What Causes blast injury? And what are the treatments?

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Title: What Causes blast injury? And what are the treatments?

Description: Blast injuries are injuries caused by the escape of energy released during a rapid chemical or nuclear reaction or the escape of high pressure gas.

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Overview of Blast injuries

Blast injuries are injuries caused by the escape of energy released during a rapid chemical or nuclear reaction or the escape of high pressure gas. They affect many organ systems.

 The first is the environment in which the explosion occurs; The water is not

compressed, so the pressure wave propagates rapidly as it slowly disperses. Therefore, it is more capable of causing injury than an airborne explosion.

 The second is the distance a person has from the explosion; The closer the blast is, the higher the blast pressure.

 The third was the site of the explosion. Explosive pressure expands as pressure waves reflect off solid surfaces and increase their energy. Therefore, people close to the wall (for example, in a confined space) are subject to better explosive pressure and the risk of injury is greater.

 Although terrorism is a growing concern, the majority of blast injuries are caused by accidents such as gas explosions. Management often implements a local major event plan.

Blast injuries are divided into four categories:

 Primary blast injury is caused by the direct effect of explosive overpressure on tissue.

Air-filled organs (eg, Ear, lung, lungs, and gastrointestinal tract) and fluid-filled cavities (eg, Brain and spinal cord) are subject to primary blast injury.

 A secondary blast injury occurs when people are exposed to debris physically displaced by an explosive pressure wave. These can cause a combination of blunt and penetrating force injuries.

 Tertiary blast injury is caused by high-energy blasts and occurs when people fly through the air and touch other objects.

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 Other injuries from explosions All other injuries caused by explosions, eg. Eg building fires or collapses, burns, exposure to toxic substances (such as radiation, carbon monoxide poisoning, cyanide poisoning), suffocation and mental injury.

Blast Injury Categories

1. Primary blast injuries

Primary blast injuries are caused by tissue damage directly from blast overpressure. Three mechanisms are described: chipping, shearing, and implosion. When the blast wave travels from high-density tissues to low-density tissues, the molecules break down and the high- density tissue breaks down into low-density. Its effect is similar to blowing water into the air, causing a large splash of water and breaking it in the air. The incision is the tearing of tissues that occurs when tissues of different densities move at different speeds. Visceral disruption occurs because the gases in the hollow organs are compressed by the explosive pressure and rapidly re-expand.

Primary blast injuries occur most often at the air-tissue interface because the blast creates sudden pressure changes. Organs commonly injured are perforations of the tympanic membrane, lungs, and ears secondary to hollow viscera in the gastrointestinal tract. The tympanic membrane has more damage at lower pressure than any other structure that serves as a rapid tool to evaluate patients for a primary blast injury. If the tympanic membranes are not damaged, the chances of continuing other primary blast injuries are reduced.

Pulmonary injuries are surpassed only by the primary eruption and the most common critical injury. Pulmonary hemorrhage, contusion, pneumothorax, pneumomediastinum, hemothorax, and arterial air embolism are manifestations of primary blast injury. Air embolism can cause stroke, myocardial or spinal cord infarction, infarction of other organs and systems, and death. Chest radiographs of explosive trauma patients with suspected barotrauma show a butterfly pattern created by bilateral perihilar infiltrates of lung contaminants.

The gastrointestinal tract is the third most frequently injured as a direct result of an explosion. There is a risk of perforation of the ileocecal area and of the colon implant mechanism and rapid change in air pressure. Barotrauma can cause contamination or intestinal bleeding. Mesenteric ischemia is caused by shear forces on the arterial supply or as a result of air embolism. Eye injuries such as globe rupture, hyphema, retinitis, and conjunctival hemorrhage are less common primary blast injuries.

Myocardial confusion, hemorrhage, and atrial fibrillation are described.

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2. Secondary blast injuries

Flying debris created during an explosion can cause secondary blast injuries. Terrorist bombs cause particularly devastating secondary injuries because they usually contain broken

objects. These injuries are the most common cause of illness and death because their impact extends beyond the primary blast injury zone. Blunt and penetrating injuries can occur. Fractures, traumatic fractures, and soft tissue injuries are the most common secondary injuries. Foreign bodies penetrate deep into the body and create small

penetrating wounds. Emergency physicians should have a low standard for imaging victims with secondary explosive injury.

3. Tertiary explosives injuries

Tertiary injuries occur when victims are physically displaced by an explosion and thrown to the ground or against stationary objects. The second etiology of tertiary injuries is the collapse of buildings or structures. Tertiary blast injury results in head injuries, fractures, blunt force injuries, crush injuries, compartment syndrome, and suffocation. Mortality among victims trapped in collapsed structures increases significantly after 24 hours mainly due to untreated crush injuries and compartment syndrome.

4.Quaternary explosion injuries

Injuries and illnesses are directly related to the explosion, but are not caused by the

previous three categories. Environmental hazards caused by explosions such as smoke, fire, chemical exposure, and radiation can cause quadrilateral injuries. The severity or instability of chronic diseases fall into this category. Burns, respiratory injuries, radiation sickness, asthma or exacerbations of COPD and severe coronary syndromes.

Symptoms of blast injuries

Most injuries (eg, fractures, lasers, brain injuries) look like other types of injuries. Explosive lung injury can cause dyspnea, hemoptysis, cough, chest pain, tachypnea, shortness of breath, shortness of breath, apnea, hypoxia, cyanosis, and hemodynamic instability. Air embolism can manifest as stroke, myocardial infarction, severe abdomen, blindness, deafness, spinal cord injury, or claudication. Damage to the tympanic membrane and inner ear can affect hearing, which should always be evaluated. Patients with abdominal trauma may present with abdominal pain, nausea, vomiting, hematemesis, rectal pain, urgency, testicular pain, and unexplained hypovolemia. Traumatic brain injury manifests

immediately, and residual neurocognitive effects can be resolved or eliminated to varying degrees. There is also concern that multiple low-level explosive exposures may have a cumulative deleterious neurocognitive effect and lead to chronic traumatic

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encephalopathy.For medical assistance immediatly consult with a ENT Doctor and take proper medication and treatment.

Diagnosis of blast injuries

Blast injury, especially of the lungs (and consequently air embolism), ear injury, concealed penetration injury, and crush injury. Apnea, bradycardia, and hypotension are clinical triads that are associated with explosive lung injury. Tympanic membrane rupture is considered to evaluate lung and lung injury, although pharyngeal petechiae may be a good presence of tic.

A chest X-ray is done and the X-rays show a characteristic butterfly pattern. Cardiac monitoring is performed in all patients. Patients with a crush injury are screened for myoglobinuria, hyperkalemia, and ECG changes.

In blast injuries, less-injured patients often skip pre-hospital triage and go directly to the hospital, where they can access more medical resources before the arrival of seriously injured patients. Triage at the scene is different from standard injury treatment, as these explosive injuries can be very difficult to detect early on, so early treatment should be directed toward the more obvious injuries, as well as rupture of the injuries. lungs, ruptured abdomen and severe crush syndromes.

Treatment of blast injuries

Focus on Airway, Breathing, Circulation, Disability (Neurological Condition), and Patient Exposure (Undressing): Approach to the Trauma Patient: Assessment and Treatment).

Administration of high flow oxygen and fluids should be considered a priority and an early appointment with a chest tube. Most injuries (eg, lasers, fractures, burns, internal injuries, head injuries) are treated as described elsewhere in the manual.

Since air embolism worsens after initiation of positive pressure ventilation, positive pressure ventilation should be avoided unless absolutely necessary. If used, slower speeds and lower induction pressure settings should be selected. Patients with suspected air-gas embolism should be placed in a coma (or recovery) position, midway between the left lateral

decubitus and the victim, at head level or below the heart. Hyperbaric oxygen therapy (HBO) is helpful (see Compression therapy).

If acute crush syndrome is diagnosed or suspected, urinary catheterization is performed to constantly monitor urine output. Using an alkaline mannitol solution for forced urination and a urinary pH of బబ 5 helps to maintain urination up to 8 L per day. The levels of blood glucose, electrolytes and muscle enzymes must be controlled. Control hyperkalemia with calcium, insulin, and glucose (see Hyperkalemia: Treatment). Hyperbaric oxygen therapy is especially useful in patients with deep tissue infections. Monitoring for compartment

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syndrome is done clinically and by measuring compartment pressure. Patients may require a fasciotomy if the difference between diastolic BP and compartment pressure is <30 mm Hg.

Hypovolemia and hypotension may not be obvious at first, but can occur suddenly after tissue release and reperfusion, so large amounts of intravenous fluid can be given (eg, 1 to 2 L of lactate Ringer or normal saline) before and after reperfusion. Liquids continue to flow at a rate sufficient to maintain a void of 300 to 500 ml / hr.

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