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INTRODUCTION AND EPIDEMIOLOGY
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More than 25,000 products are capable of producing chemical burns. Exposures occur both occupationally and in homes. As many as 10% of all burn center admissions are the result of chemical burns. Although a smaller percentage of total burns, the mortality is high and may account for as many as 30% of all burn deaths.1 Careful individual attention is required for chemical burn treatment due to the nature of concomitant tissue injury and chemical exposure.
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The skin is a barrier and transition zone between the internal and external environments. Although the outer stratum corneum layer of the skin functions as an excellent barrier against many chemicals, some penetrate it readily. Chemicals can produce burns, dermatitis, allergic reaction, thermal injury, and/or systemic toxicity.
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Most chemicals produce tissue damage by their chemical reaction rather than by thermal injury. Certainly, some chemicals produce significant heat by means of an exothermic reaction. However, most skin damage is the result of the chemical's unique characteristics. Unlike thermal burns, chemical burn injuries require tailored evaluations and treatments based on the specific agent involved. Multiple factors influence tissue damage and percutaneous absorption of chemicals (Tables 217-1 and 217-2).
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Most chemical burns are caused by acids or alkalis. At similar volumes and manner of contact, alkalis usually produce far more tissue damage than acids. Acids tend to cause coagulation necrosis with protein precipitation and form a tough leathery eschar. The eschar typically limits deeper penetration of the agent. Alkalis produce liquefaction necrosis and saponification of lipids. The result is a poor barrier to chemical penetration and deeper, ongoing burns. Other chemical injuries occur by various pathophysiologic mechanisms. Some chemical agents cause injury by more than one mechanism (Table 217-3).
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Death early after severe chemical burns is usually related to hypotension, acute renal failure, and shock ...