The skin interfaces with the external environment and constitutes a barrier and transition zone between the internal and external milieus. The outer stratum corneum layer of the skin functions as an excellent barrier against certain chemical agents, whereas others may penetrate readily. The skin contains three main layers: an outer layer of epithelial tissue (epidermis), a loose connective tissue layer (dermis), and a variable-thickness inner layer containing adipose and connective tissue (hypodermis or panniculus adiposus).

Chemicals can produce burns, dermatitis, allergic reaction, thermal injury, or systemic toxicity. Pathophysiologically, burns produced by all chemicals are similar. 1 The skin has a limited variety of toxic responses, corresponding to the major patterns of possible structural or functional changes. Toxic reactions are described mainly on the basis of morphologic rather than functional responses.2 There are morphologic, physiologic, and biochemical protective mechanisms and elements in the skin which include the epidermal barrier, eccrine sweating, phagocytic cells, metabolic detoxification, immunologic processes, and melanin pigmentation. However, these vary on a phenotypic basis and may be affected by systemic or local disease.

Skin damage by chemicals may demonstrate the classic manifestations of thermal injury (erythema, blistering, or full-thickness loss); however, an acute injury may be deceptively mild, only to be followed by extensive skin damage and systemic toxicity. A superficial (first-degree) burn causes capillary and arterial dilatation. Initially, this involves only the superficial vessels, but then extends to the deeper subcutaneous vessels by both direct and reflex action. Tissue hyperemia and congestion results in symptoms of itching, burning, or pain. More extensive inflammatory reactions result in an outpouring of fluid into the extracellular space, causing edema and vesicle or bulla formation characteristic of partial-thickness (second-degree) burns. Continued chemical damage through the dermis or into the hypodermis results in a full-thickness (third-degree) burn. Tissue damage is determined by

• Strength/concentration of the agent

• Manner of contact

• Quantity of agent

• Duration of contact

• Mechanism of action

• Extent of penetration

Factors enhancing percutaneous absorption of chemical are body site (areas of thin skin, i.e., genitalia, face; chemical contact between skinfolds; amount of surface area exposed); integrity of skin (traumatized skin, elderly skin, decreased lipid, dehydration, inflammation); nature of the chemical (lipid solubility, pH, concentration); and occlusion (garments, occlusive dressings).

The majority of 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 in general cause coagulation necrosis with protein precipitation. Tough leathery eschar may form with development of underlying ulcers. The eschar limits spread of the agent. Heat may be released during reaction of acid with skin. Alkalis produce liquefaction necrosis with loosening of material that allows deeper penetration of the unattached chemical into tissue. Not all chemicals causing burns can be considered acid or alkali. A useful classification by Jelenko groups chemicals by the manner in which they damage protein:3

1. Oxidizing agents: Damage is produced when a chemical becomes oxidized in contact with tissue. Often a toxic moiety is released during this reaction.

2. Corrosives: Extensive protein denaturation is produced, resulting in soft eschar and shallow, indolent ulcers.

3. Reducing agents: Protein denaturation is produced by binding of free electrons in tissue protein.

4. Desiccants: Severe cellular dehydration is produced, and thermal injury occurs due to exothermic reaction.

5. Vesicant: Blisters are produced, tissue amines are liberated, local ischemia and anoxic tissue damage and pandermic inflammation occurs.

6. Protoplasmic poisons: Protein is denatured by salt formation or by metabolic competition/inhibition (i.e., binding calcium or other inorganic ions necessary for tissue viability and function).

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