Epidemiology

Chemical burns are an uncommon form of burn injury, accounting for 2.1% to 6.5% of all burn center admissions. According to the 2015 National Burn Repository report of the American Burn Association, chemical injuries represented 3.4% of patients admitted to participating hospitals over the 2004 to 2015 period. The mean hospital charge for patients with chemical burns was approximately $30,000, which was significantly lower than flame, scald, or electrical injuries. More than 13 million workers in the United States are at risk for dermal chemical exposures, particularly those employed in the agricultural and industrial manufacturing industries. Skin disorders are among the most frequently reported occupational illnesses, resulting in an estimated annual cost in the United States of more than $1 billion.

Overall, chemical burns in the United States occur in roughly equal proportions at work (42.9%) and at home (45.9%), with most work-related exposures occurring in an industrial setting. The highest incidence occurred in the male population between 20 and 60 year old, representing most of the industrial work force. Similarly, a 10-year retrospective study of 690 chemical burn patients admitted to a large hospital in China reported the vast majority of chemical burns occurring in the 20- to 59-year age group (95%), which were most frequently related to work. The most common burn sites were the upper extremities (32%), followed by the head and neck (28%), and lower extremities (20%).

A vast number of hazardous chemicals are capable of damaging tissue. The Hazardous Substances Emergency Events Surveillance database of the Centers for Disease Control and Prevention published an analysis of 57,975 chemical injuries over the 1999 to 2008 time period. The chemicals most frequently associated with injury were carbon monoxide (2364), ammonia (1153), chlorine (763), hydrochloric acid (326), and sulfuric acid (318). A 2004 study of military-related chemical burns treated at Brooke Army Medical Center reported 52.9% resulting from munitions (mostly white phosphorus), followed by acid exposures (9.1%), alkali exposure (6.5%), and other chemicals, such as phenol, fluorocarbon, and oven cleaner (6.2%).

Beyond the initial tissue injury, sequelae of chemical burns can include wound infections, cellulitis, sepsis, and complications from scarring. Increasing age is associated with an increase in complications from chemical burns (mostly cellulitis and wound infections), with children under the age of 2 experiencing the lowest rate (2.5%). Complications in the 20- to 50-year age range plateau at 6.4% to 6.7%, which increases significantly with every decade greater than 50 to a maximum of 20.9% in patients older than 80. Sepsis is the most serious complication of chemical burns, which has an overall rate of around 0.6%. Mortality from chemical burns is fortunately low. In the 2014 Annual Report of the American Association of Poison Control Centers’ National Poison Data System, 151,796 dermal chemical exposures reported to the agency, and only 8 proved fatal.

Chemical burns are infrequent in children, afflicting 0.9% of admitted pediatric burns at the Parkland Burn Center. It is also not a common form of child abuse, with only 1.4% of nonaccidental pediatric burns resulting from chemical contact. Another study at Children’s Hospital Michigan grouped chemical burns in a miscellaneous category of 22% of admitted pediatric patients.

The following article focuses on the dermal and ocular chemical burns most frequently encountered by plastic surgeons. Although oral ingestion is a more common route of toxic chemical exposure, the cause and management are beyond the scope of this article. According to the 2014 Annual Report of the American Association of Poison Control Centers’ National Poison Data System, the route of exposure is usually ingestion (83.7% of cases), followed in frequency by dermal (7.0%), inhalation/nasal (6.1%), and ocular (4.3%).

Emergency Management of Chemical Burns

A general approach to the patient with chemical burns involves scene safety, protecting health care workers from exposure, removing the patient from exposure, removing any necessary clothing and jewelry, and brushing off dry chemicals with a suitable instrument. Dry lime in particular should be brushed off before attempting irrigation, because it contains calcium oxide that reacts with water to form calcium hydroxide, a strong alkali. In contrast to thermal burns, many chemicals will continue to induce injury until removed, so immediate clearance of the offending agent is paramount in the intended treatment plan.

For most chemical burn injuries, copious irrigation with water or saline is the initial treatment. The exceptions to this are elemental metals and possibly phenols. Elemental metals produce exothermic reactions when combined with water, whereas aqueous irrigation of phenols may cause deeper infiltration into tissue. Gentle irrigation of chemical burns under low pressure is essential, because higher pressure irrigation can cause deeper infiltration of the chemical into the skin and place the patient and provider at risk for splatter injury. Moderately warm water is often advised. Irrigation should be started promptly, because started initial treatment in the field has been associated with reduced severity of burn injury and a shorter length of hospitalization. Irrigation should begin with the eyes and face, which prevents further inhalation or ingestion or toxin. Treatment should continue until the pH at the skin surface is neutral, which may take 2 hours or more in the case of alkali burns. Ideally, pH at the skin surface should be measured 10 to 15 minutes after discontinuation of irrigation. Litmus paper, if available, is ideal for this purpose. Neutralizing agents are generally not recommended given the potential for an exothermic reaction to occur between the 2 substances. The delay in obtaining the neutralizing agent will also allow for deeper tissue injury if water is readily available.

Ocular injuries should be similarly irrigated with water or saline or until neutral pH is achieved. Concentrated ammonia can induce severe anterior structural injury within 1 minute of exposure, whereas lye can cause deeper injury within 3 to 5 minutes.

The initial management of phenol injuries is also somewhat controversial, with some arguing that irrigation may enhance dermal spread and penetration of the compound. Polyethylene glycol (PEG) has both hydrophilic and hydrophobic properties, which may be the ideal method of phenol decontamination. However, animal studies have not shown a significant difference in phenol plasma levels when burns were irrigated with PEG or water. Furthermore, because of the rarity of immediate phenol availability at the burn site, irrigation with water is more often advised.

Alkali Burns

Anhydrous ammonia, calcium oxide/hydroxide (lime), and sodium or potassium hydroxide (lye) are common examples of alkalis used in industrial applications or the home. Lime, found in cement and plaster, is the most common cause of alkali burns. It is also known for producing burns of limited depth owing to the precipitation of calcium soaps in fat that limit further penetration. Ammonia and lye do not produce this effect and exhibit deeper and more severe tissue injury.

Anhydrous ammonia is a pungent, colorless gas that sees use in the production of fertilizer, synthetic textiles, and methamphetamine. It is the most common injury associated with illicit methamphetamine production, which has seen a resurgence in the last decade. Anhydrous ammonia is typically stored in refrigerated vessels, and so leakages may cause concomitant chemical and cold injury. Tissue destruction is related to the production of ammonium hydroxide, and more specifically to the concentration of hydroxyl ions. The ensuing damage is a product of liquefactive necrosis, which results in any degree of burn from superficial to full thickness. Anhydrous ammonia is known to have a particularly high affinity for mucous membranes. Mucosa-associated injuries, such as hemoptysis, pharyngitis, pulmonary edema, and bronchiectasis, have all been associated with anhydrous ammonia exposure. Inhalational exposure is extremely toxic. The report of a 2013 mass casualty in China involving anhydrous ammonia described 58 exposed employees, 10 of which died at the scene from inhalational injury, another 5 succumbed en route to the hospital, and the remainder suffered various degrees of pulmonary infection and respiratory failure.

Anhydrous ammonia is soluble in water, and treatment therefore consists of immediate, copious aqueous irrigation. Because of the tendency of alkalis to linger in tissue for prolonged periods, repeat irrigation should be performed every 4 to 6 hours for the first 24 hours. Mechanical ventilation may be necessary for patients with significant facial or pharyngeal burns. Ocular exposure should be irrigated with water or saline until the conjunctival sac pH drops to less than 8.5.

Hydrofluoric Acid

Organic and inorganic acids function by release of H+ and reaction with dermal proteins, which produces coagulative necrosis of the skin. Hydrofluoric acid (HF) is commonly used in the petroleum distillation industry to produce gasoline. It is also widely used in chemical and electronics manufacturing, glass etching, and smelting. Dilute solutions are found in household rust removers and metal cleaning products.

HF displays a unique mechanism of action for an acid. More so than the free H+ released during dissociation, the free fluoride conjugate base ion is thought to be responsible for most tissue injury. Similar to strong alkalis, free H+ is scavenged from fatty acids, resulting in fat saponification and liquefactive necrosis. The free fluoride ion also affects calcium and magnesium cations in the serum, resulting in a systemic hypocalcemia and hypomagnesemia. Hypokalemia can also result from inhibition of the sodium-potassium ATPase and Krebs cycle enzymes.

Tissue damage is progressive, which can persist for days if untreated. Pain may be immediate or delayed depending on the magnitude of exposure, and affected skin will progress from a hardened, indurated appearance to a necrotic eschar. Systemic symptoms may include nausea, abdominal pain, and muscle fasciculation. In advanced cases, QT prolongation, hypotension, and ventricular arrhythmias can occur due to the profound electrolyte disturbances.

In keeping with the initial treatment of most chemical burns, immediate aqueous irrigation is indicated. Acids generally require shorter irrigation times than alkalis, which in the case of HF is approximately 15 to 30 minutes. Blisters should be debrided to allow removal of acid trapped under the desquamated epithelium. In cases of more severe HF burns, detoxification of the fluoride ion is indicated with calcium gluconate. Calcium gluconate promotes formation of an insoluble calcium salt, which can be washed from the skin surface.

Calcium gluconate can be administered by intravenous or intraarterial injection, topically with 2.5% gel, or direct subcutaneous infiltration with a 5% to 10% solution. Topical administration, although effective for superficial exposures, is incapable of neutralizing deeper burns due to the impermeability of the calcium compound. Subcutaneous infiltration may be used for localized burns, which involves injection of 0.5 mL per cubic centimeter via a 27- to 30-gauge needle. HF burns of digits have been treated with direct infiltration, although a regional nerve block is required for adequate anesthesia during the procedure. Along with the risk of digital ischemia from arterial constriction, systemic administration of calcium gluconate is recommended for digital HF burns. Intravenous or intraarterial injection with 10% calcium gluconate generally requires intensive care unit admission, telemetry, and close monitoring of serum calcium levels. Calcium chloride may also be used, although central venous access is required. The magnitude of dermal exposure need not be extensive for systemic complications to develop. An HF leakage caused by an overturned tanker truck in China in 2014 was responsible for less than 5% total body surface area (TBSA) partial- and full-thickness burns in 4 people, all of whom were treated for inhalational injury and severe hypocalcemia.

White Phosphorous

White phosphorous is a nonmetallic compound that finds widespread use in munitions manufacturing, fireworks, fertilizers, and illicit methamphetamine production. It is present throughout the military arsenal as well. Phosphorous will autoignite with atmospheric oxygen at temperatures greater than 30°C, forming phosphorous pentoxide that then hydrates with exposure to air to form phosphoric acid.

Tissue injury by white phosphorous is caused by both thermal and chemical burns. Phosphoric reacts exothermically with skin, liberating heat and causing thermal burns. Both phosphorous pentoxide and phosphoric acid are capable of inducing chemical burns. Metabolic derangements due to calcium binding and hypocalemia have been reported from white phosphorous absorption, such as bradycardia, QT prolongation, and ST- and T-wave abnormalities. In these cases, calcium gluconate may be required to sustain plasma calcium levels.

Many have recommended the use of copper-containing solutions to neutralize white phosphorous. Copper reacts with phosphorous to form black cupric phosphide, which is more easily removed. Copper sulfate also reduces the oxidation potential of phosphorous and consequently can limit deeper tissue injury. However, laboratory experiments have demonstrated no benefit of copper solutions over saline alone, and is generally less available than water or saline. Wartime experience with white phosphorous burns suggests good efficacy with water alone.

Phenol

Phenol (carbolic acid) is an aromatic hydrocarbon derived from coal tar. It has a characteristic strong, sweet odor that can be detected in burn injuries. Phenol has a notable history in surgery from the experiments by Joseph Lister in 1867 for its aseptic properties and ability to disinfect surgical instruments. Phenol is used in the production of a variety of industrial products, such as explosives, fertilizers, paints, rubber, resins, and textiles. Phenol is also used in various commercial soaps, sprays, and ointments as a germicidal antiseptic. Dilute phenol solutions are also commonly used by plastic surgeons as a chemical facial peel, which are usually admixed with water, soap, and croton oil. The solution is applied topically to produce a controlled partial-thickness burn. Upon healing, the dermal collagen reorganization improves the appearance of facial rhytids, actinic keratosis, and irregular pigmentation.

Concentrated phenol and its derivatives are highly reactive with skin, which induce tissue injury by protein denaturation and coagulative necrosis. Following initial contact, coagulative necrosis of the papillary dermis may serve to delay deeper tissue penetration, highlighting the importance of immediate irrigation. Dermal phenol exposure can cause any degree of burn injury from irritation to dermatitis to full-thickness burns. Abnormal, dark pigmentation may also result from dilute phenol exposure. Because of its anesthetic properties, extensive tissue damage can occur before pain is recognized.

Phenol is poorly soluble in water, and there is some concern that inadequate irrigation will merely spread the chemical over uninjured areas of skin, resulting in a larger burn area and potentially greater systemic absorption. PEG serves as a hydrophobic solvent, which can more readily dissolve phenol. PEG is usually available in hospital pharmacies and is probably the preferred antidote for phenol burns, although this is somewhat controversial. Although the mechanism is understood, clinical studies of phenol neutralization with PEG are lacking. In a 1978 study of swine acutely exposed to phenol, plasma phenol levels were not significantly different in swine decontaminated with PEG or water. Thus, as with most chemical burns, the recommended initial treatment is copious irrigation with water until PEG is available. Irrigation should continue with either PEG or water because dilute phenol solutions are more easily absorbed through the skin. Water irrigation should not be delayed while awaiting PEG availability. In a case series of 4 patients with extensive phenol burns in China, both water and PEG were used.

Systemic toxicity from phenol poisoning can also result, with the cardiovascular and central nervous systems primarily affected. Neurologic symptoms include mental status changes, lethargy, seizures, or coma. Cardiovascular toxicity may present as bradycardia or tachycardia. Hypotension, hypothermia, and metabolic acidosis can occur with severe exposure. Treatment of systemic toxicity is largely supportive with fluid resuscitation and vasopressors as needed.

Ocular Injuries

Chemical burns to the eye and eyelid are a frequent cause of emergency room visits, totaling approximately 2 million cases per year. Approximately 15% to 20% of facial burns involve the eye, and ocular injury stands as the second leading cause of visual impairment in the United States after cataracts. Similar to dermal chemical injuries, alkali exposures are more common and generally cause deeper and more serious tissue damage than acid. Common offending agents in the household include automobile batteries, pool cleaners, detergents, ammonia, bleach, and drain cleaners. Patients may present with decreased vision, eye pain, blepharospasm, conjunctivitis, and photophobia. In severe cases of alkali burns, the globe may appear white due to ischemia of the conjunctiva and scleral blood vessels.

Alkali injuries such as lime and ammonia penetrate readily into eye, injuring stroma and endothelium as well as intraocular structures such as the iris, lens, and ciliary body. Acid injuries are generally less severe because the immediate precipitation of epithelial proteins confers a protective barrier to intraocular penetration. Periocular injuries are common, where the depth of injury often correlates with scar formation. Debridement of devitalized periocular tissue is important to protect the ocular surface from exposure keratopathy and corneal ulceration. Profound dermal injury may result in cicatricial ectropion, which often requires tarsorrhaphy or excision and full-thickness skin grafting.

Ocular burns are categorized into 4 grades, with grade IV representing the most severe. Grade I burns are associated with hyperemia, conjunctival ecchymosis, and defects in the corneal epithelium. Grade II burns include haziness in the cornea. Grade III burns are associated with deeper penetration into the cornea and present with mydriasis, gray discoloration of the iris, early cataract formation, and ischemia in less than half of the limbus. Grade IV burns appear similar to grade III but with ischemia involving more than half of the limbus. They are also associated with necrosis of the bulbar and tarsal conjunctiva.

Immediate irrigation with water is the initial therapy for ocular injuries, beginning at the scene and continuing to the emergency department. Animal studies have consistently demonstrated better outcomes when the eye is rinsed early and thoroughly after chemical exposure, relating to the progressive neutralization of pH with water volume. Prolonged irrigation is best achieved using intravenous tubing and a polymethylmethacrylate (Morgan) lens, although when no such device is available, it is important to keep the eyelids retracted to assure adequate irrigation of the conjunctiva and cornea.