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Few injuries have the same capacity for physical destruction and emotional devastation as do thermal burns. They are relatively common presentations that often require resource-intensive management. The preceding decade saw nearly 500,000 burn injuries per year receiving medical care in the United States. Over 40,000 of these patients required inpatient treatment for their injuries, and up to 25% of these injuries were work related. The associated expenses are staggering. The mean hospital stay was in excess of 1 week and at an average cost over 50,000 dollars per admission. Over this same 10-year period, an average of over 4000 individuals per year died as a result of burn-related injuries. Fires and burns now represent the fifth leading cause of unintentional injury deaths in the United States.1 Conversely, less than 6% of the above patients who were admitted to a recognized burn center subsequently died as a result of their injuries.24 These data underscore the need for rapid and effective emergency care focused on facilitating the successful transfer of these patients to specialized burn centers. The initial management of these patients invariably falls upon the Emergency Department. The Emergency Physician needs to be well versed in the recognition of acute thermal injuries, their associated complications, and their appropriate treatment.

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Thermal injuries have the potential to affect any body surface, both internally and externally, that a heated medium comes into contact. The overall depth and degree of injury is multifactorial. It is also typically proportional to the temperature of the source medium, its unique specific heat, the actual rate of energy transfer, and the overall duration of tissue exposure. This chapter focuses on the skin and its response to burn injuries.

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Skin exposure to any significant heat source results in a spectrum of pathophysiological responses. An initial coagulation necrosis occurs as thermal energy is transmitted directly into living tissue. These cells subsequently die and lyse, spilling their intracellular contents and increasing the surrounding interstitial oncotic pressure. These processes serve to trigger a secondary edematous reaction in the surrounding tissues. Cellular breakdown releases a host of generalized inflammatory markers including histamines, prostaglandins, cytokines, and interleukins. These agents further exacerbate the localized edematous reaction via vasodilation and increased capillary permeability.5

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Burns involving over 20% of a patient's total body surface area (TBSA) can result in secondary injury extending beyond the locally involved tissues. The previously described inflammatory outburst can become significantly large enough to produce a systemic pathophysiologic response of internal fluid shifts and external fluid losses. Inadequate fluid resuscitation can result in tissue hypoperfusion and multisystem organ dysfunction. Moreover, a secondary systemic inflammatory response syndrome (SIRS) can further complicate the clinical course of patients whose burns involve greater than 30% TBSA. This frequently results in widespread intravascular hemolysis, acute renal failure, and acute lung injury.6,7 A global hypermetabolic state tends to accompany these injures. When greater than 30% to 40% of a patient's ...

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