High-energy events in which a solid or liquid is converted rapidly to a gas can occur at 3 rates (1):
Deflagration: Rapid burning but minimal blast
Explosion: Subsonic ignition and blast wind (low-grade explosive)
Detonation: Supersonic ignition and blast wave (high-grade explosive)
An example of deflagration would be the rapid flash (without a bang) that results when an open pile of black powder (gunpowder) is ignited. The same black powder confined tightly in a container would cause a low-grade explosion. In high-grade explosives, the ignition wave travels through the material at supersonic speed and causes a supersonic blast (detonation) wave; common examples include nitroglycerin and trinitrotoluene (TNT—Examples of Low-Grade and High-Grade Explosives).
Examples of Low-Grade and High-Grade Explosives
Low-grade explosives |
Black powder (original gunpowder, also in fireworks, many pipe bombs) Nitrocellulose (smokeless gunpowder) Solid rocket fuels (most) |
High-grade explosives |
Ammonium nitrate (NH4NO3) Amatol 80/20 (NH4NO3 + TNT) Ammonal (NH4NO3 + TNT + aluminum) ANFO (NH4NO3 + fuel oil) Composition B (TNT + RDX) Composition C-4 (RDX + plasticizer) Nitroglycerin (the explosive component in dynamite) PETN (pentaerythritol tetranitrate) Picric acid RDX (cyclotrimethylenetrinitramine) TNT (trinitrotoluene) |
In mass-casualty incidents involving explosions, 3 concentric zones are identified:
Blast epicenter
Secondary perimeter
Blast periphery
In the blast epicenter (kill zone), any survivors are probably mortally injured, technical rescue capabilities and extrication are likely to be required, and advanced life support and high victim-to-care-provider ratios are required for any survivors. In the secondary perimeter (critical casualty zone), survivors will have multiple injuries, and standard rescue capabilities and moderate victim-to-care-provider ratios are required. In the blast periphery (walking-wounded zone), most casualties will have non–life-threatening injuries and psychological trauma, no rescue is required, and basic support and self-help are needed.
(See also Overview of Incidents Involving Mass-Casualty Weapons.)
General reference
1. Mathews ZR, Koyfman A. Blast Injuries. J Emerg Med. 2015;49(4):573-587. doi:10.1016/j.jemermed.2015.03.013
Pathophysiology of Explosive and Blast Injuries
Blast injuries include both physical and psychological trauma. Physical trauma includes fractures, respiratory compromise, injuries to soft tissue and internal organs, internal and external blood loss with shock, burns, and sensory impairment, especially of hearing and sight. Five mechanisms of blast injury have been described (see table Mechanisms of Blast Injury).
Mechanisms of Blast Injury
Type | Mechanism | Typical Injuries |
|---|---|---|
Primary* | Impact of supersonic blast wave on body Preferentially affects hollow or gas-filled structures | Pulmonary barotrauma (blast lung) Tympanic membrane rupture and middle ear damage Abdominal hemorrhage and intestinal perforation Eyeball rupture Mild traumatic brain injury (concussion) |
Secondary | Impact of debris from blast onto body | Penetrating or blunt injuries Eye penetration (evident or occult) |
Tertiary | Impact of body thrown by blast onto environmental surfaces or debris | Fractures and traumatic amputations Closed and open brain injury |
Quaternary | Processes independent of primary, secondary, or tertiary blast injury (eg, burns, toxic inhalation, crush injury from entrapment under debris, aggravation of medical disorders) | Crush injuries with rhabdomyolysis and compartment syndrome Respiratory tract injury from inhaled toxicants Asthma, angina, or myocardial infarction triggered by the event |
Quinary† | Injuries resulting from toxic materials absorbed by the body from the blast and post detonation environment (eg, radiological, biological substances) | Radiation burns or acute radiation sickness (see also Biological Agents as Weapons and Toxins as Mass Casualty Weapons for specific symptoms) |
* Mayorga MA. The pathology of primary blast overpressure injury. Toxicology. 1997;121(1):17-28. doi:10.1016/s0300-483x(97)03652-4 † Kluger Y, Nimrod A, Biderman P, Mayo A, Sorkin P. The quinary pattern of blast injury. J Emergency Management. 2006;4(1):51-55. | ||
The supersonic blast wave in primary blast injury compresses gas-filled spaces, which then rapidly reexpand, causing shearing and tearing forces that can damage tissue and perforate organs. Blood is forced from the vasculature into air spaces and surrounding tissue. Pulmonary involvement (blast lung injury) may cause pulmonary contusion, systemic air embolism (especially in the brain and spinal cord), and free-radical–associated injuries (thrombosis, lipo-oxygenation, and disseminated intravascular coagulation); it is a common cause of delayed mortality. Primary blast injury also includes intestinal barotrauma (particularly with underwater explosions), acoustic barotrauma (including tympanic-membrane rupture, hemotympanum without rupture, and fracture or dislocation of ossicles in the middle ear), and traumatic brain injury.
Symptoms and Signs of Explosive and Blast Injuries
Most injuries (eg, fractures, lacerations, brain injuries) manifest the same as in other types of trauma. Blast lung injury may cause dyspnea, hemoptysis, cough, chest pain, tachypnea, wheezing, decreased breath sounds, apnea, hypoxia, cyanosis, and hemodynamic instability. Air embolism may manifest as stroke, myocardial infarction, acute abdomen, blindness, deafness, spinal cord injury, or claudication. Damage to the tympanic membrane and the inner ear may impair hearing, which should always be assessed. Patients with abdominal blast injury may have abdominal pain, nausea, vomiting, hematemesis, rectal pain, tenesmus, testicular pain, and unexplained hypovolemia. Traumatic brain injury may manifest immediately and resolve or leave residual neurocognitive affects of varying degree. There also is concern that multiple lower-level blast exposures may have a cumulative deleterious neurocognitive effect and perhaps lead to chronic traumatic encephalopathy.
Diagnosis of Explosive and Blast Injuries
Clinical evaluation
Imaging studies as indicated by findings
Patients are evaluated as for most multiple trauma casualties (see Approach to the Trauma Patient: Evaluation and Treatment), except that special effort is directed at identifying blast injury, particularly blast lung (and consequent air embolism), ear trauma, occult penetrating injury, and crush injury. Apnea, bradycardia, and hypotension are the clinical triad classically associated with blast lung injury. Tympanic membrane rupture has been considered to predict blast lung injury, but pharyngeal petechiae may be a better predictor. A chest radiograph is done, which may show a characteristic butterfly pattern. Cardiac monitoring is done in all patients. Patients with possible crush injury are tested for myoglobinuria, hyperkalemia, and ECG changes.
Triage
In blast injuries, less seriously injured patients often bypass prehospital triage and go directly to hospitals, possibly overwhelming medical resources in advance of the later arrival of more seriously injured patients. On-scene triage differs from standard trauma triage mainly in that blast injuries may be more difficult to recognize initially, so initial triage should be geared toward identifying blast lung, blast abdomen, and acute crush syndrome in addition to more obvious injuries.
Treatment of Explosive and Blast Injuries
The treatment principles of blast injuries are 3-fold (1):
Primary and secondary survey for traumatic injuries
Recovery position and sometimes hyperbaric oxygen therapy for air embolism
Fluid resuscitation and monitoring for rhabdomyolysis and compartment syndrome for crush injuries
Attention should be given to airway, breathing, circulation, disability (neurologic status), and exposure (undressing) of the patient (see Approach to the Trauma Patient: Evaluation and Treatment). High-flow oxygen and fluid administration are priorities, and early chest tube placement should be considered. (Also see lacerations, fractures, burns, and head injuries.)
Because air embolism may worsen after initiation of positive-pressure ventilation, positive-pressure ventilation should be avoided unless absolutely necessary. If it is used, slower rates and lower inspiratory pressure settings should be chosen. Patients suspected of having air-gas embolism should be placed in the coma (or recovery) position, halfway between left lateral decubitus and prone, with the head at or below the level of the heart. Hyperbaric oxygen (HBO) therapy may be useful (see Recompression Therapy).
If acute crush syndrome is diagnosed or suspected, urinary catheterization≥Hyperkalemia: Treatment). Hyperbaric oxygen therapy may be particularly useful in patients with deep tissue infections. Monitoring for compartment syndrome is done clinically and by measuring compartment pressure. Patients may need fasciotomy if the difference between diastolic blood pressure and compartment pressure is < 30 mm Hg. Hypovolemia and hypotension may not be apparent initially but may suddenly occur after tissue release and reperfusion, so large volumes of intravenous fluid (eg, 1 to 2 L Ringer's lactate or normal saline) are given both before and after reperfusion. Fluids are continued at a rate sufficient to maintain a urine output of 300 to 500 mL/hour.
Treatment reference
1. Beaven A, Parker P. Treatment principles of blast injuries. Surgery (Oxford). 2015. 33(9):424-429.
