds, altered percussion note, wheeze or crepitations9;15.
Chest radiographs should be performed on all patients1 and their findings will vary depending on the exact pathology within the lung (table 2). Most commonly a butterfly distribution of bilateral pulmonary infiltrates is observed14. This is thought to be due to reflection of blast forces by the mediastinum and hence a large blast load is experienced by the lung parenchyma immediately surrounding the central structures11.
Findings in blast lung. All may occur in isolation or in combination; most will be detectable on chest radiographs at presentation.
- butterfly distribution of opacification
- pulmonary haemorrhage
- pulmonary oedema
- subcutaneous emphysema
- pleural laceration
- parenchymal laceration2;11;14;1514.
All patients will require supplemental high-flow oxygen19 and large-bore6 tube thoracostomy is required for decompression of haemopneumothoraces. Although avoidance of positive pressure ventilation wherever possible is advocated to protect against systemic air embolism9;15, it is not unusual for patients with blast lung to require intubation and mechanical ventilation for management of respiratory failure. In order to limit the risk of systemic air embolism and pneumothorax, limited peak inspiratory pressures and positive end-expiratory pressures should be used. Permissive hypercapnia may be necessary to enable limited-pressure ventilation and has not been found to increase morbidity despite a relative respiratory acidosis20. Steroids are not indicated19.
Patients with blast lung are at high risk of pulmonary oedema due to increased capillary permeability. Careful fluid resuscitation should be aimed at restoring perfusion of vital organs9. Invasive monitoring may be necessary to guide fluid management13;21.
Any patient thought to be suffering from systemic air embolism should in the first instance be treated with high-flow supplemental oxygen. The gold standard definitive treatment is hyperbaric oxygen therapy although in the multiply-injured patient this is often not appropriate and for many emergency departments will be inaccessible1.
Primary blast injury affecting the GI tract is rare and usually accompanies primary blast injury to other organs. Shock waves cause first compression then rapid re-expansion of the gas-filled gut putting the gut wall under tension and causing acute, often multifocal perforation and mural haemorrhage. Mesenteries are threatened by shear waves5;11. The colon, containing more gas than the small bowel, is at the greatest risk, particularly at the ileocaecal junction10;11. Solid organs vibrate as entire entities on exposure to blast forces and are more likely to be affected by secondary or tertiary blast injury.
Symptoms and signs of abdominal primary blast injury are shown in table 3. They are likely to be evident at initial presentation but may be delayed by up to seven days if perforation occurs secondary to mesenteric infarction or ischaemia2;21.
Free gas on radiological examination
Management in the ED will involve analgesia and treatment of haemodynamic compromise with fluid resuscitation. Access to CT scanning may delay definitive management particularly in the unstable patient or be difficult to access in a situation with multiple casualties22. FAST scanning may be utilised to identify free intraperitoneal fluid although will not be able to distinguish between the different types of blast injury, and indeed may be negative in patients with perforation of a hollow viscus6;14. Patients with only mural or mesenteric haematoma and no perforation should be admitted and managed with bowel rest and nasogastric decompression and regular reassessment of abdominal signs11.
Orthopaedic injuries following explosions are most commonly the result of secondary, tertiary and quaternary blast injury. However, in the case of traumatic amputation primary blast injury has been strongly implicated as the mechanism of injury4. It is an uncommon injury in survivors1;6 as its presence indicates exposure to massive blast overpressures. The level of amputation is most commonly the level of the upper third of the tibia1;4;23. It has been postulated that the pressure transmitted from the primary blast wave to the long bone fractures through the shaft of the long bone, usually at the level of the diaphysis. The force of the subsequent blast wind then separates the limb from the body1
Mortality following blast injury has a bimodal distribution7, with most fatalities being immediate at the scene of the explosion. Mortality in those patients surviving to hospital treatment is higher than in other forms of trauma but nonetheless remains low and all patients, no matter how critically ill, should be treated aggressively19.
Patients may develop long-term hearing deficit following exposure to blast2. A rare but important complication of perforation of the tympanic membrane is the development of cholesteatoma1. Epithelial cells are implanted into the middle ear by the traumatic insult. Cellular growth is promoted and the resultant tumour is invasive with the potential to erode bony structures.
Follow-up of small numbers of patients admitted with blast lung injury has demonstrated that long-term respiratory disability is uncommon and that most will have normal lung function one year after injury19.
It has been estimated that up to 50% of soldiers injured in combat may return with some degree of traumatic brain injury (all causes) and up to a third of sufferers of even mild traumatic brain injury develop chronic symptoms27. There may be long-term neurological, cognitive, behavioural and psychiatric complications23 with the potential to cause permanent disability or even death27. Common symptoms include amnesia, poor concentration, language impairment, motor slowing and personality change27. It is essential that these symptoms are recognised and where appropriate and available support offered2.
The psychological consequences of being involved in a blast are significant and can be disabling.
Crush syndrome and acute renal failure may occur in the setting of patients rescued from collapsed structures. Maintenance of fluid and electrolyte balance and tissue perfusion is the main line of management.
The initial management of a blast victim is the same as for any multi-trauma patient
Grade D recommendation. Evidence level 5
A normal otological examination does not exclude serious blast injury to other organs
Grade D recommendation. Evidence level 5
All patients with penetrating trauma following suicide bombing should receive accelerated hepatitis B vaccination
Grade D recommendation. Evidence level 5
Symptoms of pulmonary contusion may take 12-48 hours to develop, therefore all discharged patients should return for reevaluation if they develop breathing problems, increasing abdominal pain, or vomiting.
Patients with mild traumatic brain injury and posttraumatic stress disorder (PTSD) should be referred to neurologists and mental health specialists.
Regards patients with vestibular disorders, referral to neurology and ENT should be considered for follow-up care
- Horrocks CL. Blast Injuries: Biophysics, Pathophysiology and Management Principles. JR Army Med Corps 147, 28-40. 2001. Ref Type: Generic
- DePalma RG, Burris DG, Champion HR, Hodgson MJ. Blast Injuries. The New England Journal of Medicine 352, 1335-1342. 2005. Ref Type: Generic
- Kluger Y, Kashuk J, Mayo A. Terror Bombing Mechanisms, Consequences and Implications. The Scandinavian Journal of Surgery 93, 11-14. 2004. Ref Type: Generic
- Harrisson SE, Kirkman E, Mahoney P. Lessons Learnt from Explosive Attacks. JR Army Med Corps 153, 278-282. Ref Type: Generic
- Kizer KW. Dysbarism. In: Tintinalli JE, Kelen GD, Stpczynski JS, editors. Emergency Medicine: A Comprehensive Study Guide 6th edition. 5th ed. Maidenhead: McGraw-Hill; 2003. 1269-1278.
- Wightman JM, Gladish SL. Explosions and blast injuries. Ann Emerg Med 2001; 37(6):664-678.
- Arnold JL. Mass-Casualty, Terrorist Bombings: Epidemiological Outcomes, Resource Utilization, and Time Course of Emergency Needs (Part 1). Tsai MC, Halpern P, Smithline H, Stok E, Ersoy G, editors. Prehospital and Disaster Medicine 18, 220-234. 2003. Ref Type: Generic
- Leibovici D, Gofrit ON, Stein M, Shapira SC, Noga Y, Heruti RJ et al. Blast injuries: bus versus open-air bombingsa comparative study of injuries in survivors of open-air versus confined-space explosions. J Trauma 1996; 41(6):1030-1035.
- Avidan V, Hersch M, Armon Y, Spira R, Aharoni D, Reissman P et al. Blast lung injury: clinical manifestations, treatment, and outcome. Am J Surg 2005; 190(6):927-931.
- Katz E, Ofek B, Adler J, Abramowitz HB, Krausz MM. Primary Blast Injury After a Bomb Explosion in a Civilian Bus. Ann.Surg 209, 484-488. 1989. Ref Type: Generic
- Ritenour AE, Baskin TW. Primary Blast Injury: Update on Diagnosis and Treatment. Crit Care Med 36[7 (Suppl.)], S311-S317. 2008. Ref Type: Generic
- Ciraulo DL, Frykberg ER. The surgeon and acts of civilian terrorism: blast injuries. J Am Coll Surg 2006; 203(6):942-950.
- Shuker ST. Maxillofacial Blast Injuries. Journal of Cranio Maxillo-Facial Surgery 23, 91-98. 1995. Ref Type: Generic
- Hare SS, Goddard I, Ward P, Naraghi A, Dick EA. The radiological management of bomb blast injury. Clin Radiol 2007; 62(1):1-9.
- Sasser SM, Sattin RW, Hunt RC, Krohmer J. Blast lung injury. Prehosp Emerg Care 2006; 10(2):165-172.
- Garth RJ. Blast injury of the auditory system: a review of the mechanisms and pathology. J Laryngol Otol 1994; 108(11):925-929.
- Garth RJ. Blast injury of the ear: an overview and guide to management. Injury 1995; 26(6):363-366.
- Leibovici D, Gofrit ON, Shapira SC. Eardrum perforation in explosion survivors: is it a marker of pulmonary blast injury? Ann Emerg Med 1999; 34(2):168-172.
- Almogy G, Rivkind AI. Terror in the 21st century: milestones and prospectspart I. Curr Probl Surg 2007; 44(8):496-554.
- Sorkine P, Szold O, Kluger Y, Halpern P, Weinbroum AA, Fleishon R et al. Permissive hypercapnia ventilation in patients with severe pulmonary blast injury. J Trauma 1998; 45(1):35-38.
- Shamir MY, Rivkind A, Weissman C, Sprung CL, Weiss YG. Conventional terrorist bomb incidents and the intensive care unit. Curr Opin Crit Care 2005; 11(6):580-584.
- Halpern P. Mass-Casualty, Terrorist Bombings: Implications for Emergency Department and Hospital Emergency Response (Part II). Tsai MC, Arnold JL, Stok E, Ersoy G, editors. 235-241. 2003. Ref Type: Generic
- Neuhaus SJ, Sharwood PF, Rosenfield JV. Terrorism and Blast Explosions: Lessons for the Australian Surgical Community. ANZ J.Surg. 76, 637-644. 2006. Ref Type: Generic
- Abbotts R, Harrison SE, Cooper GL. Primary blast injuries to the eye: a review of the evidence. J R Army Med Corps 2007; 153(2):119-123.
- Eshkol Z, Katz K. Injuries from biologic material of suicide bombers. Injury 2005; 36(2):271-274.
- Braverman I, Wexler D, Oren M. A novel mode of infection with hepatitis B: penetrating bone fragments due to the explosion of a suicide bomber. Isr Med Assoc J 2002; 4(7):528-529.
- Jackson GL, Hamilton NS, Tupler LA. Detecting traumatic brain injury among veterans of Operations Enduring and Iraqi Freedom. N C Med J 2008; 69(1):43-47.