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Thread: Burn-Forensic

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    Default Burn-Forensic

    Burn



    Burns are injuries of skin or other tissue caused by thermal, radiation, chemical, or electrical contact. Burns are classified by depth (1st degree, partial thickness, and full thickness) and percentage of total body surface area (BSA) involved. Complications include hypovolemic shock, rhabdomyolysis, infection, scarring, and joint contractures. Patients with large burns (> 15% BSA) require fluid resuscitation. Treatments for burn wounds include topical antibacterials, regular cleaning, elevation, and sometimes skin grafting. Burns of joints require range-of-motion exercises and splinting
    .

    Burns cause about 3000 deaths/yr in the US and about 1 million emergency department visits.
    Etiology and Pathophysiology

    Thermal burns may result from any external heat source (flame, liquids, solid objects, or gases). Fires may also result in toxic inhalation Radiation burns most commonly result from prolonged exposure to solar ultraviolet radiation (sunburn) but may result from prolonged or intense exposure to other sources of ultraviolet radiation (eg, tanning beds) or from exposure to sources of x-ray or other nonsolar radiation.

    Chemical burns may result from strong acids, strong alkalis (eg, lye, cement), phenols, cresols, mustard gas, or phosphorus. Skin and deeper tissue necrosis due to these agents may progress over several hours.
    Electrical burns result from the electrical generation of heat; they may cause extensive deep tissue damage despite minimal apparent cutaneous injury.
    Events associated with the burn (eg, jumping from a burning building, being struck by debris, motor vehicle collision) may cause other injuries.

    Burns cause protein denaturation and thus coagulation necrosis. Around the coagulated burned tissue, platelets aggregate, vessels constrict, and marginally perfused tissue (known as the zone of stasis) can necrose. Around the zone of stasis, tissue is hyperemic and inflamed. Damage to the normal epidermal barrier allows bacterial invasion and external fluid leakage; damaged tissues often become edematous, further enhancing volume loss. Heat loss can be significant because thermoregulation of the damaged dermis is impaired and because fluid leakage increases evaporative heat loss.


    Depth: Burns are classified by depth of skin affected. First-degree burns are limited to the epidermis. Partial-thickness (2nd-degree) burns involve part of the dermis and are subdivided into superficial and deep. Superficial partial-thickness burns involve the upper 1⁄2 of the dermis. These burns heal within 2 to 3 wk. Healing occurs from epidermal cells lining sweat gland ducts and hair; these cells grow to the surface, then migrate across the surface to meet cells from neighboring glands and follicles. Burns that heal within 2 to 3 wk rarely scar unless they become infected. Deep partial-thickness burns involve the bottom 1⁄2 of the dermis and take ≥ 3 wk to heal; usually, healing occurs only from hair follicles. Scarring is common. Full-thickness (3rd-degree) burns extend through the entire dermis and into the underlying fat. Healing occurs only from the periphery; these burns, unless small, require skin grafting.
    Rule of 9s

    Last edited by Asrafee; 12-10-2006 at 02:42 PM.

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