eMedicine Specialties > Dermatology > Environmental

Burns, Chemical

Author: Matthew J Mahlberg, MD, Resident Physician, Department of Dermatology, New York University School of Medicine
Coauthor(s): Mina Yassaee, BA, University of Pennsylvania School of Medicine; Richard Laws, MD, Assistant Professor, Department of Dermatology, Roger Williams Medical Center, Boston University; William D James, MD, Paul R Gross Professor of Dermatology, University of Pennsylvania School of Medicine; Vice-Chair, Program Director, Department of Dermatology, University of Pennsylvania Health System
Contributor Information and Disclosures

Updated: Jan 13, 2009

Introduction

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.

Additionally, see Burns, Electrical for information on this topic.

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

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^1,2,3
    • 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, hypomagnesemia, 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.
  • Phenol⁴
    • 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.⁵ 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 acid⁶
    • 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^7,8,9,10
    • Anhydrous ammonia is a colorless, pungent gas used in a variety of industrial settings as a fertilizer, explosive, and chemical intermediate¹¹ ; 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.¹² 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. However, one case highlights the death of an engineer after dermal absorption of concentrated tetramethylammonium hydroxide (25%; pH, 13.5), which is now widely used in the manufacture of semiconductors and liquid-crystal displays.¹³
  • Cement burns¹⁴
    • 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.¹⁵ 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^16,17,18
    • 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 liquor¹⁹
    • 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 garlic-like 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^20,21
    • 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 agents²²
    • 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).²³
  • Alternative medicine/home remedies: Several reports have implicated home remedies as the cause of chemical burns. Culinary mustard²⁴ and garlic,²⁵ 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 glue²⁶ and applications of bleach dye, highlighting solutions, and permanent wave and straightening products to the hair have been cited as causes of chemical burns.^27,28

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