CURRENT CONCEPTS

Hand Chemical Burns Elliot P. Robinson, MD, A. Bobby Chhabra, MD

There is a vast and ever-expanding variety of potentially harmful chemicals in the military, industrial, and domestic landscape. Chemical burns make up a small proportion of all skin burns, yet they can cause substantial morbidity and mortality. Additionally, the hand and upper extremity are the most frequently involved parts of the body in chemical burns, and therefore these injuries may lead to severe temporary or permanent loss of function. Despite this fact, discussion of the care of these injuries is sparse in the hand surgery literature. Although most chemical burns require only first response and wound care, some require the attention of a specialist for surgical debridement and, occasionally, skin coverage and reconstruction. Exposure to certain chemicals carries the risk of substantial systemic toxicity and even mortality. Understanding the difference between thermal and chemical burns, as well as special considerations for specific compounds, will improve patient treatment outcomes. (J Hand Surg Am. 2014;-(-):-e-. Copyright Ó 2014 by the American Society for Surgery of the Hand. All rights reserved.) Key words Chemical, burn, hydrofluoric, acid, management.

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chemical exposure make up a diverse set of injuries. They may range from mild erythema to severe tissue loss and even loss of life. The variation depends on the specific characteristics of the agent, the concentration, and duration of exposure. Chemical burns may occur in the domestic, occupational, or war setting. Each setting presents its own concerns. In the domestic setting there may be a lack of knowledge of the potential harm certain chemicals present and how to perform appropriate first aid. Non-accidental abusive or self-injurious behavior such as attempted suicide may also be involved. The industrial setting has become safer for chemical burns due to increased governmental regulations. Lastly, exposure to chemicals in warfare may be associated with other injuries. AND BURNS SECONDARY TO

From the Department of Orthopaedic Surgery, University of Virginia Health System, Charlottesville, VA. Received for publication May 21, 2014; accepted in revised form July 30, 2014. No benefits in any form have been received or will be received related directly or indirectly to the subject of this article. Corresponding author: A. Bobby Chhabra, MD, Department of Orthopaedic Surgery, University of Virginia Health System, Box 800159, Charlottesville, VA 22908; e-mail: [email protected]. 0363-5023/14/---0001$36.00/0 http://dx.doi.org/10.1016/j.jhsa.2014.07.056

Chemical burns occur most commonly in workingaged individuals.1 Additionally, the wrist and hand are the most common sites of severe burns.2 It has also been noted that chemical burns often heal more slowly than thermal burns and require surgery more frequently.3 When combined, these factors suggest that chemical burns, despite their relative rarity, are a considerable source of economic burden. Most chemical burns do not result in serious longterm sequelae. Nevertheless, the importance of vigilance and prompt treatment cannot be overstated: Despite only making up 3% of a particular burn center’s admissions, chemical burns were responsible for up to 30% of burn-related deaths.4 PATHOPHYSIOLOGY The crucial difference between a chemical burn and a thermal burn is that the damage continues until the chemical is removed or neutralized. Therefore, thorough and prompt decontamination is paramount. Several factors contribute to the characteristic of a burn after chemical exposure. 1. Responsible substance: Chemicals vary in their physical properties and mechanism of action. Although there are many chemicals that may cause burns, we will address only those substances that are important either because of their ubiquity,

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INITIAL TREATMENT Initial treatment involves decontamination, and must begin immediately after chemical exposure. Industrial settings are mandated to have procedures in place and high-flow rinsing stations. Evidence indicates that when treatment is initiated “in the field”, outcomes are improved: pH normalizes faster6 and hospital stay is decreased.7 First responders and medical center staff should continue the decontamination process and proceed along a treatment algorithm to minimize morbidity and mortality. First, the management team must take precautions not to contaminate themselves. Eyewear, gloves, and appropriate gowns are a minimum requirement. Although simple chemical burns may be managed in the community setting by an informed team, the American College of Surgeons and the American Burn Association recommend referral of severe burns to designated centers.8 Table 1 summarizes common chemicals and their characteristics and primary and secondary treatment considerations. The following are initial treatment measures for chemical burns:

or because of special considerations involved. For detailed information on any given chemical substance, the U.S. Centers for Disease Control and Prevention (CDC) compiles material safety data, which is readily available on-line. The Agency for Toxic Substances and Disease Registry is a federal public health agency of the U.S. Department of Health and Human Services. Their Web site, administered by the CDC, contains medical management guidelines (available at: http://www. atsdr.cdc.gov/mmg/index.asp). Burn percentage: The risk of systemic toxicity increases with total body surface area (TBSA) affected. Additionally, a larger area of damage may make coverage and reconstruction more difficult. Chemical concentration: Higher concentration leads to more rapid and extensive damage. Time of exposure: The extent of damage is correlated with time of exposure. Early lavage is the most important means of limiting damage. Treatment: Immediate high volume water lavage is the best early management strategy. The use of neutralizing compounds and alternative lavage substances is controversial, but generally discouraged. Certain chemicals have a high risk of systemic toxicity, which requires specific antidotes and supportive measures. Skin properties: The palmar skin has thick stratum corneum, which is more impermeable and therefore resistant to chemical insult than the dorsum. Laceration or breakdown of the resistant epidermis exposes the more sensitive underlying dermis.1

1. Removal: Loose dry agent should be dusted off, and clothing should be removed. This step is particularly important for dry chemical agents, such as lime, which may react with water exothermically and cause additional thermal damage. 2. Dilution: Copious irrigation under high flow should last at least 20 minutes, but this may be as long as several hours for concentrated alkali. Hand or limb submersion should be avoided, as this will not sufficiently dilute chemical agents and may spread the chemical to other areas. Similarly, high-pressure jet lavage may spread concentrated agent.9 pH testing of the skin with litmus paper may help determine safe end point for lavage in the case of basic or acidic burns.10

DIAGNOSIS Crucial data in the management of chemical burns are: specific chemical compound and concentration, mechanism of exposure, time of exposure and timeframe of initiation of decontamination. Trauma protocol consisting of focused assessment of airway, breathing, and circulation should be followed. Other areas of exposures such as ocular and inhalational must be ruled out. Examination of the burn should identify all involved locations. Chemical burns may not show the same early signs of skin damage as thermal burns,4,5 therefore early grading of burns may be difficult. Serial examination is recommended. An estimation of TBSA involved will guide fluid resuscitation and other treatment measures. Systemic complications are ruled out by obtaining early electrocardiography and electrolyte analysis. J Hand Surg Am.

There are exceptions to the initial use of water for lavage. Phenol is insoluble in water, so polyethylene glycol may be used initially to increase its solubility in water.11 Elemental metals such as sodium, potassium, and lithium combust when exposed to water; hence, burns from these metals should be immersed in mineral oil, and then the elemental metal with the mineral oil is then removed. Dry lime becomes caustic only when dissolved, so it should be thoroughly dusted off. Some authors caution that concentrated muriatic, sulfuric, and hydrochloric acid may generate an exothermic reaction when combined with water,1 but high flow cool water can minimize this effect. 3. Neutralization: There is controversy as to whether neutralizing substances should be used in the

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TABLE 1.

Common Chemical Burn Treatment Considerations

Chemical

Industrial Use

Domestic Use

Mechanism of Action

Special Characteristics and Systemic Effects

Primary Treatment

Secondary Treatment

Additional Workup

Fluoride binding leads High flow water decontamination to systemic hypocalcemia; painful; potentially fatal

Production of None alloys, plating, dye manufacture

Corrosion of tissue due to hydrogen ions, chromium binds cations

Chromium toxicity, renal failure

High flow water decontamination

Phosphate buffer soaks, low threshold for surgical debridement and dialysis in severe exposure

Serial electrolyte, renal function, and cardiac monitoring

Sulfuric acid

Refining and manufacturing reagent

Drain cleaner, lead-acid car batteries

Corrosion of tissue due to free hydrogen ions

Most common cause of chemical burns

High flow water decontamination

Supportive, woundspecific

Consider nonaccidental exposure. Drain cleaner is often used in asault and suicide attempt

Nitric acid

Refining and manufacturing reagent

None

Corrosion of tissue due to free hydrogen ions

Yellow staining of skin

High flow water decontamination

Supportive, woundspecific

Chemical peels, small amounts in pharmaceuticals

Corossive, cytotoxic

Painless burn, Dilute polyethylene glycol wash and hemolysis, renal high flow water injury, CNS toxicity decontamination

Supportive, woundspecific

Alkaline, corrossive Household Industrial bleaching and oxidizing cleaning products reagent, bleach, and disinfectant

Commonly associated High flow water decontamination, with inhalation dilute soapy wash exposure, metabolic acidosis with ingestion

Supportive, woundspecific

Glass etching, microchip manufacture

Chromic acid

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Phenol (carbolic Synthetics acid) manufacturing

Bleach (sodium or calcium hypochlorite)

Cement (calcium Construction oxide)

Rust remover

Construction

Forms alkaline calcium hydroxide

Delayed presentation is typical

High flow water decontamination

Serial electrolyte, renal Topical calcium function, and cardiac gluconate gel, monitoring intravenous or arterial calcium, surgical excision for severe exposure

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Corrosion of tissue due to hydrogen ions, free fluoride binds cations

Hydrofluoric acid

Monitor blood count, electrolytes, and renal function

Supportive, woundspecific (Continued)

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TABLE 1.

Common Chemical Burn Treatment Considerations (Continued)

Chemical

Industrial Use

Domestic Use

Mechanism of Action

Primary Treatment

Secondary Treatment

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Manufacture of soaps and petroleum products, paper and metal processing

Drain and oven cleaners

White phosphorus

Munitions, pesticides, fertilizers

May be combined Fireworks, illegal thermal and methamphetamine chemical corrosive production injury, high lipid solubility allows deep pentration

Complete removal with Supportive, woundHypocalcemia and specific aid of ultraviolet light, hyperphosphatemia, high flow water renal injury, decontamination hemolysis

Anhydrous ammonia

Fertilizer

Fertilizer

Alkaline when combined with water

Often stored as pressurized gas, inhalation common

High flow water decontamination

Supportive, woundspecific, avoid early ointments

Elemental Na, K, Li

Laboratory

None

Combustible when combined with water

Must be kept under inert gas or oil

Particles must be physically removed (no water)

Supportive, woundspecific

Petroleum products

Fuel, solvent, synthetic manufacturing, and other uses

Fuel, solvent

Lipid barier disruption

Potential for systemic Removal from skin with Supportive, woundmild soap followed by absorbtion, CNS, specific high flow water liver, lung, endothelial and decontamination hematologic toxicity

Additional Workup

Dry lyme causes Dust off dry lye, long Supportive, woundexothermic reaction duration high flow specific with water water decontamination

Serial electrolyte, renal function, and cardiac monitoring

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Lye (sodium hydroxide)

CNS, central nervous system.

Alkaline, corrossive

Special Characteristics and Systemic Effects

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management of chemical injury. Theoretically, a neutralizing substance would more effectively halt the activity of the offending chemical agent. However, neutralization agents may be toxic themselves, and it is difficult to control the quantity administered. Reactions between compounds and their neutralizing agent may be exothermic and cause further thermal injury. Additionally, whereas water is generally immediately available, it may take valuable time to identify and locate a specific neutralizing substance. Scientific evidence is conflicting, with some studies showing no benefit to the use of neutralizers,12 whereas others have shown more rapid return of the affected area to physiologic pH.13 However, it is generally accepted that hydrotherapy (dilution with extremely large volumes of water) is the most appropriate means of eliminating the majority of chemical contaminants.11 4. Systemic support: The ABCs of trauma apply to chemical burn management: Inhalational injury may require intubation, and electrolyte disturbance may lead to cardiovascular collapse. Conventional burn fluid resuscitation formulas should be followed with adequate monitoring of urine output. It is important to remember that irrigation with large volumes of cold water may cause hypothermia.11 Inhalational injury should be assumed whenever clothes are saturated or the injury mechanism involved an explosion.9 In such cases, evaluation and prompt treatment is critical. Ocular injury is also common and should be managed by a specialist. 5. Systemic toxicity: Electrolyte monitoring and management are important in all major burns. Remember, however, that seemingly innocuous chemical burns may cause severe electrolyte imbalance. The threshold for early and prolonged electrolyte and cardiac monitoring should be low, particularly in compounds like hydrofluoric acid (HF) and phosphorus, which are known to have high systemic toxicity. 6. Skin care: Wound care of chemical burns is similar to that of thermal burns. Ointments such as silver sulfadiazine are commonly used to keep the wound from desiccating and to suppress bacterial growth. Dressings should be changed daily and wounds should be regularly examined for signs of infection and to identify nonviable tissue in need of debridement.

hence the benefits of excision versus observation can be difficult to weigh.5,11 As in all burns, surgical debridement removes necrotic tissue, which may serve as a nidus for infection. Another important advantage of surgical debridement is the removal of residual chemicals. In severe exposures to chemicals with potentially lethal systemic toxicity (like chromic acid, HF, and phosphorus acid), this may be the only way to limit morbidity and mortality.9,14 In a patient in stable condition, timing of debridement, if necessary, is controversial. Delayed debridement of fully demarcated eschar at approximately 1 week post injury followed by split-thickness skin grafting typically leads to satisfactory results.15 However, by limiting ongoing tissue damage, early tangential excision may improve functional and cosmetic results,16,17 though this algorithm will require more frequent use of skin grafting. After early excision, skin grafting may be delayed to ensure the adequacy of the first debridement.9 Versajet (Smith & Nephew, Memphis, TN) has been reported as a useful adjunctive tool in debridement. This system creates a high velocity stream of saline. On lower settings, this will remove devitalized tissues while leaving viable tissue intact and simultaneously providing copious lavage.18 The hand contains specialized structures that warrant specific treatment considerations. The impermeable nail plate may prevent thorough decontamination efforts.8 Removal of the nail should be considered in situations like HF exposure, as this will allow application of calcium gluconate gel to the matrix and neutralize the damaging fluoride ion.8 Compartment swelling may occur after chemical injury, and the need for fasciotomy should always be considered.8 The management of skin blisters in thermal burns is not universally agreed upon, but expert opinion suggests unroofing blisters associated with chemical injury to ensure removal of any residual chemical within.8,19 In summary, decision making for debridement should favor emergent surgery for severe burns with systemic toxicity, and urgent or early surgery for burns in which progressive local tissue damage will lead to functional loss. Delayed excision and coverage of demarcated eschar also generally leads to satisfactory results. SPECIAL CONSIDERATIONS FOR SPECIFIC COMPOUNDS Cement Cement is widely used and its ability to cause burns is underappreciated, particularly outside of industry

DEBRIDEMENT Decision making for surgical treatment of a chemical injury may be challenging. Depth is difficult to estimate, J Hand Surg Am.

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circles. The predominant compound is calcium oxide, which becomes alkaline calcium hydroxide when exposed to water and the culprit for chemical burns.11 Onset of symptoms is typically insidious and may result in full-thickness burns. Loose dry agent is dusted off, then contaminated areas should be thoroughly irrigated and dressed with antibacterial ointment. Wounds are then observed for possible debridement and grafting.11

is a component of munitions and explosives, and is a frequent cause of military burns.22 However, as it is also used in pesticides, fertilizers, and fireworks, as well as illegal methamphetamine production, civilian injuries have become more common. Ignited white phosphorus creates combined thermal and chemical burns. Its lipophilic nature allows it to penetrate deeply in tissues, which is why outcomes have been noted to be worse than isolated chemical burns, with slower recoveries.3 Initial management revolves around irrigation and removal of remaining residue. White phosphorus can auto-ignite in contact with oxygen at temperatures as low as 30 C, so water for burn irrigation should be cool. Particles may become imbedded in tissue, and these must be removed to prevent further damage. Immediate and repeated surgical debridement is advocated to ensure prompt and complete removal.22 Copper sulfate, which turns phosphorus particles black, was once used to facilitate identification and removal. Systemically absorbed copper, however, can lead to severe toxicity including hemolysis, oliguria, and cardiovascular collapse.3,22 A preferable alternative is ultraviolet light from a Wood’s lamp, which causes phosphorus to fluoresce, enabling identification and removal without risk of copper toxicity. It should be noted that systemic toxicity from phosphorus is a main concern, as life-threatening hypocalcemia and hyperphosphatemia may occur. An electrocardiogram must be part of initial evaluation and electrolytes should be monitored initially and for several days postinjury.

Lye and alkaline drain cleaners Lye, or dry sodium hydroxide, is a strongly alkaline compound, which causes a vigorous exothermic reaction when combined with water. Aqueous solutions are commonly marketed as drain and oven cleaners. Alkaline substances penetrate tissue deeply, and cause progressive damage until removed or diluted. They may cause full-thickness skin loss and saponification of subcutaneous lipids.20 Very large volumes of irrigation are required to return the skin to a neutral pH.13,15 Dressing with mafenide acetate has been recommended for its antibacterial properties and inert byproducts.20 Anhydrous ammonia Widely used as a nitrogen fertilizer in the farming industry, this gas is stored and transported as a pressurized liquid. When combined with enough oxygen, it becomes combustible.10 Contact with the liquid, which is stored at e33 C, causes frostbite and tissue necrosis. When dissolved in water it is strongly alkaline.21 Ammonia is highly damaging to mucous membranes, and in its gaseous state can often be harmful by exposure to eyes and lungs. According to recent literature, lavage should be continued every few hours for 24 hours. Additionally, the use of ointments should be delayed for the first day, as they can worsen penetration of anhydrous ammonia.21

Sulfuric acid Sulfuric acid is one of the most common causes of chemical burns due to its availability in concentrated form in home-use drain cleaners. It causes dehydration of tissues and coagulation necrosis.11 As it may often result in full-thickness burns, excision and closure or split-thickness grafting of lesions may be needed.23

Sodium hypochlorite Also known as bleach, it is chemically similar to calcium hypochlorite. Both are used as oxidizing, bleaching, and disinfecting agents. The hypochlorite anion is strongly basic, and therefore causes tissue damage by liquefaction necrosis. It is important to remember that hypochlorite vapors are strongly irritating to eyes and the respiratory tract. Management is similar to other exposures to alkaline substances, with immediate high flow irrigation. Diluted soapy wash can help remove residue.

Hydrofluoric acid Hydrofluoric acid is present in a variety of over-thecounter products such as rust removers at concentrations of 6% to 12%. It may also be stored as HF gas and used in industrial glass and microchip etching in concentrations exceeding 70%. Hydrofluoric acid is particularly dangerous because of its dual mechanism of action: In addition to acidic corrosive effect, fluoride ions penetrate deeply into tissues where they react with calcium and magnesium with multiple local and systemic effects.

White phosphorus Barillo et al published an excellent review of phosphorus burns at a referral center.22 White phosphorus J Hand Surg Am.

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only 1% TBSA, and death after 10% TBSA.14 After immediate lavage, phosphate buffer soaks are applied to bind residual ions. Additionally, immediate surgical excision has been recommended as an important means of removing the cutaneous supply of chromium and to limit systemic toxicity.14

One hallmark effect is pain seeming out of proportion to the injury. This is due to shifts in potassium, which lead to continued nerve depolarization.24 Other local effects include slow-healing wounds and osteolysis. Systemic hypocalcemia and resultant hyperkalemia may cause myocardial arrhythmia. Hypocalcemia may develop with as little as 1% TBSA exposure to concentrated HF.25 Fluoride is also directly toxic to many enzymes and organs.24 Although most HF burns are more painful than dangerous,26 the potential for mortality has been documented in the literature. With TBSA exposure of 20%, mortality approaches 100%, and death has been reported with only 2.5% TBSA exposure to highly concentrated HF.24 Treatment includes the following phases:

Phenol Also known as carbolic acid, it is an isolate of coal tar used in synthetic manufacturing. Joseph Lister advocated its use as an antiseptic, but this use has been curtailed because its toxicity.27 Its contact with skin can cause a range of effects from dermatitis, depigmentation, and defatting in low concentration (1.5%) to severe necrosis at higher concentration (10% to 40%).27 It has an anesthetic effect, and because exposure is not painful, presentation may be delayed. Its lipophilic nature causes deep penetration and systemic absorption, which may lead to hemolysis and kidney, liver, and central nervous system toxicity.1 Phenol is much more soluble in polyethylene glycol than in water. Recommended treatment, therefore, is dilute polyethylene glycol wash followed by high-flow water lavage.11 In conclusion, chemical burns can cause severe local tissue damage and systemic complications. The effect is not resolved until the chemical is removed or neutralized. Therefore early and thorough decontamination of these injuries is the mainstay of treatment. Surgical debridement may be necessary when systemic complications may become life threatening, or when further damage could lead to compromise of functionally important structures. Because chemical burns frequently affect the hand and upper extremity, hand surgeons should be familiar with causative substances and principles of their surgical and nonsurgical wound management, and recognition and treatment of systemic complications.

1. Immediate, copious, and repeated lavage. Recent recommendations suggest a relatively brief initial lavage for 20 minutes in order to proceed to the next step.9 2. Topical treatment with 2.5% calcium gluconate gel is highly effective at neutralizing free fluoride ions, limiting further damage and improving pain.9,24 It is made by mixing 100 mL of watersoluble surgical lubricant with 2.5 mg of calcium gluconate powder.24 It should be applied for at least 30 minutes. Relief of pain is an indicator of its effectiveness.26 3. Local subcutaneous infiltration of calcium gluconate solution has been advocated as an adjunctive means of binding fluoride ions and limiting local and systemic toxicity. The recommended dose is 0.5 mL of 5% per square centimeter injected via small-bore needle. It should not be used in closed spaces such as the hand due to the risk of compartment syndrome and pressure necrosis.9,24,26 Intra-arterial infusion via angiographically placed catheter is an alternative means of delivering calcium to a selected vascular bed in the extremities.9,24 Infiltration techniques are suggested primarily for high concentration and delayed presentation injuries.9 4. It is important to emphasize the potential for rapid mortality with this compound, so vigilance must be high. Electrolyte and cardiac monitoring should be initiated early and electrolyte replacement may begin before laboratory results return.25

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Chromic acid Chromic acid, like HF, contains an anion that may cause severe systemic toxicity beyond the local caustic acid burn. The hexavalent form is most toxic. Acute renal failure has been reported after burns of J Hand Surg Am.

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18. Gumus N, Erkilic A, Analay H. Water jet for early treatment of chemical burn. Burns. 2010;36(3):36e37. 19. Bope ET, Kellerman RD. Chemical burns. In: Conn HF, Rakel RE, eds. Conn’s Current Therapy. Philadelphia, PA: W.B. Saunders; 1984:1127e1209. 20. Wolfort FG, Nevarre DR, De A. Alkali burns to the hand. Ann Plast Surg. 2000;44(3):346. 21. Amshel CE, Fealk MH, Phillips BJ, et al. Anhydrous ammonia burns case report and review of the literature. Burns. 2000;26(5): 493e497. 22. Barillo DJ, Cancio LC, Goodwin CW. Treatment of white phosphorus and other chemical burn injuries at one burn center over a 51year period. Burns. 2004;30(5):448e452. 23. Bond SJ, Schnier GC, Sundine MJ, et al. Cutaneous burns caused by sulfuric acid drain cleaner. J Trauma. 1998;44(3):523e526. 24. Dunser MW, Ohlbauer M, Rieder J, et al. Critical care management of major hydrofluoric acid burns: a case report, review of the literature, and recommendations for therapy. Burns. 2004;30(4): 391e398. 25. Dalamaga M, Karmaniolas K, Nikolaidou A, et al. Hypocalcemia, hypomagnesemia, and hypokalemia following hydrofluoric acid chemical injury. J Burn Care Res. 2008;29(3):541e543. 26. Burd A. Hydrofluoric acid burns: rational treatment. J Burn Care Res. 2009;30(5):908. 27. Lin TM, Lee SS, Lai CS, et al. Phenol burn. Burns. 2006;32(4): 517e521.

7. Leonard LG, Scheulen JJ, Munster AM. Chemical burns: effect of prompt first aid. J Trauma. 1982;22(5):420e423. 8. Reilly DA, Garner WL. Management of chemical injuries to the upper extremity. Hand Clin. 2000;16(2):215e224. 9. Kirkpatrick JJ, Burd DA. An algorithmic approach to the treatment of hydrofluoric acid burns. Burns. 1995;21(7):495e499. 10. Wibbenmeyer LA, Morgan LJ, Robinson BK, et al. Our chemical burn experience: exposing the dangers of anhydrous ammonia. J Burn Care Rehabil. 1999;20(3):226e231. 11. Palao R, Monge I, Ruiz M, et al. Chemical burns: pathophysiology and treatment. Burns. 2010;36(3):295e304. 12. Segal EB. First aid for skin/eye decontamination: are the present practices effective? J Chemical Health and Safety. 2007;14(4):16e22. 13. Andrews K, Mowlavi A, Milner SM. The treatment of alkaline burns of the skin by neutralization. Plast Reconstr Surg. 2003;111(6): 1918e1921. 14. Matey P, Allison KP, Sheehan TM, et al. Chromic acid burns: early aggressive excision is the best method to prevent systemic toxicity. J Burn Care Rehabil. 2000;21(3):241e245. 15. Al-Qattan MM, Pitkanen J. Delayed primary excision and grafting of full thickness alkali burns of the hand and forearm. Burns. 2001;27(4):398e400. 16. Bhat FA. Early sequential excision of chemical burns—our experience in Riyadh burns unit. Ann Burns Fire Disasters. 2006;19(2):78e79. 17. Burd A, Ahmed K. The acute management of acid assault burns: a pragmatic approach. Indian J Plast Surg. 2010;43(1):29e33.

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