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Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 8e

Chapter 217: Chemical Burns Anthony F. Pizon; Michael J. Lynch

FIGURE 217-1.

INTRODUCTION AND EPIDEMIOLOGY

More than 25,000 products are capable of producing chemical burns. Exposures occur both occupationallyand in homes. As many as 10% of all burn center admissions are the result of chemical burns. Although asmaller 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 ofconcomitant tissue injury and chemical exposure.

PATHOPHYSIOLOGY

The skin is a barrier and transition zone between the internal and external environments. Although the outerstratum corneum layer of the skin functions as an excellent barrier against many chemicals, some penetrateit 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 isthe result of the chemical's unique characteristics. Unlike thermal burns, chemical burn injuries requiretailored evaluations and treatments based on the specific agent involved. Multiple factors influence tissuedamage and percutaneous absorption of chemicals (Tables 217-1 and 217-2).

TABLE 217-1

Factors Influencing Tissue Damage

Concentration of agent

Quantity of agent

Duration of contact

Mechanism of action

Extent of penetration

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TABLE 217-2

Factors Influencing Percutaneous Absorption of Chemicals

Body site

Areas of thin skin (i.e., genitalia, face, and skinfolds are particularly vulnerable)

Amount of surface area

Integrity of skin

Increased vulnerability: traumatized skin, elderly skin, dehydration, inflammation

Nature of the chemical

Lipid solubility, pH, concentration

Duration of contact

Poor irrigation, chemical-soaked garments, occlusive dressings

Most chemical burns are caused by acids or alkalis. At similar volumes and manner of contact, alkalis usuallyproduce far more tissue damage than acids. Acids tend to cause coagulation necrosis with proteinprecipitation 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 chemicalpenetration and deeper, ongoing burns. Other chemical injuries occur by various pathophysiologicmechanisms. Some chemical agents cause injury by more than one mechanism (Table 217-3).

TABLE 217-3

Classification of Chemicals

Classification of Chemical Damage Mechanism of Injury

Acids Protein denaturation as proton donors

Alkalis Protein denaturation as proton acceptors

Organic solvents Disruption of cellular membranes

Inorganic solvents Scavenge ions and salt production within tissues

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

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TABLE 217-4

Systemic E�ects Associated with Chemical Burns

Chemical Systemic Toxicity

Hydrofluoric acid Hypocalcemia, hypomagnesemia, hyperkalemia, cardiac

arrhythmias, sudden death

Tannic acid, chromic acid, formic acid, picric

acid, phosphorus

Hepatic necrosis, nephrotoxicity

Cresol Methemoglobinemia, massive hemolysis, multiple organ

failure

Gasoline Severe pulmonary, cardiovascular, neurologic, renal, and

hepatic complications

Phenol (carbolic acid) Cardiovascular and central nervous system toxicity

Sodium nitrate, potassium nitrate Severe methemoglobinemia with refractory cyanosis

Dichromate solution Liver failure, acute renal failure, death despite hemodialysis

GENERAL APPROACH TO CHEMICAL BURNS

The initial goal of treatment is to remove the patient from the exposure and prevent any further chemicalexposure. 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 agentswill continue to damage tissue until they are removed or inactivated. Dry chemical particles such as limeshould be brushed away before irrigation. Sodium metal and related compounds should be initially coveredwith 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 toirrigate a chemical burn should not be delayed while searching for other treatment agents and should ideallybegin immediately at the scene of the accident. Almost universally, earlier irrigation means a betterprognosis.

Hospital personnel should maintain universal precautions while decontamination is ongoing. At the veryminimum, mask, face shield, chemical-resistant gown, gloves, and water-impervious boots should be worn

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at all times. The exact personal protective equipment worn will ultimately depend on the specific agentinvolved.

The amount of elapsed time to initiate dilution or removal of chemical agents is directly related to theeventual depth and degree of injury. Wounds irrigated 3 minutes a�er contact with some chemicals have atwofold greater chance of becoming full-thickness burns than wounds irrigated within 1 minute of chemicalcontact. 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 needfor 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.

A�er irrigation and debridement of remaining particles and devitalized tissue, apply topical antimicrobialagents to a�ected areas, and provide tetanus immunization as needed. Other than measures specific for aparticular 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 berequired.

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TABLE 217-5

Treatment of Select Chemical Burns

Chemical Treatment Comments

Acids

All acid burns require prompt decontamination and copious irrigation with water

Acetic acid Copious irrigation Consider systemic antibiotics for

extensive scalp burns

Phenol (carbolic acid) Copious irrigation Isopropyl alcohol may also be used

Sponge with undiluted polyethylene

glycol 200–400

Chromic acid Copious irrigation Observe for systemic toxicity

Formic acid Copious irrigation Dialysis may be needed for severe

toxicity

Hydrofluoric acid Copious irrigation Consider intradermal injection of 10%

calcium gluconate or intra-arterial

calcium gluconate for severe cases

Monitor serum calcium and magnesium

in severe exposure

10% calcium gluconate intradermal

Topical calcium gluconate gel 25 mL of 10% calcium gluconate in 75 mL

of sterile water-soluble lubricant (K-Y jelly

or US jelly)

Nitric acid Copious irrigation Consult with burn specialist

Oxalic acid Copious irrigation Evaluate serum electrolytes and renal

function

IV calcium may be required Cardiac monitoring for serious dermal

exposure

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Chemical Treatment Comments

Alkalis

All alkali burns require prompt decontamination and copious, prolonged irrigation with water

Portland cement Prolonged copious irrigation May need to remove cement particles

with a brush, such as a preoperative

scrubbing brush

Elemental Metals

Water is generally contraindicated in extinguishing burning metal fragments embedded in the skin

Elemental metals

(sodium, lithium,

potassium,

magnesium,

aluminum, and

calcium)

Cover metal fragments with sand,

foam from a class D fire extinguisher,

or mineral oil

Excise metal fragments that cannot be

wiped away

Hydrocarbons

Gasoline Decontamination

Tar Cool before removal Baby oil can be used

Remove using antibiotic ointment

containing polyoxylene sorbitan

(polysorbate)

Vesicants

Mustards Decontaminate If limited water supply, adsorbent

powders (flour, talcum powder, fuller's

earth) can be applied to the mustard and

then wiped away with a moist towel

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Chemical Treatment Comments

Copious irrigation

Reducing Agents

Alkyl mercury

compounds

Copious irrigation Blister fluid is high in metallic mercury

content

Debride, drain, and copiously irrigate

blisters

Lacrimators

Tear gas Copious irrigation May cause respiratory symptoms if

inhaled

Pepper spray Copious irrigation May cause respiratory symptoms if

inhaled

Miscellaneous

White phosphorus Remove clothing Systemic toxicity is a significant concern

Copious irrigation, keep exposed skin

areas wet or submerged until all

particles have been removed due to

risk of ignition when exposed to air

Debride visible particles

Airbag Prolonged copious irrigation

ACID BURNS

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

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With the exception of hydrofluoric acid, strong acids produce coagulation necrosis from the denaturation ofproteins in the superficial tissue. Injury severity is related to the physical characteristics of the acid. Mostsubstances with a pH <2 are strong corrosives. Other important tissue-damaging properties of acids includeconcentration, molarity, and complexing a�inity for hydroxyl ions. The higher each of these factors is, thegreater is the tissue damage. Contact time with the skin is the most important chemical burn feature thathealthcare professionals may alter. For example, instantaneous skin decontamination of 18M sulfuric acidwill 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 commoncause of chemical burns to the scalp in women. Prolonged contact, especially with an already damagedscalp, can cause a partial-thickness burn that heals slowly and is prone to infection. Initial treatment iscopious 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 andcauses chemical burns characterized by a relatively painless white or brown coagulum. Paradoxically, dilutephenol 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 at0.047 parts per million, and its low volatility help prevent airborne exposure. Although commerciallyavailable in concentrations up to 90%, even dilute solutions of 1% to 2% phenol may cause a burn if contactis 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, butphenol may become entrapped under the eschar. Remove contaminated clothing and begin water irrigationimmediately. Water lavage alone may not be totally e�ective, because the necrotic coagulum inhibits waterpenetration to the deeper layers.

Decontamination is more e�ective by the use of an undiluted polyethylene glycol solution of molecularweight 200 to 400 or by a gentle wash with isopropyl alcohol. Adequate supplies of either irrigation solutionshould remain stored for such use. Either irrigation solution reduces the extent of cutaneous corrosion andalso 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 norisopropyl alcohol is available in adequate supplies, large volumes of water should be used.

CHROMIC ACID

Chromium hexavalent compounds (Cr6+) are powerful oxidizers. The chromate ion in chromic acid producesa chronic penetrating ulcerating lesion of the skin. Associated signs and symptoms of chromic acid exposure

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are conjunctivitis, lacrimation, and ulceration of the nasal septum. Systemic chromium toxicity can causeliver or renal failure, GI bleeding, coagulopathy, and CNS disturbances. Significant symptoms may occur a�eronly 1% to 2% body surface area burns. A 10% body surface area cutaneous burn caused by chromic acid canbe fatal due to systemic toxicity. Any acute skin exposure to chromic acid should be treated with copiouswater irrigation and observation for systemic e�ects. Aggressive excision is the best method for prevention ofsystemic e�ects because depth of the burn is di�icult to determine and absorption of chromium may

continue a�er irrigation.4

FORMIC ACID

Formic acid in 60% solution is used by acrylate glue makers, cellulose formate workers, and tanning workers.Formic acid produces coagulation necrosis of the skin. Systemic e�ects, including decreased respiration,

anion gap metabolic acidosis, and hemolysis have been reported.5 Treatment includes immediatedecontamination and irrigation with water. Systemic toxicity may require intravenous sodium bicarbonatefor the metabolic acidosis or exchange transfusions for severe hemolysis.

HYDROCHLORIC AND SULFURIC ACIDS

The dermal toxicity of hydrochloric acid and sulfuric acid is so well recognized that early decontaminationand water irrigation usually prevent severe burns to the skin. These acids can burn the skin dark brown orblack. Toilet bowl cleaners may contain 80% solutions of sulfuric acid, and some drain cleaners may be 95%to 99% sulfuric acid solutions. Munitions, chemical, and fertilizer manufacturers commonly use 95% to 98%sulfuric acid solutions in their industrial processes. Automobile battery fluid is 25% sulfuric acid. Mosthousehold bleaches are only 3% to 6% hypochlorite solutions, which, although acidic, cause little damageunless they are in contact with skin for a prolonged time. Treatment is the same as for formic acid burns.

HYDROFLUORIC ACID

Hydrofluoric acid is used in the production of high-octane fuel, etching and frosting glass, semiconductors,microelectronics/microinstruments, germicides, dyes, plastics, tanning, and fireproofing material and is usedin cleaning stone and brick buildings. It is also a very e�ective rust remover.

Unlike other acids, hydrofluoric acid penetrates deeply and will cause progressive tissue loss. It producesburns in two ways. First, hydrogen ions cause direct cellular damage as other acids do through proteindenaturation. Second, free fluoride ions scavenge intracellular cations, such as calcium and magnesium,disrupt cellular membranes, and inhibit the sodium/potassium/ATPase. This leads to systemic hypocalcemia,hypomagnesemia, and hyperkalemia. Locally, free fluoride ions cause spontaneous depolarization of nervetissue and severe pain. Pain will persist until all free fluoride ions have been neutralized.

The dermal e�ects may not be immediately noted and appear to be more related to the concentration ofhydrofluoric acid than to the duration of exposure. Solutions >50% produce immediate pain and tissue

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destruction. Solutions <20% may not produce signs and symptoms until 12 to 24 hours a�er exposure. Theskin o�en develops a blue-gray appearance with surrounding erythema.

The treatment of hydrofluoric acid burns consists of two phases. The first, immediate phase is copious waterirrigation of the a�ected skin for 15 to 30 minutes. This may be the only treatment that is needed if thehydrofluoric acid solution is <20% concentration, the duration of exposure was very brief, anddecontamination is begun immediately. Severe, persistent pain denotes a more serious injury requiring thesecond phase of treatment.

The second phase of treatment is aimed at replacing calcium and magnesium and detoxifying the enzyme-

poisoning fluoride ion. Two ions—calcium (Ca2+) and magnesium (Mg2+)6—bind the fluoride ion and curtailits toxic e�ects. However, the overwhelming clinical experience to date has been with calcium gluconate, soit is the agent of choice. Calcium gluconate can be administered as a topical preparation,subcutaneous/intradermal injection, or intra-arterial infusion. A calcium gluconate gel made with a water-soluble lubricant is generously applied to the a�ected skin. The topical preparation is made by mixing 3.5grams of calcium gluconate powder in 5 oz of water-soluble lubricant, or 25 mL of 10% calcium gluconate in75 mL of water-soluble lubricant. Calcium chloride or calcium carbonate can be substituted if no calciumgluconate is available. The main limitation of topical therapy is the impermeability of the skin to calcium,and therefore, topical therapy is limited to use in mild, superficial burns. Most importantly, topical therapyshould not delay intradermal or intra-arterial injections for severe burns.

Treatment with intradermal injection of a 10% calcium gluconate solution through a 27-gauge needle intothe hydrofluoric acid–burned skin is a very e�ective treatment. A typical dose of 0.5 mL of 10% calciumgluconate per square centimeter of burned skin is recommended. Pain relief is nearly immediate, and,indeed, the elimination of pain may be used as a guide for further therapy. Recurrence of pain indicates theneed for further therapy. Unfortunately, injection therapy has several disadvantages: (1) only limitedamounts of calcium are delivered to the tissue; (2) hyperosmolarity and inherent toxicity of free calcium ionscause more pain initially, and more tissue damage is possible if calcium is not bound to fluoride; (3) vascularcompromise can result if too much fluid is injected, especially into digits; and (4) rapid penetration ofhydrofluoric acid beneath the nail requires nail removal to administer the calcium gluconate into the nail bedadequately. Acute hydrofluoric acid contamination of the hands, feet, digits, or nails requires consultationwith a medical toxicologist and plastic surgeon.

Intra-arterial infusion of calcium gluconate may be used to prevent tissue necrosis and stop the pain

associated with hydrofluoric acid burns.7 This should be performed as soon as possible a�er the initial burn,preferably within 6 hours of insult. Place an intra-arterial catheter in the appropriate vascular supply (thebrachial artery if the entire hand is a�ected) and connect to a three-way stopcock to which is attached anarterial pressure-monitoring device and the infusion syringe of calcium gluconate. A 50-mL syringe may befilled with 10 mL of a 10% calcium gluconate solution and 40 mL of 5% dextrose in water and infused over 4hours. The arterial pressure-monitoring device ensures that the catheter has not dislodged from the lumen ofthe cannulated artery. Repeat infusion may be needed if pain recurs within 4 hours. Intra-arterial infusion

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avoids the disadvantages of local infiltration therapy, but it has its own disadvantages: it is an invasivevascular procedure that (1) may result in arterial spasm or thrombosis, (2) requires more time and hospitalresources, and (3) requires experience in the technique.

Inhalation of hydrofluoric acid can cause immediate or delayed pulmonary injury. All cases of suspectedinhalation injury should be admitted for observation even if asymptomatic. Nebulized calcium gluconatemay be attempted in these cases, but no controlled studies exist for its use. The solution is made by adding1.5 mL of 10% calcium gluconate solution into 4.5 mL of sterile water or saline and is administered bynebulizer.

Ocular exposure to hydrofluoric acid requires water irrigation for at least 30 minutes and requires emergentophthalmologic consultation. An animal study suggests that calcium-containing irrigation fluids for eye

exposures may be harmful.8 Therefore, standard eye irrigation practices should be used. The possibility ofsevere injury and eye necrosis should not be taken lightly. In severe ocular exposures, systemic absorption ispossible as well.

Systemic toxicity from dermal hydrofluoric acid exposure can result in ventricular fibrillation as a result ofsystemic acidosis, hyperkalemia, hypomagnesemia, and hypocalcemia. In major hydrofluoric acid burns,immediately administer IV calcium and magnesium, using standard slow IV rates, before laboratory resultsare available. Once patients develop hypocalcemia or hypomagnesemia, it is very di�icult to restore theseelectrolyte deficiencies. Cardiac monitoring, IV access, and electrolyte monitoring should be performed in allcases of significant hydrofluoric acid dermal burns (Table 217-6).

TABLE 217-6

Options for Treatment of Hydrofluoric Acid Skin Burns

1. Copious irrigation for 15–30 min immediately.

2. Application of calcium gluconate gel, 25 mL of 10% calcium gluconate in 75 mL of water-soluble lubricant.

3. Further treatment options as dictated by patient response:

a. Dermal injection of 10% calcium gluconate at the rate of 0.5 mL/cm2 of skin surface using a small-

gauge needle.

b. Arterial infusion over 4 h (40 mL of 5% dextrose in water with 10 mL of 10% calcium gluconate).

c. Consider supplemental magnesium and calcium IV.

METHACRYLIC ACID

Methacrylic acid, found in many artificial nail cosmetic products, can produce severe dermal burns, usuallyin preschoolers. Emergency treatment is copious water irrigation.

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NITRIC ACID

Nitric acid is used in industry for casting iron and steel, electroplating, engraving, and fertilizermanufacturing. Upon contact with skin, nitric acid can produce tissue damage by oxidation and may turn theskin yellowish as it is burned. Emergency treatment consists of copious water irrigation and standard burncare (see chapter 216, "Thermal Burns").

OXALIC ACID

Oxalic acid is used for leather tanning and blueprint paper. Oxalic acid binds calcium and prevents musclecontraction. The wounds should be irrigated with water, and IV calcium may be required. Serum electrolytesand renal function should be evaluated, and cardiac monitoring should be instituted a�er serious dermalexposure.

ALKALI BURNS

Alkalis penetrate skin deeper and longer than acids and present a greater danger of toxicity from systemicabsorption. Wounds may initially look superficial only to become full-thickness burns in 2 to 3 days. Alkaliscombine with protein and lipids in tissue to form soluble protein complexes and soaps that permit passage ofhydroxyl ions deep into tissue. So�, gelatinous, friable, brownish eschars are o�en produced (Figure 217-1).Strong alkalis have a pH >12.

FIGURE 217-1.

Deep alkali burn. [Reproduced with permission fromhttp://www.burnsurgery.org/Modules/initial_mgmt/sec_6.htm.]

LYES

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Strong, corrosive alkalis ("lyes") include ammonium, barium, calcium, lithium, potassium (caustic potash),and sodium (caustic soda) hydroxides. Lyes are widely used in industry and are found in home products such

as drain and toilet cleaners, detergents, and paint removers. The urine sugar reagent tablet Clinitest® (Bayer)

contains anhydrous sodium hydroxide.9 Ammonium hydroxide is used in the production of synthetic fibersand extensively in agriculture. Exposure to these chemicals can result in severe toxicity including mucousmembrane, ocular, dermal, GI, and inhalational/pulmonary injury. As a mode of assault, lyes have a lowermortality rate than gunshot wounds or stabbings, but victims o�en su�er long-term pain, scarring, andblindness. Suicidal ingestion of lye may result in rapid death from upper airway occlusion. Late morbidityrelated to esophageal and gastric necrosis may be minimized by early surgical intervention with

esophagogastrectomy. The mainstay of treatment is immediate, voluminous, and persistent irrigation.10 Lyesare extremely corrosive and penetrating. Burns require copious irrigation for long periods of time.

LIME

Lime (calcium oxide) is found in agricultural products and cements. There is considerable variability of limecontent in di�erent grades of cement, with fine to textured masonry cement having more lime than concrete.Lime is converted by water to the alkali calcium hydroxide. Upon skin contact, lime draws water out of theskin. All dry lime particles should be brushed away before irrigation. Even a small amount of water maygenerate an exothermic reaction resulting in calcium hydroxide formation and tissue injury. Brisk irrigationwith a large volume of water (taking care to avoid splashing in eyes) should be used and will permitdissipation of heat.

PORTLAND CEMENT

Portland cement, which accounts for a major proportion of the cement used in the United States, is a mixtureof sand, lime, and other metal oxides. In the presence of water, calcium hydroxide, sodium hydroxide, andpotassium hydroxide may all be formed. Workers who kneel in wet cement or get cement in their boots maydiscover burns hours a�er initial contact. In addition, skin may become irritated from gritty material, and acontact dermatitis may develop in individuals sensitive to the chromate contained in the material. Treatmentof cement burns may require cleaning the wound with a brush, such as a preoperative scrubbing brush, toremove cement particles imbedded in the dermis. Careful attention to appropriate donning of personalprotective equipment should be emphasized to patients su�ering dermatitis or burns from contact withcement.

METALS

Foundry workers are sometimes burned by molten metal, which may spill or splash on body parts and rundown into the boots. Elemental metals, sodium, lithium, potassium, magnesium, aluminum, phosphorus,and calcium may all cause burns. When exposed to air, some elemental metals spontaneously ignite. Water isgenerally contraindicated in extinguishing burning metal fragments embedded in the skin because theresultant explosive exothermic reaction can lead to significant tissue injury. Burning metal may be

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extinguished with a class D fire extinguisher, smothered with sand, or covered with mineral oil. Wounddebridement should include excision of metal fragments that cannot be wiped away. Metal fragments shouldbe placed in mineral oil to prevent further ignition.

HYDROCARBONS

GASOLINE

Hydrocarbons cause a fat-dissolving corrosive injury to the skin referred to as defatting dermatitis. Gasoline,a complex mixture of alkanes, cycloalkanes, and aromatic hydrocarbons, is the most common hydrocarbonburn treated in the ED.

A hydrocarbon chemical burn typically resembles a thermal scald or a partial-thickness burn, although full-

thickness burns can result from prolonged contact with gasoline.11 During extremely cold weather, topicalgasoline exposure may lead to frostbite when rapid gasoline evaporation causes heat loss from the skin.Systemic e�ects of hydrocarbon absorption include neurologic, pulmonary, cardiovascular, GI, and hepaticinjuries. For further discussion, see chapter 199, "Hydrocarbons and Volatile Substances."

The primary treatment is decontamination by removing saturated clothing and irrigating exposed skin withsoap and water. Otherwise, management is as for a thermal burn.

HOT TAR

Hot tar is derived from long-chain petroleum and coal hydrocarbons. Roofing tars and asphalt are heated totemperatures up to 500°F (260°C), and the burns sustained are usually more thermal than chemical. Althoughthe surface area size of the burn is usually small, solidified material stuck to skin and hair is di�icult toremove. If hot, the tar should be cooled to prevent continued thermal injury. Manual mechanicaldebridement can be painful and destructive to skin structures. Polyoxylene sorbitan (polysorbate), containedin many antibiotic ointments, is an emulsifying agent that can be used to remove tar. Industrial removal

agents such as De-Solv-It®, a citrus and petroleum distillate, are also e�ective in tar removal. Baby oil is alsoe�ective for tar removal.

VESICANTS (DIMETHYL SULFOXIDE, CANTHARIDES, AND SULFURMUSTARD)

Dimethyl sulfoxide, cantharides, and mustard gas are vesicant or drying agents. Skin burns with edema andblister formation occur due to production of ischemia and anoxic necrosis at the site of contact. Dimethylsulfoxide is a water-soluble organic solvent used in industry. It is available without prescription and is usedtopically for sprains, bruises, minor burns, and joint pain. Due to its chemical composition and solubility,dimethyl sulfoxide can penetrate barrier surfaces such as nitrile gloves. Cantharides ("Spanish Fly") isoccasionally used for its supposed aphrodisiac e�ects. Sulfur mustard is a vesicant historically used in

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chemical warfare. An alkylating agent, exposure results in inhibition of cellular enzymatic activity, leading tonecrosis. For further discussion, see chapter 8, "Chemical Disasters."

Skin damage following vesicant exposure can be severe and result in deep skin penetration, edema, blisters,ulcers, and serious morbidity. Immediate, copious irrigation with water or saline may mitigate the extent oftissue injury. Skin can also be decontaminated by using adsorbent powders such as flour, talcum powder,and fuller's earth if the supply of water is limited. These powders adsorb the mustard from the skin andshould be wiped away with a moist towel. Almost any material can be used to brush the vesicant away fromskin. The military uses M258A1 kits for skin decontamination. These kits contain three sets of towelettes, oneof each containing phenol, sodium hydroxide, and sodium benzene sulphonochloramine (chloramine).Chloramine produces "free" chlorine, which inactivates sulfur mustard. Povidone iodine shows great promisein the prevention and early treatment of skin damage caused by sulfur mustard. Human data are currentlylacking, but in animal models, both prevention of burns and immediate (<10 minutes) treatment of exposure

yielded impressive skin protection.12

POTASSIUM PERMANGANATE

Potassium permanganate is an oxidizing agent that is mildly irritating in dilute solution, but in concentratedsolution, it can produce dermal burns with a thick, brownish purple eschar of coagulated protein. Burnsshould be copiously irrigated with water.

ALKYL MERCURY COMPOUNDS

Alkyl mercury compounds, which are reducing agents used in disinfectants, fungicides, and woodpreservatives, can produce dermatitis or burn lesions. Lesions typically are erythematous with blisterformation. The blister fluid is high in metallic mercury content. The burning process continues as long as theagent remains in contact with skin. Partial-thickness burns deepen if the blister fluid is allowed to remain, sothe blisters should be debrided, drained, and copiously irrigated. Repeated or prolonged exposure to topicalmercury compounds may lead to systemic mercury toxicity.

LACRIMATORS OR TEAR GAS

Lacrimators, or tear gas, such as 2-chloroacetophenone, o-chlorobenzylidene malonitrile, and oleoresincapsicum (pepper spray), cause skin and mucosal irritation within 20 to 60 seconds of exposure and can leadto development of contact dermatitis. Although the skin injury is usually limited, inhalation and eye injuriesmay be severe. Treatment of skin exposure is rapid removal from the o�ending agent followed by salineirrigation. Ocular irritation is treated with copious water irrigation, followed by slit-lamp examination forcorneal damage. Arrange ophthalmology follow-up in 24 hours. High concentrations of lacrimators causestructural damage of the cornea. Inhalation injuries are treated with respiratory support including oxygen

and bronchodilators. There is no role for steroid therapy.13

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WHITE PHOSPHORUS

White phosphorus is used as an incendiary in munitions and fireworks and as a component of insecticides,rodenticides, and fertilizers. It ignites spontaneously when exposed to air and is rapidly oxidized tophosphorus pentoxide. Burns caused by both its solid and liquid forms are seen in both the military andcivilian populations. In munitions, white phosphorus is solid, but some of it may liquefy with detonation.Death has been reported in burns covering <10% body surface area.

Flaming droplets of inorganic phosphorus may embed beneath the skin. The heat of the reaction causestissue destruction. Particles continue to oxidize slowly until debrided, neutralized, or completely oxidized. Aslong as phosphorous is exposed to air, it will continue to burn. Remove contaminated clothing and visibleparticles, and copiously irrigate burns with normal saline or water. Skin exposed to white phosphorus mustremain wet or immersed in water until completely debrided to prevent further injury. Wood's lampexamination aids identification of remaining phosphorus as it fluoresces. Copper sulfate solution should notbe used despite its ability to detoxify phosphorous because it causes hemolysis and increases mortality.

White phosphorus burns are characterized by slow healing and ongoing burning, necessitating early andaggressive treatment. Systemically absorbed phosphorous is a serious concern. Hypocalcemia,hyperkalemia, and hepatic and renal injury all have been reported. Even patients with small burns should beconsidered for admission or transfer to a burn center for aggressive hydration, monitoring, and further

treatment.14 Treatment providers should take care to wear protective equipment and avoid direct contactwith the patient's clothing, feces, and emesis.

AIRBAG BURNS

Approximately 8% of individuals su�ering injuries related to airbag deployment are burned. Airbags deployby ignition of solid propellant—sodium azide and cupric oxide—that creates an exothermic reaction leadingto rapid inflation of the airbag. Many other gases are created during activation, including corrosives such assodium hydroxide, nitric oxide, ammonia, and multiple hydrocarbons. An airbag is deflated within 2 secondsof inflation through exhaust side ports on the bag. Burns associated with airbags include friction, thermal,

and chemical burns.15 Sodium hydroxide produced during airbag activation can cause chemical keratitis.Full-thickness skin burns have been reported. Perform slit-lamp examination for eye irritation to detectkeratitis. Treatment of airbag chemical burns is similar to any alkali burn: immediate and copious waterirrigation.

OCULAR BURNS

Chemical burns to the eyes are ocular emergencies requiring immediate treatment.16

If the nature of the chemical is not known, use pH paper to determine the presence of acid or alkali. Acidquickly precipitates the superficial tissue proteins of the eye, producing the typical "ground glass"

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appearance of the cornea. Damage sustained secondary to acid burns is, in most cases, immediate andlimited to the area of contact. The posterior segment of the eye rarely su�ers injury, but prolonged exposure,highly concentrated solution, or exposure to hydrofluoric acid may lead to deeper penetration andpermanent injury.

Alkali burns are generally more severe, frequently with unsightly and disastrous results. Higher pH, moreconcentrated solution, and longer duration of exposure are associated with greater injury. In a short periodof time, strong alkalis can penetrate the cornea, anterior chamber, and retina, with destruction of all sensoryelements, thus causing complete blindness (see Figure 241-50 in chapter titled "Eye Emergencies").

The penetration of alkali can continue for hours to days, resulting in globe perforation. The vessels of theconjunctiva and sclera as well as collecting veins of the anterior chamber may be destroyed, leading tosecondary glaucoma. Second- and third-degree burns of surrounding tissue can complicate the burn.

Treatment of eye burns should not be delayed. Immediate treatment is copious and continuous waterirrigation at the scene, in transport, and at the hospital. Eye-irrigation kits may be used. Although specificsolutions may be beneficial in irrigation of the injury, delay in irrigation cannot be justified. Sterile water orsaline is recommended. In general, 1 to 2 L of normal saline for each eye for 30-minute continuous irrigationis the minimum treatment. Neutralizing substances should not be used.

Acid burns may not require as much volume or treatment time as alkali burns. For treatment of severe alkaliburns, 24 hours or more of continuous irrigation may be necessary. Checking the pH in the conjunctival sacto see whether it has returned to 7.4 is helpful in determining need for further irrigation. However, extended2- to 3-hour irrigation, despite apparent conjunctival pH correction, is recommended in the setting of strongalkaline or hydrofluoric acid burns with obvious examination abnormality to correct anterior chamber pH aswell as conjunctival pH. During irrigation, the eyelid may have to be held open manually or with retractorsdue to severe orbicularis spasm (see chapter 241). The eyelids should be everted. Sweep the fornices with awet cotton applicator to remove any particulate matter, especially if the pH is not responding well toirrigation.

Pain control with topical anesthetics during evaluation and treatment is necessary. Systemic opioids may benecessary for severe pain or associated injuries. Emergency ophthalmology consultation is needed forcorneal burns. For additional discussion, see chapter 241.

IATROGENIC CHEMICAL BURNS

Iatrogenic chemical burns have been caused by the use of potassium permanganate at an inappropriatelyhigh concentration to treat dermatologic problems. Dimethyl sulfoxide used as a transcutaneous vehicle forminor sprains has caused burns. Patients in the operating room may develop burns from skin preparationsolutions. Thimerosal, which has a high mercury content, is the most common agent implicated. Mechanicalabrasion of the skin from scrubbing and from pooling of the skin preparation agent under the torso ortourniquet predisposes patients to burns. Blister formation, skin sloughing, and eschar development have

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been reported in neonates when isopropyl alcohol pledgets were substituted for conducting paste beneathlimb electrocardiograph electrodes. Silver nitrate used to cauterize umbilical granulomas in infantsreportedly has caused periumbilical burns.

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USEFUL WEB RESOURCES

Information on personal protective gear for Hazmat responders from U.S. Department of Transportation—www.phmsa.dot.gov/hazmat/library/erg

International poison control listings from the World Health Organization—www.who.int/gho/phe/chemical_safety/poisons_centres/en/index.html

Handbook for medical personnel caring for victims of hazardous substances from Occupational Safety andHealth Administration—www.osha.gov/dts/osta/bestpractices/html/hospital_firstreceivers.html#appa2132

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