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.

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 217-1 and 217-2).

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).

Death early after severe chemical burns is usually related to hypotension, acute renal failure, and shock as a result of fluid loss. However, systemic toxicity and subsequent morbidity and mortality may also occur if chemicals are absorbed. Acidosis, hypotension, hyperkalemia, dysrhythmia, and shock can occur with systemic absorption of acids (Table 217-4).

The initial goal of treatment is to remove the patient from the exposure and prevent any further chemical exposure. If not performed prior to arrival, remove all exposed clothing immediately. With few exceptions, aggressive irrigation with water is the cornerstone of initial treatment for chemical burns. Chemical agents will continue to damage tissue until they are removed or inactivated. Dry chemical particles such as lime should be brushed away before irrigation. Sodium metal and related compounds should be initially covered with mineral oil or excised, because water can cause a severe exothermic reaction. Dilution of phenol (carbolic acid) with water may enhance penetration. For the most part, however, use of water or saline to irrigate a chemical burn should not be delayed while searching for other treatment agents and should ideally begin immediately at the scene of the accident. Almost universally, earlier irrigation means a better prognosis.

Hospital personnel should maintain universal precautions while decontamination is ongoing. At the very minimum, mask, face shield, chemical-resistant gown, gloves, and water-impervious boots should be worn at all times. The exact personal protective equipment worn will ultimately depend on the specific agent involved.

The amount of elapsed time to initiate dilution or removal of chemical agents is directly related to the eventual depth and degree of injury. Wounds irrigated 3 minutes after contact with some chemicals have a twofold greater chance of becoming full-thickness burns than wounds irrigated within 1 minute of chemical contact. The time required for irrigation varies. Severe alkali burns may require several hours of irrigation. Use pH indicator paper to determine continued presence of alkali or acid in burn wounds and possible need for further irrigation. Irrigation should continue until pH is neutral or near neutral.

Although thermal energy is produced in an exothermic reaction when using water irrigation, copious amounts of water will decrease the rate and intensity of the chemical reaction and dissipate the heat.² Continue irrigation at a gentle flow to avoid continued skin contact with chemicals.

After irrigation and debridement of remaining particles and devitalized tissue, apply topical antimicrobial agents to affected areas, and provide tetanus immunization as needed. Other than measures specific for a particular chemical burn, treatment following initial therapy is similar to that of thermal burns (Table 217-5). Aggressive fluid replacement is needed if extensive chemical burns are sustained. Analgesics may be needed, and in the case of allergic responses to chemicals, epinephrine, antihistamines, and steroids may be required.

Do not limit the examination of a patient with a significant chemical acid burn to the skin because acids may cause respiratory and mucous membrane irritation as well. Furthermore, skin absorption of some compounds may occur and result in systemic signs and symptoms.

With the exception of hydrofluoric acid, strong acids produce coagulation necrosis from the denaturation of proteins in the superficial tissue. Injury severity is related to the physical characteristics of the acid. Most substances with a pH <2 are strong corrosives. Other important tissue-damaging properties of acids include concentration, molarity, and complexing affinity for hydroxyl ions. The higher each of these factors is, the greater is the tissue damage. Contact time with the skin is the most important chemical burn feature that healthcare professionals may alter. For example, instantaneous skin decontamination of 18M sulfuric acid will cause no burn, but a 1-minute exposure can cause full-thickness skin damage.

ACETIC ACID

The dilute (<40%) acetic acid solution found in hair-wave neutralizer solutions is perhaps the most common cause of chemical burns to the scalp in women. Prolonged contact, especially with an already damaged scalp, can cause a partial-thickness burn that heals slowly and is prone to infection. Initial treatment is copious water irrigation. Oral antibiotics should be prescribed if the scalp burn has created open skin lesions.

CARBOLIC ACID (PHENOL)

Phenol (carbolic acid), a corrosive organic acid used widely in industry and medicine, denatures proteins and causes chemical burns characterized by a relatively painless white or brown coagulum. Paradoxically, dilute phenol penetrates tissue more readily than the concentrated form. Systemic absorption may result in life-threatening cardiac dysrhythmias or seizures. The unpleasant, acrid odor of phenol, detecTable in air at 0.047 parts per million, and its low volatility help prevent airborne exposure. Although commercially available in concentrations up to 90%, even dilute solutions of 1% to 2% phenol may cause a burn if contact is prolonged or extensive. Chemically related phenolic compounds that induce skin damage include cresol, creosote, and cresylic acid.

Coagulation necrosis of the involved area is common. Necrotic tissue may delay absorption temporarily, but phenol may become entrapped under the eschar. Remove contaminated clothing and begin water irrigation immediately. Water lavage alone may not be totally effective, because the necrotic coagulum inhibits water penetration to the deeper layers.

Decontamination is more effective by the use of an undiluted polyethylene glycol solution of molecular weight 200 to 400 or by a gentle wash with isopropyl alcohol. Adequate supplies of either irrigation solution should remain stored for such use. Either irrigation solution reduces the extent of cutaneous corrosion and also decreases systemic toxicity. An isopropyl alcohol rinse is equivalent to polyethylene glycol in removing phenol.³ The advantage of isopropyl alcohol is its ready availability. If neither polyethylene glycol nor isopropyl alcohol is available in adequate supplies, large volumes of water should be used.

CHROMIC ACID

Chromium hexavalent compounds (Cr⁶⁺

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