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OVERVIEW

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SPECIAL CONSIDERATIONS IN CHILDREN

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  • Developmental immaturity: unable to flee or seek medical attention, unable to describe symptoms or give history

  • Increased respiratory exposure: closer to the ground, higher minute ventilation

  • Increased dermal exposure: less fat, thinner, more permeable skin, larger body surface area:mass ratio

  • Increased risk of dehydration due to toxin-induced vomiting and diarrhea

  • Increased risk of hypothermia during decontamination procedures

  • Immunologic immaturity, resulting in more virulent disease manifestations, greater permeability of blood–brain barrier

  • Increased incidence of head injuries: head is larger proportionally, calvarium is thinner

  • Increased incidence of multiple-organ injury

  • Provider unfamiliarity with pediatric dosing, lack of pediatric equipment, pediatric-sized antidotes, and vaccines

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BLAST INJURIES

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Explosive charges can be low order (lower energy, no overpressure wave) or high order (high energy, overpressure wave) such as TNT, C4, or ammonium nitrate. High-order explosives are used in up to 66% of terror attacks.

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There are four types of blast injuries. Most victims suffer injuries from multiple mechanisms.

  • Primary: direct effect of the overpressure wave moving through tissues

  • Secondary: penetrating injuries from fragments

  • Tertiary: result from the victim impacting a hard surface (fractures, traumatic brain injury [TBI], abrasions)

  • Quaternary: burns and injuries caused by the blast itself

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Primary blast injuries (PBIs) may not be immediately visible but can be life threatening. The incidence and mortality of PBI are higher when the blast occurs in enclosed rather than open areas because the overpressure wave bounces off solid walls.

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BLAST INJURIES BY SYSTEMS

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  • Primary blast lung injury (PBLI): 3% to 14% of initial survivors, highest mortality risk

    • Pathophysiology: Disruption of capillary-alveolar interface, leading to pulmonary hemorrhage, pulmonary edema, pneumothorax, pulmonary fat or air embolus, and IL-8–mediated inflammatory response

    • Presentation: Cough, tachypnea, dyspnea, chest pain, cyanosis, hemoptysis, bilateral opacities on chest x-ray (CXR), hypoxemia

    • Management: Supportive care with 100% oxygen and maintaining a patent airway, judicious fluid management (avoid fluid overload), lung-protective ventilator strategy with permissive hypercapnia to minimize risk of pneumothorax

      • Prophylactic chest tubes are recommended prior to anesthesia or transport.

      • Maintain high suspicion for air or fat embolus and obtain appropriate imaging (CT, echocardiogram, bronchoscopy). Emboli are likely to be multifocal so thoracotomy may not be feasible; use alternative positioning (e.g., lateral decubitus, prone) to increase venous pressure in the damaged lung and prevent more air from embolizing.

      • Selective ventilation may be necessary for severe pulmonary hemorrhage.

      • Extracorporeal membrane oxygenation support (ECMO) can be considered as a last resort.

  • Cardiovascular blast injuries:

    • Pathophysiology: Primary blast injury results in bradycardia, hypotension, and apnea immediately after the blast (perhaps through a vagal mechanism). Air emboli can cause coronary vessel obstruction and myocardial ischemia. Secondary and tertiary injury can cause cardiac contusion or tamponade.

    • Management: Supportive care. Maintain euvolemia. Atropine may be a helpful adjunct.

  • Primary blast gastrointestinal injuries: 3% to 6.7% of initial survivors

    • Pathophysiology: Overpressure wave causes ...

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