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CHAPTER 218:  Chemical Burns      1391 compromised renal function. Mafenide and nitrofurazone have little utility in the ED management of the acutely burn-injured patient. Dressings should ideally be changed twice daily, gently removing residual ointment, for as long as the wounds continue to weep, then daily until healing is complete. Synthetic occlusive, solid, or biological dressings are alternative methods of managing partial-thickness burns in outpatients. Wounds are cleansed and debrided prior to application of these dressings. Examples include clear occlusive synthetics, foam or hydro-fiber dressings impregnated with antiseptics, or treated biologic membranes. Consider contacting the director of the local or regional burn center to identify the center's preferred topical antimicrobial agent and/or specific burn dressing to integrate local and tertiary burn care. The goal is for the dressing to act as artificial skin. Wounds should be reevaluated at 24 to 48 hours. Wounds treated with synthetic solid, or biological dressings are well tolerated by patients, require few dressing changes, and heal with good appearance. Reassess burn wounds at 24 to 48 hours for depth and extent of burn. Explain the follow-up visit schedule and prescribe analgesics. Discharge instructions should include home burn care, pain control, and the symptoms and signs of infection. Burned extremities should be elevated for 24 to 48 hours to prevent edema. Advise patients to return to the ED with signs or symptoms of infection or if pain is inadequately controlled. Patients with deep partial-thickness, full-thickness, and mixed-thickness burns not requiring admission should be referred to a plastic surgeon or burn care specialist in 2 to 4 days for reevaluation and consideration for skin grafting. Patients with self-inflicted burns have additional social and psychological needs that must be addressed either during inpatient admission or prior to discharge from the ED. They have been associated with substance abuse and decreased likelihood of follow-up. 35 Consider psychiatric evaluation early if self-harm is suspected. REFERENCES The complete reference list is available online at www.TintinalliEM.com. Chemical Burns Anthony F. Pizon Michael Lynch INTRODUCTION AND EPIDEMIOLOGY More than 25,000 products can produce chemical burns. Most expo sures 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. PATHOPHYSIOLOGY 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.

hemicals, 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. CHAPTER TABLE 218-1 Factors Influencing Tissue Damage •   Duration of contact •   Concentration of agent •   Quantity of agent •   Mechanism of action •   Extent of penetration 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). Most chemical burns are caused by acids or alkalis. At similar vol umes 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). Death early after severe chemical burns is usually related to hypotension, acute renal failure, and hypovolemic shock. 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 certain caustics (Table 218-4). GENERAL APPROACH TO CHEMICAL BURNS The initial goal of treatment is to remove the patient from the exposure and prevent any further chemical contact. 4 If not performed prior to arrival, remove all exposed clothing immediately. With few exceptions, aggressive large-volume irrigation with water is the cornerstone of initial treatment. 4 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. 5 Sodium metal and related compounds should be initially covered with mineral oil or excised, because water can cause a severe exothermic reaction. 6 Dilution of phenol (carbolic acid) with water may enhance penetration.5 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. 4,5 Almost universally, earlier irrigation means a better prognosis. New amphoteric and hypertonic chelating agents offer promise as more effective irrigation solutions for chemical burns as more evidence becomes available. 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. The amount of elapsed time to initiate dilution or removal of chemi cal agents is directly related to the eventual depth and degree of injury. The time required for irrigation varies.

mination is ongoing. At the very minimum, mask, face shield, chemical-resistant gown, gloves, and water-impervious boots should be worn. The amount of elapsed time to initiate dilution or removal of chemi cal agents is directly related to the eventual depth and degree of injury. The time required for irrigation varies. Severe alkali burns may require TABLE 218-2 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 Tintinalli_Sec16_p1333-1418.indd 1391 8/2/19 8:23 PM

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 Tintinalli_Sec16_p1333-1418.indd 1391 8/2/19 8:23 PM 1392 SECTION 16: Environmental Injuries several hours of irrigation. Use pH indicator paper to determine con tinued 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. 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. 1 Other than measures specific for a particular chemical burn, treatment following initial ther apy is similar to that of thermal burns (Table 218-5). 5 Aggressive fluid replacement is needed if extensive chemical burns are sustained. Anal gesics may be needed, and in the case of allergic responses to chemicals, epinephrine, antihistamines, and steroids may be required. ACID BURNS Perform a complete examination of a patient with a significant chemi cal acid burn to the skin because acids may also cause respiratory and mucous membrane irritation. Furthermore, skin absorption of some compounds may occur and result in systemic illness. Apart from 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 antibiot ics 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. Although commercially available in concentrations up to 90%, even dilute solutions of 1% to 2% phenol may cause a burn if con tact 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.

ly 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 using an undiluted polyethylene glycol solution of molecular weight 200 to 400 or by a gentle wash with isopropyl alcohol. An isopropyl alcohol rinse is equivalent to polyethylene glycol in removing phenol. 5,9 Either irrigation solution reduces the extent of cutaneous corrosion and decreases systemic toxicity. If neither polyethylene glycol nor isopropyl alcohol is available in adequate supplies, large volumes of water should be used.  CHROMIC ACID Chromium hexavalent compounds (Cr 6+) are powerful oxidizers. The chromate ion in chromic acid produces a chronic penetrating ulcerating lesion of the skin. Generalized exposure to powdered chromic acid can result in conjunctivitis, lacrimation, and ulceration of the nasal septum. Systemic chromium toxicity can cause liver or renal failure, GI bleeding, coagulopathy, and CNS disturbances. Significant symptoms may occur after only 1% to 2% body surface area burns. A 10% body surface area cutaneous burn caused by chromic acid can be fatal due to systemic toxicity. Any acute skin exposure to chromic acid should be treated with copious water irrigation and observation for systemic effects. Aggressive excision is the best method for prevention of systemic effects because depth of the burn is difficult to determine and absorption of chromium may continue after irrigation.  FORMIC ACID Formic acid in 60% solution is used by acrylate glue makers, cellulose formate workers, and tanning workers. Formic acid produces coagula tion necrosis. Systemic effects, including decreased respiration, anion gap metabolic acidosis, and hemolysis, have been reported. 11 Treatment includes immediate decontamination and irrigation with water. 5 Sys temic toxicity may require IV sodium bicarbonate for 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 decontamination and water irrigation usually prevent severe burns to the skin. These acids can burn the skin dark brown or black. 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. Most household bleaches are only 3% to 6% hypochlorite solutions, which, although acidic, cause little damage unless they are in contact with skin for a prolonged time. Treatment is the same as for formic acid burns.

% sulfuric acid solutions in their industrial processes. Automobile battery fluid is 25% sulfuric acid. Most household bleaches are only 3% to 6% hypochlorite solutions, which, although acidic, cause little damage unless 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, glass etching, semiconductors, microelectronics/microinstruments, TABLE 218-3 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 TABLE 218-4 Systemic Effects 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 CNS toxicity Sodium nitrate, potassium nitrate Severe methemoglobinemia with refractory cyanosis Dichromate solution Liver failure, acute renal failure, death despite hemodialysis Tintinalli_Sec16_p1333-1418.indd 1392 8/2/19 8:23 PM CHAPTER 218:  Chemical Burns      1393 TABLE 218-5 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 Sponge with undiluted polyethylene glycol of molecular weight 200–400 Isopropyl alcohol may also be used. Chromic acid Copious irrigation Observe for systemic toxicity. Formic acid Copious irrigation Dialysis may be needed for severe toxicity. Hydrofluoric acid

CHAPTER 218:  Chemical Burns      1393 TABLE 218-5 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 Sponge with undiluted polyethylene glycol of molecular weight 200–400 Isopropyl alcohol may also be used. Chromic acid Copious irrigation Observe for systemic toxicity. Formic acid Copious irrigation Dialysis may be needed for severe toxicity. Hydrofluoric acid Copious irrigation 10% calcium gluconate intradermal for severe cases Consider intradermal injection of 10% calcium gluconate or intra-arterial calcium gluconate for severe cases. Monitor serum calcium and magnesium in severe exposure. Topical calcium gluconate gel, 2.5% for mild cases 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 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 Remove using antibiotic ointment containing polyoxylene sorbitan (polysorbate) Baby oil can be used. Vesicants Mustards Decontaminate Copious irrigation 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. Reducing Agents Alkyl mercury compounds Copious irrigation Debride, drain, and copiously irrigate blisters Blister fluid is high in metallic mercury content.

Decontaminate Copious irrigation 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. Reducing Agents Alkyl mercury compounds Copious irrigation Debride, drain, and copiously irrigate blisters Blister fluid is high in metallic mercury content. 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 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 Systemic toxicity is a significant concern. Air bag Prolonged copious irrigation germicides, dyes, plastics, tanning, and fireproofing material and is used in cleaning stone and brick buildings. It is also a very effective rust remover. Unlike other acids, hydrofluoric acid penetrates deeply and will cause progressive tissue loss. It produces burns in two ways. First, hydrogen ions cause direct cellular damage as other acids do through protein denaturation. 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 nerve tissue and severe pain. Pain will persist until all free fluoride ions have been neutralized. The dermal effects may not be immediately noted and are more related to the concentration of hydrofluoric acid than to the duration of exposure. Solutions >50% produce immediate pain and tissue destruc tion. Solutions <20% may not produce signs and symptoms until 12 to 24 hours after exposure. The skin often develops a blue-gray appearance with surrounding erythema. Tintinalli_Sec16_p1333-1418.indd 1393 8/2/19 8:23 PM

oric acid than to the duration of exposure. Solutions >50% produce immediate pain and tissue destruc tion. Solutions <20% may not produce signs and symptoms until 12 to 24 hours after exposure. The skin often develops a blue-gray appearance with surrounding erythema. Tintinalli_Sec16_p1333-1418.indd 1393 8/2/19 8:23 PM 1394 SECTION 16: Environmental Injuries should be used. The possibility of severe injury and eye necrosis should not be taken lightly. In severe ocular exposures, systemic absorption is possible as well. Systemic toxicity from dermal and oral hydrofluoric acid exposure can result in ventricular fibrillation because of systemic acidosis, hyperkalemia, hypomagnesemia, and hypocalcemia. In major hydrofluoric acid burns or oral exposures, immediately administer IV calcium and magnesium, using standard slow IV rates, before laboratory results are available. Once patients develop hypocalcemia or hypomagnesemia, it is very difficult to restore these electrolyte deficiencies. Cardiac monitoring, IV access, and electrolyte monitoring should be performed in all cases of significant hydrofluoric acid dermal burns or oral exposures (Table 218-6).  METHACRYLIC ACID Methacrylic acid, found in many artificial nail cosmetic products, can produce severe dermal burns, usually in preschoolers. Emergency treatment is copious water irrigation.  NITRIC ACID Nitric acid is used in industry for casting iron and steel, electroplating, engraving, and fertilizer manufacturing. Upon contact with skin, nitric acid can produce tissue damage by oxidation and may turn the skin yellowish as it is burned. Emergency treatment consists of copious water irrigation and standard burn care (see Chapter 217, “Thermal Burns”).  OXALIC ACID Oxalic acid is used for leather tanning and blueprint paper. Oxalic acid binds calcium and prevents muscle contraction. The wounds should be irrigated with water, and IV calcium may be required. Serum electrolytes and renal function should be evaluated, and cardiac monitoring should be instituted after serious dermal exposure. ALKALI BURNS Alkalis penetrate skin deeper and longer than acids and present a greater danger of toxicity from systemic absorption. Wounds may initially look superficial only to become full-thickness burns in 2 to 3 days. Alkalis combine with protein and lipids in tissue to form soluble protein complexes and soaps that permit passage of hydroxyl ions deep into tissue. Soft, gelatinous, friable, brownish eschars are often produced (Figure 218-1). Strong alkalis have a pH >12.  LYES 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.15 Ammonium hydroxide is used in the production of synthetic fibers and extensively in agriculture. Exposure to these The treatment of hydrofluoric acid burns consists of two phases. The first, immediate phase is copious water irrigation for 15 to 30 minutes. This may be the only treatment that is needed if the hydro fluoric acid solution is <20% concentration, the duration of exposure was very brief, and decontamination is begun immediately. Severe, persistent pain denotes a more serious injury requiring the second 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 (Ca 2+) and magnesium (Mg 2+)13—bind the fluoride ion and curtail its toxic effects. However, the overwhelming clinical experience to date has been with calcium gluconate, so it is the agent of choice.

atment is aimed at replacing calcium and magnesium and detoxifying the enzyme-poisoning fluoride ion. Two ions—calcium (Ca 2+) and magnesium (Mg 2+)13—bind the fluoride ion and curtail its toxic effects. However, the overwhelming clinical experience to date has been with calcium gluconate, so it is the agent of choice. Calcium gluconate can be administered as a topical prepara tion, subcutaneous/intradermal injection, or intra-arterial infusion. If commercial 2.5% gel is not available, a calcium gluconate gel can be made with a water-soluble lubricant and should be generously applied to the affected skin. The topical preparation is made by mixing 3.5 grams of calcium gluconate powder in 5 oz of water-soluble lubri cant, or 25 mL of 10% calcium gluconate in 75 mL of water-soluble lubricant. Calcium chloride or calcium carbonate can be substituted if no calcium gluconate is available. The main limitation of topical ther apy is the impermeability of the skin to calcium, and therefore, topical therapy is limited to use in mild, superficial burns. Most importantly, topical therapy should not delay intradermal or intra-arterial injec tions for severe burns. Treatment with intradermal injection of a 10% calcium gluconate solution through a 27-gauge needle into the hydrofluoric acid–burned skin can be effective. A typical dose of 0.5 mL of 10% calcium glu conate 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. Unfortunately, injection therapy has several disadvantages: (1) only limited amounts of calcium are delivered to the tissue; (2) hyperosmolarity and inherent toxicity of free calcium ions cause more pain initially, and more tissue damage is possible if calcium is not bound to fluoride; (3) vascular compromise can result if too much fluid is injected, especially into digits; and (4) rapid penetration of hydrofluoric acid beneath the nail requires nail removal to administer the calcium gluconate into the nail bed ade quately. Acute hydrofluoric acid contamination of the hands, feet, digits, or nails requires consultation with 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. 13 This should be performed as soon as possible after the ini tial burn, preferably within 6 hours of insult. Place an intra-arterial catheter in the appropriate vascular supply (the brachial artery if the entire hand is affected) and connect to a three-way stopcock to which is attached an arterial pressure-monitoring device and the infusion syringe of calcium gluconate. A 50-mL syringe may be filled with 10 mL of a 10% calcium gluconate solution and 40 mL of 5% dextrose in water and infused over 4 hours. The arterial pressure-monitoring device ensures that the catheter has not dislodged from the lumen of the cannulated artery. Repeat infusion may be needed if pain recurs within 4 hours. Intra-arterial infusion avoids the disadvantages of local infiltration therapy, but it has its own disadvantages: it is an invasive vascular procedure that (1) may result in arterial spasm or thrombosis, (2) requires more time and hospital resources, and (3) requires experi ence in the technique. Inhalation of hydrofluoric acid can cause immediate or delayed pul monary injury. All cases of suspected inhalation injury should be admitted for observation even if asymptomatic. Nebulized calcium gluconate may be attempted in these cases, but no controlled studies exist for its use. The solution is made by adding 1.5 mL of 10% calcium gluconate solution into 4.5 mL of sterile water or saline and is administered by nebulizer.

ation injury should be admitted for observation even if asymptomatic. Nebulized calcium gluconate may be attempted in these cases, but no controlled studies exist for its use. The solution is made by adding 1.5 mL of 10% calcium gluconate solution into 4.5 mL of sterile water or saline and is administered by nebulizer. Ocular exposure to hydrofluoric acid requires water irrigation for at least 30 minutes and emergent ophthalmologic consultation. An animal study suggests that calcium-containing irrigation fluids for eye exposures may be harmful. 14 Therefore, standard eye irrigation practices TABLE 218-6 Options for Treatment of Hydrofluoric Acid Skin Burns •   Copious irrigation for 15–30 min immediately. •   Application of calcium gluconate gel; use commercial 2.5% gel or mix 25 mL of 10% calcium gluconate in 75 mL of water-soluble lubricant. •   Further treatment options as dictated by patient response: •   Dermal injection of 10% calcium gluconate at the rate of 0.5 mL/cm2 of skin surface using a small-gauge needle. •   Arterial infusion over 4 h (40 mL of 5% dextrose in water with 10 mL of 10% calcium gluconate). •   Consider supplemental magnesium and calcium IV. Tintinalli_Sec16_p1333-1418.indd 1394 8/2/19 8:23 PM

•   Dermal injection of 10% calcium gluconate at the rate of 0.5 mL/cm2 of skin surface using a small-gauge needle. •   Arterial infusion over 4 h (40 mL of 5% dextrose in water with 10 mL of 10% calcium gluconate). •   Consider supplemental magnesium and calcium IV. Tintinalli_Sec16_p1333-1418.indd 1394 8/2/19 8:23 PM CHAPTER 218:  Chemical Burns      1395 FIGURE 218-1. Deep  alkali  burn. [Reproduced  with  permission  from  http://www .burnsurgery.org/Modules/initial_mgmt/sec_6.htm.] chemicals can result in severe toxicity including mucous membrane, ocular, dermal, GI, and inhalational/pulmonary injury. Suicidal inges tion of lye may result in rapid death from upper airway occlusion. Late morbidity related to esophageal and gastric necrosis may be minimized by early surgical intervention with esophagogastrectomy. The mainstay of treatment is immediate, voluminous, and persistent irrigation. 16 Lyes are extremely corrosive and penetrating. Lye 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 lime content in different 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 the skin. All dry lime par ticles should be brushed away before irrigation. 5 Even a small amount of water may generate an exothermic reaction resulting in calcium hydroxide formation and tissue injury. Brisk irrigation with a large volume of water (taking care to avoid splashing in eyes) should be used and will permit dissipation of heat.  PORTLAND CEMENT Portland cement, which accounts for a major proportion of the cement used in the United States, is a mixture of sand, lime, and other metal oxides. In the presence of water, calcium hydroxide, sodium hydroxide, and potassium hydroxide may all be formed. Workers who kneel in wet cement or get cement in their boots may discover burns hours after initial contact. In addition, skin may become irritated from gritty material, and a contact dermatitis may develop in indi viduals sensitive to the chromate contained in the material. Treatment of cement burns may require cleaning the wound with a brush, such as a preoperative scrubbing brush, to remove cement particles imbed ded in the dermis. METALS Foundry workers are sometimes burned by molten metal, which may spill or splash on body parts and run down into the boots. Elemental metals, sodium, lithium, potassium, magnesium, aluminum, phos phorus, and calcium may all cause burns. When exposed to air, some elemental metals spontaneously ignite. Water is generally contrain dicated in extinguishing burning metal fragments embedded in the skin because the resultant explosive exothermic reaction can lead to significant tissue injury. Burning metal may be extinguished with a class D fire extinguisher, smothered with sand, or covered with mineral oil. Wound debridement should include excision of metal fragments that cannot be wiped away. Metal fragments should be 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 hydro carbon burn treated in the ED. A hydrocarbon chemical burn typically resembles a thermal scald or a partial-thickness burn, although full-thickness burns rarely result from prolonged contact with gasoline. 17 During extremely cold weather, topical gasoline exposure may lead to frostbite when rapid gasoline evaporation causes heat loss from the skin.

A hydrocarbon chemical burn typically resembles a thermal scald or a partial-thickness burn, although full-thickness burns rarely result from prolonged contact with gasoline. 17 During extremely cold weather, topical gasoline exposure may lead to frostbite when rapid gasoline evaporation causes heat loss from the skin. Systemic effects of hydrocarbon absorption include neurologic, pulmonary, cardiovascular, GI, and hepatic injuries. For further discussion, see Chapter 199, “Hydrocarbons and Volatile Substances. ” The primary treatment is decontamination by removing saturated clothing and irrigating exposed skin with soap 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 to temperatures up to 500°F (260°C), and the burns sustained are usually more thermal than chemical. Although the surface area size of the burn is usually small, solidified material stuck to skin and hair is difficult to remove. If hot, the tar should be cooled to prevent continued thermal injury. Manual mechanical debridement can be painful and destructive to skin structures. Polyoxylene sorbitan (polysorbate), contained in 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 effective in tar removal. Baby oil is also effective for tar removal. VESICANTS (DIMETHYL SULFOXIDE, CANTHARIDES, AND SULFUR MUSTARD) Dimethyl sulfoxide, cantharides, and mustard gas are vesicant or drying agents. Skin burns present with edema and blister formation due to production of ischemia and anoxic necrosis at the site of contact. Dimethyl sulfoxide is a water-soluble organic solvent used in industry. It is available without prescription and is used topically 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”) is occasionally used for its supposed aphrodisiac effects. Sulfur mustard is a vesicant historically used in chemical warfare. An alkylating agent, exposure results in inhibition of cellular enzymatic activity, leading to necrosis. For further discussion, see Chapter 8, “Chemical Disasters. ” Skin damage following vesicant exposure is often severe and can result in deep skin penetration, edema, blisters, ulcers, and serious morbidity. Immediate, copious irrigation with water or saline may mitigate the extent of tissue 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 and should be wiped away with a moist towel. Almost any material can be used to brush the vesicant away from skin. The military uses M258A1 kits for skin decontamination. These kits contain three sets of towelettes, one of each containing phenol, sodium hydroxide, and sodium benzene sulphonochloramine (chloramine). Chloramine pro duces “free” chlorine, which inactivates sulfur mustard. Povidone iodine shows great promise in the prevention and early treatment of skin damage caused by sulfur mustard. Human data are currently lacking, but in animal models, both prevention of burns and immediate (<10 minutes) treatment yielded impressive skin protection. Tintinalli_Sec16_p1333-1418.indd 1395 8/2/19 8:23 PM