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Explosives and Blast Injuries
High-energy events in which a solid or liquid is converted rapidly to a gas can occur at 3 rates:
An example of deflagration would be the rapid flash (without a bang) that results when an open pile of black powder 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—see Table: Examples of Low-Grade and High-Grade Explosives).
Examples of Low-Grade and High-Grade Explosives
In mass casualty incidents involving explosions, 3 concentric zones are identified:
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 psychologic trauma, no rescue is required, and basic life support and self help are needed.
Blast injuries include both physical and psychologic 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
The supersonic blast wave in primary blast injury (PBI) 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. PBI 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.
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, MI, 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.
Patients are evaluated as for most multiple trauma casualties (see page 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. Chest radiography is done, and x-rays 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.
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.
Attention should be given to airway, breathing, circulation, disability (neurologic status), and exposure of the patient (see page Approach to the Trauma Patient : Evaluation and Treatment). High-flow O2 and fluid administration are priorities, and early chest tube placement should be considered. Most injuries (eg, lacerations, fractures, burns, internal injuries, head injuries) are managed as discussed elsewhere in The Manual.
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 position, halfway between left lateral decubitus and prone, with the head at or below the level of the heart. Hyperbaric O2 (HBO) therapy may be useful (see page Recompression Therapy).
If acute crush syndrome is diagnosed or suspected, urinary catheterization is done to allow continual monitoring of urine output. Forced diuresis using an alkaline mannitol solution to maintain urine output up to 8 L/day and a urinary pH of ≥ 5 may help. ABGs, electrolytes, and muscle enzymes should be monitored. Control hyperkalemia with calcium, insulin, and glucose (see page 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 BP 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 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/h.
The views expressed in this article are those of the author and do not reflect the official policy of the Department of Army, Department of Defense, or the US Government.
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