INTRODUCTION AND EPIDEMIOLOGY
More than 25,000 products can produce chemical burns. Most exposures occur occupationally, but home exposures are common as well. As few as 10% of all burn center admissions are the result of chemical burns; however, the morbidity and mortality are high and may account for as many as 30% of all burn deaths.1,2 Burn injuries from corrosives, mostly to the face and neck, are unfortunately a common and growing method of assault in low- and middle-income countries. Long-term psychological and physical effects are debilitating.3 Careful individual attention is required for chemical burn treatment due to the nature of concomitant tissue injury as well as chemical exposure.
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.
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 218-1 and 218-2).
TABLE 218-1Factors Influencing Tissue Damage ||Download (.pdf) TABLE 218-1 Factors Influencing Tissue Damage
Duration of contact
Concentration of agent
Quantity of agent
Mechanism of action
Extent of penetration
TABLE 218-2Factors Influencing Percutaneous Absorption of Chemicals ||Download (.pdf) TABLE 218-2 Factors Influencing Percutaneous Absorption of Chemicals
Integrity of skin
Nature of the chemical
Duration of contact
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 forming 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 allowing deeper burns and persistent tissue injury. Other chemical injuries occur by various pathophysiologic mechanisms. Some chemical agents cause injury by more than one mechanism (Table 218-3).
TABLE 218-3Classification of Chemicals ||Download (.pdf) TABLE 218-3 Classification of Chemicals
|Classification of Chemical Damage
|Mechanism of Injury
|Protein denaturation as proton donors
|Protein denaturation as ...