TABLE 1815 Dermally Adsorbed Agents Through Intact Skin Resulting in Systemic Toxicity

CORROSIVES Local dermal injury from corrosive agents may be obvious immediately after exposure to mineral acids or may be delayed following exposure to alkaline corrosives or hydrofluoric acid. Alkaline burns (sodium hydroxide, cement) are most common. These agents tend to penetrate tissues and cause liquefaction necrosis. In general, injury to the skin is more extensive than that from acids, which coagulate proteins and do not penetrate tissues deeply. Acids may cause desiccation of the skin and form darkened areas or eshcars. Treatment may involve prolonged irrigation or hydrotherapy of the area. The use of nitrazine paper to monitor pH may guide therapy. Contact with other substances may cause frostbite or freezing injuries to the skin, including liquid forms of phosphine, phosgene, ammonia, chlorine, ethylene oxide, hydrogen sulfide, and propane. Hydrocarbons such as gasoline may cause dermal burns or a defatting dermatitis.

PHENOL Phenol and its derivatives, creosol, carboxylic acid, and the polycyclic phenols, cause intense cutaneous destruction. They are then rapidly absorbed through the skin and may produce CNS depression, hypotension, intravascular hemolysis, pulmonary edema, and hepatic and renal dysfunction. Theoretically, phenol absorption may be enhanced by small volumes of water. Deluge volumes of water, however, should remove the toxin safely. The burn area may then be lavaged or soaked for 5 to 10 min with gauze impregnated with polyethylene glycol (PEG 300 or 400). Glycerol or isopropanol may be substituted if PEG solutions are not available. Because phenol acts as a local anesthetic, pain may not be an appropriate indicator of ongoing tissue destruction.

HYDROFLUORIC ACID Hydrofluoric acid is an aggressive substance commonly used in the semiconductor or glass-etching industry and also marketed for household use as a metal or brick cleaner, wheel brightener, and rust remover. Dermal contact with concentrations greater than 50% cause immediate throbbing pain, blanching, and blistering. Contact with lower concentrations causes no immediate symptoms but results in delayed pain, swelling, and potentially serious injury 8 to 24 h later. Accidents involving only 2.5 percent surface area exposure to concentrated forms may be fatal. Systemic absorption may result in malignant cardiac dysrhythmias, seizures, local tissue destruction, bone demineralization, hypocalcemia, hyperkalemia, and hypomagnesemia. Inhalation of hydrofluoric acid vapor is rare but may result in delayed fatal pulmonary edema. Overall management involves cardiac monitoring, intravenous calcium or magnesium administration as indicated, skin decontamination, topical application of calcium gluconate gel to the affected area, and narcotics for pain. Injection of calcium gluconate (never calcium chloride) into the affected area at a maximum of 0.5 mL/cm2 of tissue may be considered for intractable pain to neutralize the fluoride ion. Since such infiltration may cause fingertip ischemia, intraarterial calcium through a radial arterial line has been recommended for digital burns (10 mL 10% calcium gluconate in 50 mL D 5W infused over 4 h). Hydrofluoric acid burns are often much more painful than the appearance of the wound would indicate, and persistent pain represents continuous injury. Newer decontamination solutions such as Hexafluorine are currently under evaluation. There is little data to support the instillation of calcium or magnesium solutions into the eyes.

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