Author: Alison Tompkins / Editor: Adrian Boyle / Reviewer: Mohamed Elwakil, Caitriona Considine / Codes: HAP11 / Published: 14/04/2020 / Review Date: 14/04/2023
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.
The incidence of explosions and resultant blast injuries increased throughout the twentieth century.
Although some of these events are attributable to increasing industrialisation, they are predominantly the result of attacks using explosive weapons .
Physics and Pathophysiology
On detonation, a blast wave is generated by the rapid transformation of explosive material from a solid or liquid to a gas as it almost instantaneously increases in volume up to 100,000 times . This 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) pressure.
Types of blast Injury
There are four major types of blast injury:
The magnitude of the peak over-pressure and the duration of the blast wave correlates with the risk of primary blast injury .
Loose objects are displaced and become 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 explosion.
They are usually blunt injuries but may include impalement.
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 explosion .
The table 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.
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.
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.
Effect on Tissues
Two types of pressure waves are generated by the interaction of the blast wave with the body:
Stress waves are longitudinal forces moving at supersonic speeds which create spalling effects at tissue-gas interfaces [1,7].
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 damage .
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 interfaces .
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 the tearing of tissues and organs and may result in injury to their attachments .
Evaluation and Management
Patients attending the emergency department (ED) 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-trauma .
Initial management should be given in accordance with standard trauma management [7,9].
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 ED.
In order to adequately assess a patient at risk of primary 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 a 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 assessment .
Many victims will suffer a short-lived but profound period of sensorineural deafness and tinnitus that resolves within hours .
Persisting deafness and tinnitus results from tympanic membrane rupture that may occur at pressures as low as 5 psi  and this usually occurs at the pars tensa .
Although intact tympanic membranes were once relied upon as a marker of absence of exposure to significant over-pressures, significant primary blast injuries may occur in its absence . In one study, 36.7% of patients with blast lung injury had intact tympanic membranes.
Less typical injuries
Disruption of the ossicular chain, most often at the incudomalleolar joint , and distortion or destruction of the oval or round windows, are rarer primary blast injuries but cause significant morbidity.
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 injury .
In the ED, little treatment is required for tympanic membrane rupture .
ED medics must ensure that otological examination is performed and recorded  and all patients, whether conscious of deafness or not, should undergo audiometric follow-up [1,11].
Simple advice can be given to patients regarding:
- The avoidance of submersion in water
- Probing the ear canal
- Seeking early antibiotics in the event of infection
Intact tympanic membranes do not exclude primary blast injury to other organs.
The second most susceptible organ to blast injury is the lung .
It is found on autopsy in a high proportion of immediate fatalities [3,5] and body armour is not protective against injury .
Blast forces are propagated through lung parenchyma, causing widespread disruption at the capillary-alveolar membrane and tearing of alveolar septae .
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 embolism 
Patients may show no signs of external trauma, but usually have clinical and radiological evidence of blast lung at the time of presentation to hospital [5,6,9].
They may, however, be asymptomatic in early stages [1,6].
It is vital to measure pulse oximetry in all patients and a decrease in peripheral oxygen saturation may be the earliest sign of the development of blast lung.
Other symptoms include:
- Chest pain
- Wheeze and cough with haemoptysis
On examination, there may be:
- Increased work of breathing
On auscultation there may be:
- Absent or reduced breath sounds
- Altered percussion note
- Wheeze or crepitations [5,9]
Chest radiographs should be performed on all patients and their findings will vary depending on the exact pathology within the lung.
All may occur in isolation or in combination and most will be detectable on chest radiographs at presentation. The following are typical findings in blast lung:
- Butterfly distribution of opacification
- Pulmonary haemorrhage
- Pulmonary oedema
- Subcutaneous emphysema
- Pleural laceration
- Parenchymal laceration
Most commonly a butterfly distribution of bilateral pulmonary infiltrates is observed . The mediastinum is thought to reflect blast forces, increasing the blast load affecting the lung parenchyma surrounding the central structures .
Treatment in the ED
Treatment for blast lung in the ED should take into consideration the following:
All patients will require supplemental high-flow oxygen .
Large-bore tube thoracostomy is required for decompression of haemopneumothoraces .
Intubation and ventilation
although avoidance of positive pressure ventilation wherever possible is advocated to protect against systemic air embolism [5,9], 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 acidosis .
Steroids are not indicated .
Intubation and ventilation should not be withheld in hypoxic patients with blast lung, but should be initiated with caution.
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 organs .
Invasive monitoring may be necessary to guide fluid management .
Systemic air embolism
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 therapy is hyperbaric oxygen, although in the polytrauma patient this is often not appropriate and will be inaccessible for many EDs .
Primary blast injury affecting the GI tract is rare and usually accompanies primary blast injury to other organs.
- Shock waves cause 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 (Fig 1)
- Mesenteries are threatened by shear waves
- The colon, containing more gas than the small bowel, is at the greatest risk, particularly at the ileocaecal junction (Fig 2)
- Solid organs vibrate as entire entities on exposure to blast forces and are more likely to be affected by secondary or tertiary blast injury (Fig 3)
- A negative FAST examination in stable patients with increased pain or vomiting, should be followed up with CT examination of the abdomen and pelvis.
The following are symptoms and signs of abdominal primary blast injury.
- Abdominal pain
- Haemodynamic instability
- Free gas on radiological examination
These may be evident at initial presentation, but may be delayed by up to 7 days if perforation occurs secondary to mesenteric infarction or ischaemia 
Management in the ED
Management in the ED involves analgesia and fluid resuscitation.
Access to CT scanning may delay definitive management, particularly in the unstable patient, or be difficult to access with multiple casualties.
FAST scanning may identify free intraperitoneal fluid, although will not be able to distinguish between the different types of blast injury, and may miss a perforated hollow viscus [4,8].
Patients with only mural or mesenteric haematoma should be admitted and managed with bowel rest and nasogastric decompression. They should undergo regular reassessment of abdominal signs .
Patients with abdominal pain following exposure to a blast should be admitted and regularly reassessed.
Orthopaedic injuries following explosions are most commonly the result of secondary, tertiary and quaternary blast injury.
In the case of traumatic amputation, however, primary blast injury has been strongly implicated as the mechanism of injury . It is an uncommon injury in survivors as its presence indicates exposure to massive blast over-pressures [1,4].
The level of amputation is most commonly the level of the upper third of the tibia .
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 body .
Management in the ED should focus on control of haemorrhage, analgesia and meticulous exclusion of other life-threatening primary blast injuries.
In cases of life-threatening extremity trauma secondary to blast injuries, early use of tourniquets may prove lifesaving beside haemostatic agents.
Acceleration-deceleration forces acting directly on the mediastinum may cause cardiac contusion .
Air embolism can affect the coronary arteries and result in myocardial ischaemia and infarction [1,6,14].
Animal studies have demonstrated that a vagally-mediated response to thoracic blast injury results in a prolonged period of bradycardia with hypotension in the presence of normal systemic vascular resistance, which may explain why some patients with significant blast injury may be hypotensive without evidence of haemorrhage [6,12].
- Patients complain of chest pain, breathlessness, sweating and nausea
- ECG may reveal typical ischaemic changes or arrhythmia
- These patients should be managed initially with high-flow oxygen with expedient correction of any arrhythmia
- Nitrates are not indicated in the management of myocardial ischaemia due to systemic air embolism and thrombolytic agents should be avoided
- Hyperbaric oxygen therapy may be indicated
The mechanism behind severe head injury following explosion is usually that of secondary and tertiary blast injuries.
However, exposure to blast forces may result in primary blast injury to the brain and the degree of injury ranges from concussion through mild traumatic brain injury to diffuse axonal injury .
At higher over-pressures, skull fractures can occur and these, when occurring as a primary blast injury, are closely associated with blast lung injury .
Focal neurological deficit may be the result of systemic air embolism to the brain or spinal cord.
Management in the ED follows usual practice, with induction of anaesthesia and initiation of mechanical ventilation in unconscious patients.
Results of CT scanning will depend on the mechanism of injury. There are a significant number of radiology negative concussive injuries following blast injury .
Monitoring of intracranial pressures may be undertaken by the neurosurgical team and patients should be discharged to specialist neurological critical care units .
The retinal vessels may be affected by systemic air embolism and this may be directly visible on fundoscopic examination.
Patients complain of blurred vision. Hemi- or quadrantopias may be discovered on visual field testing.
The presence of primary blast injury to the eye itself implies exposure to massive blast forces and these injuries are rare in survivors. Risk to the eye continues to be from flying debris (secondary blast injury) .
There are three major areas of maxillofacial injury caused by blasts:
The middle third of the face, being comprised of wafer-thin sheets of bone, has similarities to an egg shell.
It sustains external forces up to a point and any force applied above that threshold results in its shattering into small pieces.
Following exposure to a blast, patients therefore may have severely comminuted fractures of the maxillary and ethmoid sinuses and the cribriform plates [7,8].
Fracture of the orbital walls may lead to globe injuries and, if severe, may threaten sight if not recognised .
The mandible is more likely to be injured by blast forces striking the face laterally and fractures under shear forces.
The resultant mandibular body fractures are usually unilateral, horizontal and occur below the apices of the teeth.
There is usually no associated soft tissue injury although the patient may show signs of flash burns .
Teeth fractures due to primary blast injury are usually multiple and occur at the cemento-enamel junction .
Management in the ED
Patients with facial primary blast injuries are likely to be suffering from primary blast injury affecting other organs, most of which will take priority during stabilisation.
Establishment of an early definitive airway may be essential in deforming trauma of the face .
Management of ‘crushed egg shell’ injury to the middle third of the face is difficult because of haemorrhage from the comminuted maxillary sinus and orbital floor. It may be necessary to contact the maxillo-facial surgeon for consideration of early surgical intervention .
The following special considerations should be taken into account in patients presenting with blast injuries:
In some ways the foetus is protected from primary blast injury, having no gas-filled organs. However, being suspended in amniotic fluid does potentially expose it to substantial blast forces.
As with other forms of trauma, the best way to look after the foetus is to look after the mother.
Sonography should be performed for all pregnant patients exposed to a blast, to exclude uterine rupture and placental abruption.
Rhesus-negative pregnant women should receive anti-D immunoglobulin within 72 hours of blast injury.
A suicide bomber’s fragmented body may cause penetrating (secondary) blast injury.
In recent years there has been concern that this biological material may cause cross-infection with the hepatitis and human immunodeficiency viruses.
In Israel there have been a number of incidents where human material from suicide bombers has tested positive for HBV or HbsAg [16,17].
Any biological fragments removed from wounds in patients involved in a blast should be sent for virological examination .
It is the author’s recommendation that accelerated hepatitis B vaccination should be considered in all patients with open wounds who have been involved in a blast, if it is possible that the explosion has been the result of a suicide bombing. Patients should also receive anti-tetanus toxin.
All patients with penetrating trauma following suicide bombing should receive accelerated hepatitis B vaccination.
Disposition of Patients Following Exposure to Blasts
Patients may be considered for discharge if they have normal oxygen saturations and a normal chest x-ray, even in the presence of perforation of the eardrum .
Patients who physically felt the impact of a blast wave and those who sustained loss of consciousness following an explosion should be admitted for observation, probably for at least 24 hours .
All patients will need to be discharged with written and verbal advice regarding:
- Symptoms of other blast injuries
- Symptoms that should prompt return to the ED
- Who to contact in the case of emergency
- If and when to return for a follow up
Monitoring and reassessment of injuries
Patients with evidence of blast lung, but not initially requiring critical care, must be admitted and closely monitored for any deterioration, preferably with continuous oxygen saturation monitoring.
Patients with abdominal primary blast injury may need emergent laparotomy. If this is not necessary they are best admitted under the surgical team for regular reassessment of their haemodynamic status and abdominal examination, any deterioration of which should prompt repeat imaging of the abdomen or exploratory surgery.
Above all, patients with any sign of primary blast injury must be reassessed regularly for any deterioration.
The following complications can ensue in patients presenting to the ED with blast injury:
1 – Mortality following blast injury has a bimodal distribution, with most fatalities being immediate at the scene of the explosion.
Mortality in patients surviving to hospital treatment is higher than in other forms of trauma, but nonetheless remains low.
All patients, no matter how critically ill, should be treated aggressively .
2 – Patients may develop long-term hearing deficit following exposure to blast.
A rare but important complication of perforation of the tympanic membrane is the development of cholesteatoma .
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.
3 – 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 injury .
4 – 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 symptoms.
There may be long-term neurological, cognitive, behavioural and psychiatric complications  with the potential to cause permanent disability or even death.
Common symptoms include amnesia, poor concentration, language impairment, motor slowing and personality change. Its essential that these symptoms are recognised and, where appropriate, support offered.
The psychological consequences of being involved in a blast are significant and can be disabling.
Crush syndrome, rhabdomyolysis and acute renal failure may occur after blast injuries.
- Horrocks CL. Blast Injuries: Biophysics, pathophysiology and management principles. JR Army Med Corps 2001;147:28-40.
- Kluger Y, Kashuk J, Mayo A. Terror bombing – mechanisms, consequences and implications. Scand J Surg 2004;93:11-14.
- Kizer KW. Dysbarism. In: Tintinalli JE, Kelen GD, Stpczynski JS, eds. Emergency Medicine: A Comprehensive Study Guide 6th edn. Maidenhead: McGraw-Hill, 2003:1269-1278.
- Wightman JM, Gladish SL. Explosions and blast injuries. Ann Emerg Med 2001;37:664-678.
- 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.
- Ritenour AE, Baskin TW. Primary Blast Injury: Update on Diagnosis and Treatment. Crit Care Med 2008;36[7 (Suppl.)]:S311-S317.
- Shuker ST. Maxillofacial Blast Injuries. Journal of Cranio Maxillo-Facial Surgery 1995;23:91-98.
- 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.
- Almogy G, Rivkind AI. Terror in the 21st century: milestones and prospects–part 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.
- Neuhaus SJ, Sharwood PF, Rosenfield JV. Terrorism and Blast Explosions: Lessons for the Australian Surgical Community. ANZ J.Surg 2006;76:637-644. 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;15(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.