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INTRODUCTION

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.1-3 Over 40,000 of these patients required inpatient treatment for their injuries and up to 73% of these injuries occur at home. The associated expenses are staggering. The mean hospital stay was over 1 week and at an average cost over $50,000 per admission. An average of over 4500 individuals per year died from burn-related injuries. Fires and burns represent the fifth, third, sixth, and eighth leading causes of unintentional injury deaths in the United States for the age groups of 1 to 4 years, 5 to 9 years, 10 to 14 years, and ≥ 65 years, respectively.1 Less than 6% of the above patients who were admitted to a recognized burn center subsequently died from their injuries.2-4 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.

Thermal injuries have the potential to affect any body surface, both internally and externally, with which a heated medium comes into contact. The overall depth and degree of injury is multifactorial. It is 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.

ANATOMY AND PATHOPHYSIOLOGY

Skin exposure to any significant heat source results in a spectrum of pathophysiologic 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 (e.g., histamines, prostaglandins, cytokines, and interleukins). These agents further exacerbate the localized edematous reaction via vasodilation and increased capillary permeability.5

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 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. 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...

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