AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

INTRODUCTION

Section 2 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Background

Chemical exposure is a frequent cause of burns, accounting for 2.1-6.5% of all admissions to burn units. Thousands of different products used for industrial, agricultural, military, and home purposes are capable of producing chemical burns. Most of these injuries occur in the workplace as a result of an industrial exposure.

The cutaneous implications of chemical burn injuries are often similar to those caused by other types of burns. Clinical manifestations include areas of necrosis at sites of maximal injury with surrounding zones of stasis and erythema as well as blistering. Chemical burns tend to be deep because of continued tissue necrosis caused by prolonged exposure. Therefore, the primary concern in treating patients with suspected chemical burns is the removal of the offending agent.

Pathophysiology

Agents that cause chemical burns are described by mechanism of injury. The chemical classification scheme includes such categories as desiccants, vesicants, oxidizing agents, protoplasmic poisons, acids, and alkali agents.

Acids act through coagulative necrosis, forming an eschar that limits the penetration of the acid. Strong alkali cause liquefactive necrosis, resulting in saponification of fats and denaturation of proteins, ultimately allowing deeper penetration of the chemical. Oxidizing agents also denature proteins and often cause cell damage via cytotoxic effects. Protoplasmic poisons, such as hydrofluoric acid (HF), can form salts with cellular proteins. Desiccants dehydrate cells through an exothermic reaction. Finally, vesicants are thought to produce physiologic reactions that cause the release of amines along with a variety of other damaging processes. Despite these categories, precise classification of chemical agents remains difficult because agents often cause injury by more than one mechanism.

In addition to local injury, systemic effects are an important consideration in any burn patient because of the associated electrolyte imbalances and fluid loss. These effects are compounded in chemical burns because the chemical material can often be absorbed and result in systemic toxicity. Several chemical agents with deleterious consequences and the mechanism by which they cause those effects are discussed. For additional information about other causative agents, see Burns, Chemical in the Emergency Medicine section of the eMedicine journal.

Frequency

United States

Chemical burns account for 2.1-6.5% of all admissions to burn units.

CLINICAL

Section 3 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

History

The clinical evaluation and treatment of patients with chemical burns depends on a careful history and physical examination. Because some agents can lead to systemic complications, determining the type of chemical that caused the injury is important. Some patients do not know the causative agent of their injuries, so knowledge of offending chemicals can assist the clinician in determining treatment recommendations. Additionally, examining the extent and depth of the burn helps guide monitoring and treatment; however, the physical examination findings are often nonspecific with respect to determining the causative agent.

• The following should be determined from the patient history:
• • Offending agent, physical form, and concentration
  • Route and volume of exposure
  • Timing and extent of irrigation
  • Coexisting injuries

Physical

Examining the extent and depth of the burn helps guide monitoring and treatment; however, the physical examination findings are often nonspecific with respect to determining the causative agent.

• The following should be determined from the skin examination:
• • Location of injury
  • Body surface area (BSA) affected
  • Depth of burn

Causes

• Acids
• • Hydrofluoric acid
    • HF is used commonly in industrial settings and is found in fertilizers, pesticides, solvents, dyes, plastics, refrigerant fluid, high-octane fuels, rust removers, aluminum brighteners, and heavy-duty household cleaners. Because of its ability to dissolve silica, HF is also used to polish glass and ceramics, to remove sand from metal castings, to clean stone and marble, and to treat textiles. Despite its many practical applications, HF represents a great risk for chemical injury.
    • The 2 forms of HF are the anhydrous form and the aqueous form. The anhydrous form is the purified form and is considered a strong acid. The more dilute aqueous form is considered a weak acid. Most exposures involve dilute HF contacting small surface areas. Differentiating the 2 forms of HF is important because even minimal exposure (2% BSA) to the concentrated anhydrous form can be fatal.
    • HF produces chemical burns by 2 processes. Superficial injury is caused by the corrosive effect of HF as an acid. Secondary injury results from a protoplasmic poison mechanism with deep penetration of lipophilic fluoride ions. While most acids remain superficial, HF penetrates deeply because of the nonionic nature of the very toxic and reactive fluorine atom. Fluoride ions penetrate into the intracellular compartment and bind calcium and magnesium ions, causing a painful liquefactive necrosis of soft tissues and decalcification and corrosion of bone. Pain results from the immobilization of calcium ions in the tissues, resulting in shifting potassium ions and nerve stimulation.
    • The clinical manifestations of HF burns vary depending on the site and duration of the exposure and the concentration of the acid. The concentration of the acid and the duration of the exposure determine the latency period before symptoms develop. Patients exposed to HF with concentrations up to 20% may not experience pain or erythema for as long as 24 hours. Burns from HF with concentrations of 20-50% become apparent within 1-8 hours, and burns from acid concentrations greater than 50% produce immediate pain and tissue destruction.
    • Most HF burns are caused by the weak acid (approximately 3% HF acid) found in household cleaners, which produces pain with intense throbbing, often in the fingertips. Contact with concentrated acid produces intense pain, rapid tissue destruction, and white areas of coagulation and blistering that appear after the erythematous stage. A classic silvery-gray scale may be seen. Weaker forms of HF can produce effects similar to stronger concentrations if left untreated.
    • Systemic complications are an important consideration when evaluating a patient with cutaneous HF burns, given their potential to cause systemic fluorosis, hypocalcemia, and hyponatremia. Clinical symptoms suggestive of systemic toxicity include nausea, vomiting, abdominal pain, muscular pain, fibrillations and convulsions, pareses, cyanosis, hypotension, cardiac arrhythmias, and cardiac failure.
  • Phenol
    • Phenol (C6H6O) is an aromatic hydrocarbon and a weak organic acid derived from coal tar. Common synonyms for phenol include carbolic acid and hydroxybenzene. Historically, phenol was used for sewage treatment, but it now has a variety of uses in medicine. Because of its anesthetic properties, physicians use phenol for chemical face peels, nerve injections, and topical anesthesia for skin and mucous membranes.
    • Phenol damages the skin through a corrosive effect, denatures proteins, and acts as a protoplasmic poison, leading to severe systemic effects. Skin contact leads to a white covering of precipitated protein, which may turn red and slough. Depigmentation caused by phenol is thought to occur by competitive inhibition of the tyrosinase enzyme and melanocyte damage. Phenol is absorbed rapidly and binds reversibly to albumin in the plasma.
    • Clinical findings from phenol burns vary from small partial-thickness burns to florid systemic complications. The anesthetic properties of phenol allow extensive damage to occur before the patient is aware of the tissue injury.
    • Systemic complications are a primary concern in patients with phenol exposure. Acutely, rapid phenol absorption can result in cardiovascular complications, with premature ventricular contractions and the possibility of ventricular tachycardia. An initial period of bradycardia may occur, followed by tachycardia and hypotension. Other acute effects of phenol exposure include CNS depression and the potential for respiratory arrest. Direct toxicity to a number of types of tissues leads to subacute systemic injuries from phenol. Such injuries may include RBC lysis, peripheral nerve demyelination, central lobular necrosis of the liver, and renal failure due to direct damage to the glomeruli.
  • Chromic acid
    • Chromic acid is an industrial chemical used for electroplating in alloy and dye production. In its hexavalent ionic form, it is particularly dangerous because it easily penetrates cell membranes. Once in the blood, hexavalent chromium is absorbed by RBCs and is reduced to the trivalent form. In its trivalent form, chromium can bind to hemoglobin, impairing oxygen-carrying capacity. Chromium's ability to move across membranes also allows it to bind to intracellular proteins, which results in absorption in the kidneys, liver, bones, lungs, and spleen.
    • Like most acids, chromic acid burns produce localized coagulative necrosis
    • Systemic toxicities have been reported with chromic acid burns involving as little as 1% BSA. Systemic symptoms include gastrointestinal hemorrhage, vomiting, diarrhea, renal or hepatic failure, CNS disorders, anemia, and coagulopathies.
  • Formic acid
    • Formic acid is also known as formate. It is used in industry as a descaling agent, rubber processor, and a textile-tanning substance.
    • Beyond a localized chemical burn, formic acid can have profound systemic effects. Systemic acidosis is the primary concern with formic acid exposure. A primary anion gap acidosis may develop. Furthermore, formic acid's interference with cellular respiration may result in a secondary, lactate-dependent acidosis. By diminishing the central respiratory drive, formic acid may cause a respiratory acidosis. The complex acidosis reinforces itself by increasing proximal tubule reabsorption, thereby decreasing the elimination of formic acid. Symptoms of systemic toxicity also include hypotension, hematuria, hemoglobinuria, renal failure, CNS depression, and other end organ damage.
  • Monochloroacetic acid
    • Monochloroacetic acid (MCAA) is a strong acid used as an herbicide and in the synthesis of organic chemicals. In some European nations, MCAA is used as a wart remover. Dermatologists in the United States do not use MCAA because of its systemic toxicity, instead choosing to use the less toxic trichloroacetic acid. Although MCAA is an unusual cause of chemical burns, its severe systemic toxicity warrants its inclusion in this discussion.
    • MCAA is thought to cause injury by blocking cellular energy supplies, probably by decreasing the activity of pyruvate dehydrogenase and ketoglutarate dehydrogenase, leading to lactic acidosis. It is also thought to damage the blood-brain barrier.
    • MCAA is rapidly absorbed through the skin, causing localized coagulative necrosis. Systemic effects are delayed for 1-3 hours after exposure. Most often, vomiting occurs initially; then, CNS disturbances may develop. Cardiovascular involvement is common, creatinine levels increase, and a severe metabolic acidosis can develop. When exposed to an 80% solution of MCAA (the concentration used for treatment of warts), a burn over a BSA of up to 5% poses a moderate risk of systemic poisoning; a burn over a BSA of 6-10% poses a risk for severe, potentially lethal poisoning; finally, a burn over a BSA of greater than 15% suggests an expected lethal systemic poisoning.
• Alkali agents
• • Anhydrous ammonia
    • Anhydrous ammonia is a colorless, pungent gas used in a variety of industrial settings; it is usually stored and transported in a pressurized liquid form. It has also been reported to cause eye injuries in patients involved in illicit methamphetamine production. Most commonly, it is found in a dilute form in household cleaning products such as drain and oven cleaners. In a prior case series of patients admitted for chemical burns, anhydrous ammonia accounted for a third of admissions to burn units.
    • Although it is highly water soluble, the alkaline nature of anhydrous ammonia allows it to rapidly penetrate the epidermis and enter the more hydrophilic dermis. Once in the dermis, the alkaline ammonia causes liquefactive necrosis. Because anhydrous ammonia is stored at very low temperatures (-28°C [-18.4°F]), the chemical burn injury is complicated by a freeze injury, which can result in thrombosis of superficial vessels and ischemic necrosis.
    • Clinically, burns can be of partial or full thickness, although full-thickness burns are uncommon. Anhydrous ammonia burns are often gray-yellow and soft, although severe exposure can result in black, leathery tissue.
    • The systemic effects of anhydrous ammonia exposure are unrelated to the skin injury. The most common extracutaneous symptoms include inhalation injury and eye exposure, which can produce a spectrum of pulmonary and ocular diseases, respectively.
  • Cement burns
    • Cement is a material commonly used in construction projects that consists of approximately 64% calcium oxide (also called lime) and 21% silicon oxide and has an alkaline pH of approximately 12.5. The prevalence of chemical burns caused by wet cement appears to be increasing. The peak incidence of cement burns appears to be in the spring and summer months, concordant with periods of increased construction work.
    • Cement burns can result from 3 different processes. First, prolonged contact with wet cement allows the alkaline calcium oxide to penetrate and cause tissue destruction through liquefactive necrosis. This type of burn is complicated by the coarse texture of the cement, which causes abrasions in the skin, allowing penetration of the cement. A second form of cement burns results from thermal injury due to contact with hot cement powder during manufacturing. The third type of burn also occurs during manufacturing and is due to the explosive discharge of alkaline and acidic elements. Of these 3 types of burns, only those caused by the alkaline wet cement are considered true chemical burns.
    • Clinically, wet cement burns produce findings similar to other chemical burns, with a delayed onset of pain, erythema, and vesicles. Progression to partial- or full-thickness burns occurs 12-48 hours later. Full-thickness burns are relatively common, occurring in 50% and 66% of patients in a British and German series, respectively. The lower limbs are most often affected, being the site of injury in 86% of patients admitted to the burn unit with a cement burn in a British retrospective study. In one report, calcium oxide (the alkaline ingredient of cement) was mistakenly used to line a football field, leading to second- and third-degree burns in most of the players who were exposed.
  • Airbag injuries
    • Chemical burns caused by automobile airbag deployment are a combined injury of thermal, abrasive, and chemical origin.
    • Activation of the airbag releases sodium azide and sodium hydroxide, which may induce alkaline chemical irritation and burns.
    • Thermal injury occurs as gases released by deployment of the airbag are ignited.
    • Finally, talcum released at airbag deployment can result in abrasive irritation on the skin.
    • Injuries to the skin account for 7-8% of all injuries related to airbag deployment.
  • Black liquor
    • Black liquor is a heated mixture of sodium bicarbonate (10%), sodium sulfide (4%), sodium thiosulfate (5%), and sodium sulfate (4%). It is an alkaline chemical solution (pH 11-13) used in the papermaking industry to convert wood chips to pulp. During production, the solution is heated to 85-95°C (185-203°F).
    • Clinical burns reported after exposure to this substance are a combination of chemical and thermal burns. The chemical component of the burn results from the alkali nature of the black liquor. Injuries from black liquor can be severe, but they have only been reported in workers in the pulp and paper industry.
• Oxidizing agents
• • White phosphorus
    • White phosphorus is used in weaponry, manufacturing of various insecticides and fertilizers, and fireworks. It is a frequent cause of chemical burns in military personnel.
    • White phosphorus has unusual physical properties, melting at temperatures greater than 44°C (111.2°F) and autoigniting at temperatures greater than 30°C (86°F). When it ignites, white phosphorus spontaneously oxidizes, forming phosphorous pentoxide. With contact with skin, white phosphorus continues to oxidize until debrided, neutralized, or consumed as it is converted to phosphoric acid. Cutaneous damage results from corrosion caused by phosphoric acids, thermal effects of the chemical reaction that produces phosphorus pentoxide, and the hydroscopic activity of phosphorus pentoxide.
    • Clinically, white phosphorus produces a combined chemical and thermal burn. Active burning yields a yellow flame and dense white smoke. Contact with skin yields a painful, necrotic, yellow chemical burn with a garliclike odor. Embedded white phosphorus, which should be removed, can be identified with a Wood lamp.
    • Systemic effects include hypocalcemia and hyperphosphatemia and are present as early as 1 hour after the burn is induced. High fat solubility can result in hepatic necrosis or renal damage. Burns over greater than 10-15% BSA have caused sudden death.
• Vesicants
• • Sulfur mustard
    • Sulfur mustard (SM) is the most important agent in the class of vesicants, or blistering agents. Historically, mustard has been used as a chemical warfare agent from World War I until most recently in the Iraq-Iran conflict in the 1980s. Given its ability to inflict mass casualties and recent concerns about terrorism, much has been written recently on this topic.
    • The mechanism by which SM causes chemical burns is incompletely understood. As an alkylating agent, it may cross-link DNA and cause a G2-, G1-, or S-phase block. SM is also known to be an inflammatory activator. Other in vitro studies have suggested an apoptotic mechanism or one related to altered keratin biochemistry.
    • Clinically, dermatologic exposure results in chemical burns with a predilection for the intertriginous areas. After exposure, frequently an asymptomatic latent period occurs, followed by pain, erythema, or pruritus. Blistering generally begins 48 hours after exposure and can continue for up to 2 weeks, with the blisters sometimes coalescing into large bullae.
    • Systemic effects include airway involvement, nausea and vomiting, and delayed hematopoietic suppression, which can manifest as leukopenia days to weeks after exposure. Burns over greater than 25% of BSA can be fatal.
• Other agents
• • Skin preparation agents
    • Povidone-iodine solution (Betadine) is a widely used antiseptic. It is water soluble and contains water, iodine, and polyvinylpyrrolidone.
    • Chemical burns due to povidone-iodine solution are rare, but most occur in patients undergoing gynecologic, urologic, or orthopedic operations.
    • Burns induced by povidone-iodine solution usually occur in dependent parts of the body, such as the buttocks or under a tourniquet, where the agent has not been allowed to dry. Irritation and long-term pressure both appear to play roles in the pathogenesis of these injuries.
    • Alcohol-based skin cleansers such as chlorhexidine gluconate 0.5% in 70% methanol are also used frequently in medical settings. While innocuous to most individuals, severe chemical burns have been reported after alcohol-based skin cleansers were used on babies with immature skin (<28 wk of gestation).
  • Alternative medicine/home remedies: Several reports have implicated home remedies as the cause of chemical burns. Culinary mustard and garlic, when applied to the skin, can result in minor chemical burns. Knowledge of this potential complication may be helpful for physicians practicing in cross-cultural settings.
  • Cosmetic products: Nail glue and bleach hair dye have been cited as causes of chemical burns.

DIFFERENTIALS

Section 4 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

WORKUP

Section 5 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Lab Studies

• Some minor chemical burns are localized injuries and laboratory studies may be unnecessary. However, burns over moderate-to-large skin surface areas and any burn caused by an agent known to have systemic effects warrant, at minimum, careful monitoring of fluid and electrolyte status in a hospital setting. The following agents are prone to causing systemic effects and deserve special attention.
• • Acids
    • Hydrofluoric acid: Perform a chemistry panel to monitor sodium, calcium, and magnesium levels. Monitor cardiovascular and respiratory status with cardiac monitors to assess for electrocardiographic changes. Include frequent blood pressure, pulse, and respiration measurements.
    • Phenol: Perform respiratory and cardiac monitoring. Evaluate hepatic and renal function.
    • Chromic acid: Renal and hepatic function should be monitored, given the risk for liver or kidney failure. A complete blood cell count and coagulation studies help assess for anemia and coagulopathies that may develop from systemic toxicity due to chromic acid.
    • Formic acid: A chemistry panel and arterial blood gas determination should be performed to evaluate for an anion gap metabolic acidosis. A secondary lactic acidosis may be present from respiratory depression. Renal function should be monitored carefully, and a urinalysis is appropriate because hematuria and hemoglobinuria may be early signs of systemic toxicity. A complete blood cell count should be obtained to evaluate for intravascular hemolysis. Finally, monitor vital signs to assess for hypotension.
    • Monochloroacetic acid: Cardiovascular monitoring is essential because cardiovascular involvement is common. A chemistry panel helps evaluate for renal failure. Lactate levels are directly proportional to the clinical signs of toxicity and the mortality rate.
  • Others
    • White phosphorus (oxidizing agent): Evaluate hepatic and renal function. Systemic consequences of nephrotoxicity and hepatotoxicity include progressive anuria, decreased creatinine clearance, and increased blood urea nitrogen levels. Chemistry panel values and serum calcium and phosphorus levels should be monitored. White phosphorus burns may cause hypocalcemia and hyperphosphatemia; therefore, serum calcium and phosphorus levels should be monitored for at least 48-72 hours. Cardiovascular monitoring, especially for bradycardia and other electrocardiographic changes, is warranted.
    • Sulfur mustard (vesicant): Serial complete blood cell counts should be performed for several weeks following the burn, given the risk of leukopenia.

TREATMENT

Section 6 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical Care

The initial management of chemical burns is universal regardless of the agent. Treatment begins with ending the exposure. Contaminated clothing should be removed, and the affected area should be irrigated profusely, preferably with a high-density shower. Immediate irrigation of the chemical with water has been shown to limit the depth of the burn and the duration of the hospital stay. Notable exceptions to the exclusive use of water irrigation include chemical burns induced by dry lime, phenol, hydrochloric acid, and sulfuric acid. Phenol and dry lime are discussed below. For more information on the treatment of hydrochloric and sulfuric acid burns, see Burns, Chemical in the Emergency Medicine section of the eMedicine journal.

Extensive burns from any cause warrant careful monitoring of fluid and electrolyte status, with early fluid resuscitation. This is especially important in the case of chemical burns, which can be deceptive because they tend to be deeper than other types of burns. To prepare for possible systemic toxicities, consultation with a poison control center toxicologist is important. Other, more specific guidelines for treating chemical burns caused by individual agents are listed below. Some of these treatments are controversial because many have not been tested in randomized controlled trials.

• Acids
• • Hydrofluoric acid
  • • Immediately irrigate the chemical burn with water; continue irrigating for approximately 20 minutes. Irrigation cleans the wound of unreacted chemicals and dilutes the chemical that is in contact with the skin. Washing is especially important in HF burns because the acidic properties of the chemical are derived from complex ions that are not present at concentrations of less than 10%.
    • After the initial washing stage, the objective is to inactivate free fluoride ions by forming an insoluble fluoride salt. High-molecular–weight quaternary ammonium compounds such as 0.2% benzalkonium chloride (Hyamine 1622) or 0.13% benzalkonium chloride (Zephiran) are widely used. Quaternary ammonium compounds may inactivate the fluoride ion by a variety of mechanisms. The compounds may produce nonionized fluoride complexes by exchanging chloride for fluoride or they may directly affect the permeability of the cell membrane. These quaternary ammonium compounds also help control invasive microorganism infection. Nevertheless, the use of these compounds is controversial because of the discomfort associated with using iced solutions and the possible toxicities associated with 0.2% benzalkonium chloride. In addition, 0.2% benzalkonium chloride may be ineffective in deeper tissues.
    • Divalent cations can neutralize the reactive fluoride ions from an HF burn. Calcium gluconate gels have been widely used as topical treatments of major burns. Minor burns may be treated by applying topical 2.5% calcium gluconate jelly; pain resolution is the end point of treatment. The addition of dimethyl sulfoxide (DMSO) as a solvent is being investigated because anecdotal reports indicate its usefulness in difficult treatment areas such as the nailfold. Calcium carbonate gels are also used, but a large amount is required for treatment and they may stain the skin.
    • Some authors recommend a subcutaneous injection of 10% calcium gluconate, which has proven effective for pain resolution. A 27- to 30-gauge needle is used for the subcutaneous tissue injection (0.5 mL of 10% calcium gluconate per cm²), and it should be injected at the periphery of the burn. Often, the use of calcium gluconate therapy is reserved for patients with severe throbbing pain or with a central hardened, gray area and surrounding erythema.
    • Infiltration therapy is invasive and may introduce infection and hypercalcemia. However, in patients with severe hand burns, a regional, intra-arterial infusion of calcium gluconate solution should be considered. The route of infusion is generally via the brachial, ulnar, or radial artery. Continuing to monitor the serum calcium level, and provide supplementation, is extremely important.
  • Phenol: The initial treatment of a phenol injury generally includes decontamination with 50% polyethylene glycol (PEG) and extensive irrigation with water. In addition, a solvent cleaner with hydrophilic and hydrophobic properties may be used to remove phenol from the skin prior to initial treatment.
  • Chromic acid
  • • Treatment initially involves water irrigation, a phosphate buffer, or 5% thiosulfate soaks, which converts the hexavalent chromium ion to its less toxic trivalent form. Topical use of 10% calcium ethylenediamine tetraacetic acid (EDTA) ointment; 5-10% sodium citrate; lactate- or tartrate-soaked dressings; or cream containing ascorbic acid, sodium pyrosulfate, ammonium chloride, tartaric acid, and glucose is recommended to prevent further absorption. These treatments allow chelation with the chromium or reduction of the hexavalent chromium ion to the less toxic trivalent ion.
    • Dimercaprol, ascorbic acid, or sodium calcium edentate is often used as a systemic treatment.
    • In burns involving greater than 2% BSA, the patient should receive peritoneal dialysis in the first 24 hours to prevent parenchymal absorption.
  • Formic acid
  • • Treatment is similar to that for other acidic burns and begins with removal of affected clothing and profuse water irrigation. Treatment also includes elimination of the acidotic state and removal of formate from the body, which may be accomplished by means of intravenous hydration and aggressive bicarbonate therapy.
    • Folic acid may be used to increase the rate of formate metabolism.
    • In severe cases, dialysis may be necessary.
  • Monochloroacetic acid
  • • The European Centre for Ecotoxicology and Toxicology of Chemicals recommends the use of dichloroacetate (DCA) as an antidote for MCAA exposure.
    • DCA acts directly on the affected enzyme systems to reduce the accumulation of lactic acid.
    • DCA is recommended for all exposures involving greater than 5% BSA. Hemodialysis should also be performed in all cases of systemic toxicity.
• Others
• • Cement (alkali agent): Treatment of cement injuries includes removing the agent with a cloth, followed by washing the affected area with soap and copious amounts of running water. Dry lime (a form of calcium oxide) should be dusted off the skin before washing it away with water.
  • White phosphorus (oxidizing agent): White phosphorus is difficult to remove and, in liquid form, often becomes embedded. Thus, aggressive and prompt removal is required to prevent injury progression. The first priority after removal is to stop the oxidation process. Thorough irrigation should be followed by covering the wound with wet compresses. The wet compresses serve to prevent contact with oxygen, which causes ignition of white phosphorus. Immediate surgical debridement should also be considered.

Surgical Care

As with other types of burns, surgical intervention is an important aspect to the treatment of chemical burns and includes debridement, wound care, and, in some cases, skin grafting. Surgical debridement is most important in full-thickness and deep partial-thickness burns and serves to remove eschar and any remaining chemical material. Topical antimicrobials play an important role in the surgical aspect of burn wound care, particularly 1% silver sulfadiazine cream, 0.5% silver nitrate solution, and 11.1% mafenide acetate cream. Application of an occlusive dressing maintains a moist environment, allowing epithelialization to occur more readily. While these general guidelines hold true for most chemical burns, several causative agents deserve special mention in regards to surgical treatment.

• Acids
• • Hydrofluoric acid: The role of surgery in HF burns is to debride blisters that form and to excise any necrotic tissue from the burned area so that treatment with topical agents or infiltration can be effective. Excision of the involved tissue may also serve to remove residual HF and thereby reduce systemic toxicity.
  • Chromic acid: Immediate excision of the burn reduces chromium absorption, which ultimately reduces systemic effects. Therefore, wide excision with the application of autograft or homograft split skin is advocated. Literature reviews suggest that superficial burns involving greater than 2% BSA require immediate excision to reduce chromium absorption. If the burn involves less than 2% BSA and is superficial, calcium EDTA dressings may be used.
• Alkali agents: Surgical treatments are used in alkali burns to prevent further chemical penetration. Extensive debridement may require the use of autographs, allografts, or synthetic skin substitutes for wound coverage and to prevent desiccation. As in all burn wounds, antimicrobial agents should be included in the management of wound care. Mafenide acetate solution, 5%, has been reported in the treatment of alkali burns.
• Oxidizing agents: For white phosphorus burns, immediate surgical debridement to remove all particles or smoking areas should be considered if irrigation is not effective. Avoid oily or greasy dressings because they contribute to the tissue permeability of the lipid-soluble white phosphorus. Wound closure should be deferred until adequate debridement is ensured.

MEDICATION

Section 7 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical therapy for burn care consists of antidotes, wound care, and analgesia. For information regarding wound care and analgesia, see Burns, Chemical in the Emergency Medicine section of the eMedicine journal or Wound Care in the Internal Medicine section of the journal. The following medication section focuses on specific antidotes recommended for chemical burns discussed in detail in this article.

Drug Category: Antidotes/decontamination agents

Used as a decontaminate or antidote for specific chemical agents.

Drug Category: Divalent cations

Used in HF burns. May reduce pain, minimize systemic toxicity, or both.

FOLLOW-UP

Section 8 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Deterrence/Prevention

• Workers should be familiar with the material data safety sheets for different compounds to which they may be exposed.

Patient Education

• For excellent patient education resources, visit eMedicine's Burns Center. Also, see eMedicine's patient education articles Chemical Burns and Thermal (Heat or Fire) Burns.

MISCELLANEOUS

Section 9 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical/Legal Pitfalls

• If any question exists as to the extent of a burn, patients should be treated for the worst possible injury. This is especially pertinent for burns caused by chemical agents with known systemic toxicities, such as HF.
• Because chemical burns often occur in industrial and other occupational settings, physicians should be aware of the potential for legal matters regarding disability or workers' compensation.

REFERENCES

Section 10 of 10

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

• Amshel CE, Fealk MH, Phillips BJ, Caruso DM. Anhydrous ammonia burns case report and review of the literature. Burns. Aug 2000;26(5):493-7. [Medline].
• Baker JG, Tarantino DA Jr, Miller ML. Lime disease?. Arch Dermatol. Oct 2000;136(10):1277-8. [Medline].
• Barillo DJ, Cancio LC, Goodwin CW. Treatment of white phosphorus and other chemical burn injuries at one burn center over a 51-year period. Burns. Aug 2004;30(5):448-52. [Medline].
• Burd A. Hydrofluoric acid-revisited. Burns. Nov 2004;30(7):720-2. [Medline].
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• Chou TD, Lee TW, Chen SL, Tung YM, Dai NT, Chen SG, et al. The management of white phosphorus burns. Burns. Aug 2001;27(5):492-7. [Medline].
• Corazza M, Bacilieri S, Morandi P. Airbag dermatitis. Contact Dermatitis. Jun 2000;42(6):367-8. [Medline].
• Corazza M, Trincone S, Virgili A. Effects of airbag deployment: lesions, epidemiology, and management. Am J Clin Dermatol. 2004;5(5):295-300. [Medline].
• Davis KG, Aspera G. Exposure to liquid sulfur mustard. Ann Emerg Med. Jun 2001;37(6):653-6. [Medline].
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Article Last Updated: Jan 23, 2007