INTRODUCTION — Chemical burns, which are often work-related [1], are unique injuries that require individualized treatment and management depending upon the causative agent. They account for 4 percent of admissions to burn units in developed countries and up to 14 percent in underdeveloped countries [2].
A variety of chemicals are manufactured for household, agricultural, industrial, and military use, with an estimated 60,000 new chemicals produced each year [3]. For management of toxic exposures, it is helpful to organize these chemicals into general categories, keeping in mind that some have overlapping properties or incompletely understood pathophysiology.
The evaluation and treatment of common topical chemical burns will be reviewed here with a focus on the basic principles of management. Thermal burns, chemical ingestions, chemical eye injuries, and agents used for chemical warfare are discussed elsewhere. (See "Emergency care of moderate and severe thermal burns in adults" and "Caustic esophageal injury in adults" and "Caustic esophageal injury in children" and "Corneal abrasions and corneal foreign bodies: Clinical manifestations and diagnosis" and "Chemical terrorism: Rapid recognition and initial medical management".)
PRINCIPLES OF MANAGEMENT
General approach — The potency and concentration of the toxic agent and the duration of contact primarily determine the degree of tissue destruction. Therefore, it is critical that treatment be started immediately. In the great majority of cases, the management of topical chemical burns consists of the following general steps:
●Ensure protection of rescuers and health care workers from exposure.
●Remove the patient from the area of exposure.
●Remove all clothing and jewelry.
●Brush any dry chemicals off the patient; any suitable instrument may be used (eg, dry brush, towel).
The most important component of active therapy is irrigation of all wounds and areas of exposure thoroughly with copious amounts of water [4]. Irrigation is begun at the site of contamination and the eyes and face, if they are involved or adjacent to the exposed area. Some experts suggest cleaning the exposed area with a mild soap following irrigation.
There are a small number of exceptions to this approach. Among the few chemical toxins that should not be irrigated immediately with water are dry lime, phenols, and elemental metals (eg, sodium, potassium, calcium oxide, magnesium, phosphorous). (See 'Chemicals NOT treated with immediate water irrigation' below.)
Patients entering the medical system via emergency medical services (EMS) or other first responder systems (eg, fire department) are often decontaminated, including water irrigation, using portable decontamination units prior to entering the hospital. Decontamination may also be performed by hospital-based decontamination teams. Plans for the decontamination of patients exposed to hazardous substances are generally determined by the hospital's disaster planning committee and local and state emergency management departments. A table summarizing the signs and symptoms of some common chemical burns is provided (table 1).
Protection of providers — Before initiating irrigation for patients with chemical burns, first responders and clinicians must don appropriate protective gear to prevent contamination or injury. The clothing and equipment needed to protect an individual from a chemical or biological threat depends upon the type of threat and the duration of exposure. In the United States, the Occupational Safety and Health Administration (OSHA) classification system is often used to describe the levels of personal protection [5,6]:
●Level A: Maximal protection includes encapsulation boots and gloves and a self-contained breathing apparatus (SCBA).
●Level B: Non-encapsulating splash protective suit that is not airtight but provides full respiratory protection and SCBA.
●Level C: Splash suit and full or half-face respirator.
●Level D: Work clothes, boots, safety goggles, and gloves; no respiratory protection.
Available equipment varies considerably among EMS systems and hospitals. For most hospital decontaminations of an unknown substance, OSHA believes the following protection is adequate for those working in the decontamination zone [7]:
●Powered air-purifying respirator (PAPR) that provides a protection factor of 1000 combined with a 99.97 percent high-efficiency particulate air (HEPA)/organic vapor/acid gas respirator cartridges.
●Double layer protective gloves.
●Chemical resistant suit; suit openings are sealed with tape.
●Head covering with eye and face protection (if not part of respirator).
●Chemical protective boots.
A parent or other adult holding or helping a child who is being treated with decontamination should also don protective equipment appropriate for the agent involved and clinical circumstance. For those providing post-decontamination care, protection comparable to that used for infection control should be used (ie, gown, glove, mask).
Removal of chemical — Complete removal of the toxic chemical is essential. Tissue damage continues for as long as the chemical remains in contact with skin. Furthermore, destruction of the epidermis allows substances to reach the dermis, which is more permeable to chemical toxins and may permit systemic absorption. To ensure thorough decontamination, remove all clothing (including footwear and jewelry), brush off all dry agents, and begin irrigation with copious amounts of water immediately at the scene of exposure. Water irrigation is continued upon arrival at the emergency department (ED).
Irrigation
Basic approach — Copious irrigation with water dilutes and removes the large majority of chemicals (a common mnemonic is: "the solution to pollution is dilution") [4]. A small number of chemicals should not be irrigated with water and these are discussed immediately below.
When initiated in the field, water irrigation reduces burn severity and the length of hospitalization [8]. Immediate water irrigation also represents the essential first aid for chemical burns of the skin and eye, reducing the risk for chronic conjunctivitis and sight-threatening corneal ulceration.
Moderately warm water in high volumes but at low pressures should be used for irrigation. High pressure irrigation should be avoided as it can splash chemicals on to unexposed areas and drive them deeper into tissue [9]. During cold weather, warmer water is needed to prevent hypothermia. Either a shower or a hose can be used.
Irrigation should begin at the site of contamination and the eyes and face, if they are involved or adjacent to the exposed area. Decontamination of the face prevents further inhalation or ingestion of any toxin.
Concentrated strong acids, such as muriatic acid (hydrochloric acid) and sulfuric acid, may theoretically liberate heat due to ionization when irrigated with water, which has led some to caution against immediate irrigation [10]. However, based on a review of limited evidence and the experience of a few clinicians, it appears that the most important factor in mitigating tissue damage is early decontamination [11]. We therefore suggest that strong acid exposures be decontaminated as quickly as possible, with copious water if that is most readily available, and with a dry towel or rag followed by copious water if immediate water decontamination is not possible.
Diphoterine is an amphoteric, hypertonic, polyvalent, chelating solution that has been in use in Europe, primarily in industrial settings, as a first-line irrigation solution for chemical exposures, both alkaline and acidic. Limited research of Diphoterine suggests that it is well tolerated, free of harmful effects, and potentially a good first-line decontaminating agent [12-16]. However, additional study is needed to determine whether Diphoterine and similar buffered solutions (eg, Cederroth) are substantially superior to water irrigation, and concerns have been raised about bias stemming from industry-sponsored research [12,17,18].
While the European Union has classified Diphoterine solution as a Class II medical device, disputes between the manufacturer and the US Food and Drug Administration (FDA) are ongoing. The issue is whether Diphoterine should be designated as a medical device or a drug. The delivery system uses a pressurized canister to deliver the solution in a manner that removes chemicals physically in addition to Diphoterine's chemical effects.
Once imminent threats to human health and life are addressed, reasonable efforts to contain and mitigate environmental damage should be made. The effluent from decontamination is dilute following copious irrigation and generally does not pose an environmental threat. Many decontamination units include equipment to manage irrigation runoff, which can be collected and disposed of in an environmentally safe manner.
Skin irrigation — Evidence to guide the method and duration of water irrigation is lacking. For acid burns of the skin, we suggest continuous water irrigation until the pH of any exposed tissue becomes neutral. For alkali burns of the skin, we suggest the same approach, but a much longer period of irrigation is necessary. Two hours or more of continuous irrigation may be required before the pH of tissue exposed to a strong alkali returns to neutral. It is best to measure the pH approximately 10 to 15 minutes after stopping irrigation to ensure the measurement accurately reflects the presence of any residual chemical rather than the water used for irrigation [9].
Neutralization of alkali burns using a weak acid, such as 5 percent acetic acid (household vinegar), may be a useful treatment, but further research is needed [19].
Eye exposure — Eye contact with acids or alkalis requires immediate evaluation and treatment to prevent permanent vision loss. Burn severity depends upon the agent involved, duration of exposure, and depth of penetration (table 2) [20,21]. In the United States, injury from chemical ocular burns occurs most often in residential settings, with children age 1 to 2 years the most common victims [22].
Alkaline substances usually cause more severe damage than acids because they saponify phospholipid membranes. This action leads to rapid epithelial cell death and caustic penetration into the eye. Concentrated ammonia can inflict severe injury to anterior ocular structures after less than one minute of exposure, and lye can cause deep eye injury within three to five minutes leading to irreversible blindness [20]. Glaucoma is a potential long-term sequelae from the internal damage caused by alkaline exposure. Acid burns cause coagulation necrosis that may result in sight-threatening corneal ulceration and scarring, but tend to be self-limited.
Patients with chemical eye burns present with decreased vision, moderate to severe eye pain, blepharospasm (inability to open the eyelids), conjunctival redness, and photophobia. In severe cases of alkali exposure, the eye may appear white due to ischemia of the conjunctiva and scleral vessels (picture 1).
Many solvents penetrate the cornea or eye only to a limited extent and irrigation longer than 15 to 30 minutes may not be necessary. However, with any significant ocular exposure to alkali or acid, ophthalmologists generally recommend continuous irrigation until a neutral pH is achieved in the eye [20,23-25]. Water or isotonic saline may be used. Irrigation initiated at the scene is continued at the emergency department. If available, we suggest that a buffered eye wash solution (eg, Diphoterine, Cederroth) be used to irrigate any significant ocular exposure to alkali or acid. Observational evidence suggests that the use of these solutions reduces the severity of eye injury [16,26-28].
Once at the hospital, prolonged irrigation is best performed using intravenous tubing and a polymethylmethacrylate scleral lens (ie, Morgan lens) (figure 1 and picture 2 and picture 3 and picture 4). While convenient, a Morgan lens may leave some material trapped in the fornices. Direct manual irrigation is preferred when retained material (eg, cement, plaster) must be removed.
If a Morgan lens is not available, it is important to keep the eyelids retracted for maximal exposure of the conjunctiva and cornea. If a concomitant globe rupture or penetrating injury is suspected or confirmed, a Morgan lens should not be used, and only careful, gentle irrigation is advised to avoid exacerbating the injury [29]. (See "Open globe injuries: Emergency evaluation and initial management".)
It is often necessary to apply topical analgesics to an eye that has sustained a chemical injury to permit irrigation and examination. Proparacaine (one to two drops of 0.5 percent) may be used; repeat doses may be needed. Intravenous analgesics should be used to supplement topical treatment as necessary.
A "normal" eye pH depends upon the method of measurement. Typically a pH of 6.5 to 7.5 is considered normal, particularly if using pH paper. Urine dipsticks, which contain litmus paper, can be used safely to measure the ocular pH [30]. If only one eye is affected, the uninvolved eye should be used to determine the normal pH. Measurements of pH are generally taken at the fornix (region between the conjunctiva and the lower eyelid).
Initial irrigation is performed continuously for 30 minutes before assessing pH. Thereafter, pH is reassessed every 15 to 30 minutes until it is in the neutral range. Irrigation alone is insufficient to normalize pH if there is caustic particulate matter embedded in the globe or sequestered in the fornices. Therefore, after initial irrigation, the eyelids must everted and particulate matter removed by gentle swabbing with a moistened cotton or synthetic fiber swab. Facial exposure to cement, drain cleaner, explosives, and fireworks all have a tendency to cause particulate matter or depots of alkali to become embedded or sequestered in the fornices.
Occasionally, more than two hours may be required to achieve a neutral pH at the eye surface. The pH should be remeasured at 5 and 30 minutes after the completion of irrigation to confirm that a neutral pH has been maintained. If these measurements are abnormal, attention should be directed toward removing any particulate matter before irrigation is continued for another 30 minutes. The cycle of remeasuring pH and irrigating is continued until a neutral pH is achieved and maintained.
Weak acids do not readily penetrate into the anterior chamber. Therefore, prolonged irrigation is not generally necessary. However, with alkali burns, irrigation should be continued for two to three hours regardless of the eye surface pH in order to normalize the pH of the anterior chamber. Once irrigation is complete, a broad spectrum topical antibiotic (eg, erythromycin ointment; polymyxin/trimethoprim drops) should be applied to the eye following any alkali or other severe exposure. Management of corneal injuries, including antibiotic selection, is reviewed separately. (See "Corneal abrasions and corneal foreign bodies: Management", section on 'Management'.)
Immediate ophthalmologic consultation is mandatory for significant eye exposures. Severe burns occasionally require prolonged continuous irrigation, which may exceed 12 hours [30].
Chemicals NOT treated with immediate water irrigation — Immediate water irrigation is contraindicated for a few chemicals because it causes a harmful exothermic (heat-producing) reaction or releases hazardous byproducts. Such chemicals include dry lime, phenol, and metals such as elemental potassium and sodium (table 3). In the event of ocular exposure, the fornices should be inspected and swabbed.
●Dry lime should be brushed off the skin prior to irrigation. It contains calcium oxide, which reacts with water to form calcium hydroxide, a strong alkali. (See 'Alkali' below.)
If water irrigation is begun inadvertently, it is important to stop as soon as the presence of dry lime is recognized and to brush off any remaining particles prior to restarting water irrigation. Intravenous pain medication is likely to be needed in such instances.
●Elemental metals and certain reactive metal compounds combust or release hazardous byproducts when exposed to water. Examples include: sodium, potassium, magnesium, phosphorous, lithium, cesium, and titanium tetrachloride. All fragments of such materials should be carefully removed with dry forceps and placed in a nonaqueous solution (eg, mineral oil). Once this is done, the affected area should be covered with mineral oil (or a comparable nonaqueous solution) to prevent further exposure to air and moisture. The mineral oil may be wiped off and reapplied to ensure that any remaining metal fragments are removed. Surgical debridement may be necessary if fragments are embedded in the skin.
●Phenol is not readily soluble in water. Removal of phenol requires that it be wiped off the skin by sponges soaked in 50 percent polyethylene glycol (PEG). Decontamination may be started with large amounts of water until PEG is obtained. It is important to use copious amounts of water because dilute solutions of phenol are more rapidly absorbed through the skin. (See 'Phenol (carbolic acid) and derivatives' below.)
Antidotes — Antidotes do not play a major role in the treatment of most chemical burns. Water irrigation is of primary importance and should not to be delayed while an antidote is sought. (See 'Irrigation' above.)
There are a few toxic substances that require antidotal treatment. As an example, hydrofluoric acid burns cause intense pain and tissue destruction, as well as electrolyte abnormalities that may precipitate cardiac arrest. Calcium salts are the mainstay of treatment of hydrofluoric acid burns; the dose and route depend upon the clinical situation. (See 'Hydrofluoric acid' below.)
White phosphorus is found in military explosives and fireworks. In the past, some toxicologists recommended treating white phosphorus burns with 1 or 2 percent copper sulfate solution along with copious water irrigation [31]. However, the copper solution can be toxic, and we do not recommend its use. (See 'White phosphorus' below.)
Burn assessment — Chemical burns can be difficult to assess and burns that appear superficial may be associated with severe deep tissue injury. As a result, the extent of injury is often underestimated, leading to insufficient irrigation [31]. To avoid such mistakes, we recommend that clinicians err on the side of treating with copious water irrigation. Frequent reexamination of the patient and all wounds should be performed with any chemical burn.
Systemic toxicity — Toxic chemicals absorbed through the skin can cause systemic toxicity, and inhaled chemical vapors can cause both systemic toxicity and lung injury. Management of such exposures can be complex and we recommend that clinicians consult with a medical toxicologist or poison control center. (See 'Additional resources' below.)
Vaping (e-cigarettes) — A series of case reports describe burns sustained by users of vaping devices, which have become popular and include millions of users in the United States alone [32,33]. Explosions of lithium batteries have resulted in significant thermal burns, including a case of systemic absorption of chemicals found in the devices. In one case, toxicology consult was obtained due to elevated plasma levels of cobalt and manganese from burns sustained from a vaping device [32]. Lithium levels were also obtained but were within normal limits. (See "Vaping and e-cigarettes", section on 'Adverse health effects'.)
Treatment of thermal burns from chemical exposure — Chemical burns differ from thermal burns in that they continue to cause damage as long as some active component of the chemical remains in the wound [2]. Chemical burns heal slowly and generally require a hospitalization period that is 30 percent longer than a thermal burn of comparable surface area and depth [2].
Other than the importance of immediate decontamination, including extensive water irrigation, the principles of management for chemical burns are similar to those for thermal injuries. These include rapid airway assessment and stabilization as indicated, fluid resuscitation, tetanus prophylaxis, and analgesia. Like thermal burns, chemical burns to a large body surface area can lead to significant fluid shifts requiring treatment with aggressive intravenous fluid resuscitation. Topical antibiotics should be applied to all nonsuperficial burns. The management of thermal burns is reviewed elsewhere. (See "Emergency care of moderate and severe thermal burns in adults".)
SPECIFIC AGENTS AND TREATMENTS
Riot control agents (eg, pepper spray) — Riot control agents can cause not only topical burns but also direct trauma, ocular damage, and pulmonary complications. The management of ocular exposure from these chemicals does not differ and is discussed above; assessment and management of other aspects of these agents are reviewed separately. (See 'Eye exposure' above and "Chemical terrorism: Rapid recognition and initial medical management", section on 'Crowd-control agents'.)
Acids — Inorganic and organic acids denature the skin's proteins, ultimately causing coagulation necrosis. The agent involved often determines the color of the coagulum. As examples, nitric acid causes a yellow eschar, while sulfuric acid causes a black or brown eschar. Initial treatment in the majority of cases consists of extensive irrigation with water. A table summarizing the signs and symptoms of some common chemical burns is provided (table 1). (See 'Irrigation' above.)
Hydrofluoric acid — Hydrofluoric acid (HF) is a highly corrosive inorganic acid with numerous applications. It is widely used in glass etching, electronic industries, and cleaning solutions. When hydrofluoric acid contacts skin, it causes both local injury and a potentially fatal systemic reaction [34]. Solutions with concentrations of 15 percent or greater cause symptoms immediately, while less concentrated solutions may take hours but remain capable of causing severe injury [35].
HF penetrates quickly through the epidermal layer into the dermis and deeper. Fluoride ions complex with calcium and magnesium, which can lead to hypocalcemia and hypomagnesemia [36,37]. These electrolyte abnormalities and the direct cardiotoxic effects of fluoride ions contribute to the development of cardiac arrhythmias, which are the primary cause of death in HF burns [38,39]. Hypocalcemia may stimulate an efflux of potassium ions from cells resulting in hyperkalemia, and predisposing to cardiotoxicity [40,41]. QTc interval prolongation, due to hypokalemia, hypomagnesemia, and/or hypocalcemia may be seen. (See "Acquired long QT syndrome: Definitions, pathophysiology, and causes", section on 'Metabolic abnormalities'.)
Ophthalmic injury from topical HF exposure can be severe [42], and inhalation of HF vapor can cause severe pulmonary injury [43].
Management of hydrofluoric acid burns — Symptomatic hydrofluoric acid (HF) burns are treated with copious water irrigation and calcium. Calcium ions complex free fluoride ions to prevent further toxicity, and also help to correct cellular and systemic hypocalcemia. Initial treatment consists of applying calcium gluconate gel (2.5 percent) to burned areas [44,45].
Commercially available calcium gel may be used or it can be made by mixing 3.5 g of calcium gluconate powder with approximately 140 g (5 oz) of water soluble surgical lubricant. The gel is massaged into the skin for 30 to 60 minutes. Topical calcium gel treatment may be repeated as necessary. The patient or clinician performing the massage should wear two pairs of surgical gloves.
Many HF injuries occur on the hands and upper extremities. To treat hand burns, the gel can be put in a surgical glove, which is then placed on the patient's hand and used as a dressing over the burn. Inactivation of free fluoride ions by the calcium results in pain relief.
If pain persists following a topical exposure despite initial treatment, 5 percent calcium gluconate (0.5 mL per square cm of wound area) may be injected intradermally directly into and around the affected areas. Injection directly into digits is not recommended [1]. Resolution of pain suggests that treatment is successful, and generally occurs soon after injection.
If within approximately one hour local pain is not adequately controlled by topical application or direct injection, calcium can be given via an artery or vein. Intraarterial injection of 10 to 15 mL of calcium gluconate in 40 mL of Ringer's lactate may be given via an arterial line in the affected extremity over three hours [35]. Arterial placement must be definitively confirmed (eg, arterial tracing on a pressure monitor) before injecting calcium gluconate, which is caustic to soft tissue. Alternatively, a mixture of 10 to 15 mL of 10 percent calcium gluconate and 3000 to 5000 IU of heparin may be added to 40 mL of Ringer's lactate and instilled intravenously using a Bier block [1,31,35,46].
Immediate treatment using intraarterial injection or a Bier block may be necessary in the setting of large burns or burns involving concentrated hydrofluoric acid. This is best done in consultation with a medical toxicologist or a comparable expert. (See 'Additional resources' below.)
Systemic toxicity from hydrofluoric acid — HF burns can lead to systemic toxicity resulting in severe electrolyte abnormalities, particularly hypocalcemia and hyperkalemia. Intravenous (IV) access, serum electrolyte concentrations, an electrocardiogram, and cardiac monitoring should be obtained in patients exposed to HF.
Inhalational exposures may be severe and the airway of any patient with such an exposure should be rapidly assessed and managed as indicated. Patients with inhalation injuries are treated with oxygen and nebulized calcium gluconate (4 mL of 2.5 to 5 percent). Succinylcholine is best avoided if rapid sequence intubation must be performed in the setting of HF exposure due to the possibility of hyperkalemia.
If systemic toxicity is suspected (due to QTc prolongation, cardiac arrhythmia, or obvious systemic illness), calcium is administered intravenously. Calcium gluconate can be given as 1000 mg (10 mL of a 10 percent solution) infused slowly over two to three minutes; several repeat doses may be necessary if profound hypocalcemia is present. In cases of systemic toxicity, we also give magnesium replacement (4 g IV over 20 minutes).
There is a case report of severe fluoride intoxication from hydrofluoric acid exposure resulting in severe burns and recurrent ventricular fibrillation successfully treated with emergency hemodialysis [47]. Hemodialysis is generally not considered standard treatment for HF acid toxicity. However, fluoride ions are renally excreted and therefore hemodialysis may be of benefit in the setting of renal failure.
Phenol (carbolic acid) and derivatives — Phenol is a colorless or white solid but is often sold in liquid form. It has a strong sweet odor and is widely used in disinfectants and in the production of resins and plastics. It is readily absorbed through the skin and across the lungs when its vapor form is inhaled. Severe dermal burns from phenol can cause severe systemic toxicity and death.
Phenol is only moderately soluble in water and swabbing merely spreads the chemical, increasing the area of absorption and thereby toxicity. The solvent polyethylene glycol (PEG) is used to remove phenol from the skin [31]. PEG can generally be found in hospital pharmacies or areas where phenol is used. After swabbing thoroughly with a 50 percent PEG 400 solution, exposed areas are then irrigated with copious amounts of water. Isopropanol or glycerol may be substituted if PEG is unavailable. Decontamination may be started with large amounts of water until PEG is obtained. It is important to use copious amounts of water because dilute solutions of phenol are more rapidly absorbed through the skin.
The toxicity of phenol depends upon the free plasma concentration. Systemic toxicity most often manifests as central nervous system or cardiac abnormalities [48]. CNS dysfunction can manifest as agitation, seizures, or coma, while cardiac dysfunction generally manifests as hypotension or dysrhythmia. Phenol also demyelinates peripheral nerves and causes lysis of erythrocytes.
White phosphorus — White phosphorus is a solid element that spontaneously ignites in air forming phosphorus pentoxide. White phosphorus is used as an incendiary agent in weapons and fireworks. Oxidation may produce yellow flame, while the production of white smoke indicates ongoing formation of phosphoric acid [49]. The corrosive action of phosphoric acids and the heat from their chemical reactions contribute to tissue damage.
White phosphorus produces a combined chemical and thermal burn. Particles of white phosphorus that become embedded in wounds can continue to oxidize, causing tissue damage, until debrided, treated, or consumed. Systemic toxicity can lead to severe hypocalcemia or hyperphosphatemia and hepatic necrosis. There is no reliable method to predict which patients will develop severe metabolic abnormalities. Death can occur from burns covering a total body surface area of only 10 to 15 percent. Serum calcium and phosphorus levels should be monitored for 48 to 72 hours while caring for these patients.
Following the removal of all clothing, the initial management of white phosphorus injuries consists of copious water irrigation. White phosphorus particles embedded in wounds must be kept wet; particles will reignite if allowed to dry. Wounds should be covered with saline-soaked gauze to prevent drying. Immediate surgical debridement is often necessary and repeated debridements may be needed to remove all phosphorus particles.
Animal studies demonstrate that vigorous water irrigation of white phosphorus wounds is superior to topical treatment with water soaked dressings, 3 percent copper sulfate solution, copper sulfate emulsion, or intralesional superoxide dismutase injection [49].
Copper sulfate solution is no longer considered an antidote for white phosphorus burns and is potentially dangerous: it is readily absorbed via the wound and can cause acute renal failure, cardiovascular collapse, and death [50]. We recommend that copper sulfate not be used in the treatment of white phosphorous exposure.
Alkali — Alkali agents dissolve proteins and collagen resulting in the formation of soluble protein complexes and causing extensive tissue damage (picture 5). The soluble protein complexes allow the alkali agent to penetrate deeper into tissues creating further damage and making irrigation more difficult. Alkali burns are notable for their degree of edema and fluid loss. Anhydrous ammonia and cement are among the more common causes of alkali burns. Initial treatment in the majority of cases consists of extensive irrigation with water. A table summarizing the signs and symptoms of some common chemical burns is provided (table 1). (See 'Irrigation' above.)
Anhydrous ammonia — Anhydrous ammonia is a colorless, pungent gas used extensively as a fertilizer and in the manufacturing of synthetic fibers and methamphetamine. The compound is usually stored as a pressurized liquid at -33º Celsius (-28º Fahrenheit). Exposures therefore often cause a combination of cold injury and alkali burn [51]. Injuries to eyes and lungs are common. Symptom severity and tissue damage from dermal exposure are related to the concentration of hydroxyl ions. Severe anhydrous ammonia burns result in black, leathery tissue, while less severe burns are grey-yellow and softer.
Anhydrous ammonia is extremely soluble in water and immediate treatment consists of copious water irrigation, once all clothing has been removed. Repeat irrigation should be performed every four to six hours for the first 24 hours. Eye exposures are treated with topical analgesics (eg, proparacaine one to two drops of 0.5 percent) and copious water irrigation. (See 'Eye exposure' above.)
Acute contact with high concentrations of ammonia damages the lung parenchyma via collagen degradation and other means and can produce laryngospasm and glottic edema. Mild pulmonary insults produce coughing, laryngitis, pharyngitis, or tracheobronchitis. Severe pulmonary injury results in pulmonary edema and bronchiectasis. We recommend early intubation for patients with significant facial or pharyngeal burns or signs of upper airway injury (eg, dyspnea, stridor, hoarseness, hemoptysis). There is no specific treatment for inhalation injury.
Anhydrous ammonia is a key ingredient for illicit methamphetamine production in makeshift laboratories. Producers of illicit methamphetamine often steal anhydrous ammonia from storage areas (eg, farms, industrial refrigeration systems, railroad tanker cars). During thefts, exposure can occur when valves of storage containers are left open while ammonia is removed [52]. (See "Methamphetamine: Acute intoxication".)
Cement burns — Wet cement is a poorly recognized and under-reported cause of alkali burns. A cement mixture has an initial pH of 10 to 12 that may rise as high as 14 as hydrolysis occurs and the cement sets.
Cement burn injuries occur most often on the lower legs and knees [53]. Presenting symptoms generally occur several hours after exposure and include burning sensations, erythema, pain, and vesicle formation. Twelve to 48 hours later, partial to full thickness burns become evident [54]. Treatment consists of copious water irrigation. In the event of ocular exposure, inspection and swabbing of the fornices is necessary.
Cement burns can be prevented by wearing appropriate skin protection. Many patients are unaware of the potential hazards of cement and fail to take preventive measures [55].
Automobile airbag burns — Several case reports document burns resulting from automobile airbag deployment. Airbags may occasionally perforate and release sodium azide or sodium hydroxide resulting in alkali chemical burns [56]. Thus, damaged, deployed airbags may cause both chemical and thermal injury. Clinicians may underestimate the degree of injury from such wounds, which may require aggressive treatment [57]. When treating patients with burns following airbag deployment, clinicians should ask the patient and paramedics whether the airbag was perforated. If eyes are involved, it is wise to swab and irrigate the fornices in the event that there is embedded or sequestered particulate matter.
Hydrocarbons — Hydrocarbons are ubiquitous. They can be found in a wide range of kitchen cleaning products, chemical solvents, and automobile products. Contact with gasoline and other hydrocarbons may cause dermatitis, itching, and inflammation. Significant burns and systemic toxicity may occur, especially in the setting of trauma, such as industrial or motor vehicle accidents.
Hydrocarbons cause cell membrane injury and dissolution of lipids, which results in skin necrosis with prolonged exposure [58]. Most burns are superficial or partial thickness. However prolonged exposure may cause full thickness burns. Once skin damage has occurred, hydrocarbons are readily absorbed. This can result in systemic toxicity, including severe pulmonary, neurologic, renal, cardiovascular, and gastrointestinal injuries [59].
Treatment of dermal exposure consists of removal from the scene and decontamination, including copious water irrigation. The management of systemic hydrocarbon toxicity is beyond the scope of this review and should be undertaken with the assistance of a toxicologist. (See 'Additional resources' below.)
Tar and asphalt — Tar is obtained from bituminous coal; asphalt is produced from crude petroleum. Both are used for paving and roofing. For construction use, both substances must be heated to high temperatures (approximately 140ºC for paving; approximately 245ºC for roofing). Thermal burns occur when heated tar or asphalt comes into contact with skin [60]. However, both tar and asphalt cool rapidly.
Treatment at the scene of injury consists of accelerating cooling by immediately applying cold water. In the emergency department, tar and asphalt can be removed by applying any of several organic solvents. Solvents that have been used successfully include: polymyxin-neomycin-bacitracin (ie, Neosporin) ointment, which has the added benefit of infection prophylaxis, polyoxyethylene sorbitan, petrolatum, sunflower oil, olive oil, butter, and baby oil [61-64].
Several hourly reapplications of the solvent may be necessary to remove the tar or asphalt. For minor exposures without complications, this may be done as an outpatient with follow-up the next day. Once the wound is clean, thermal burns are treated in standard fashion. (See "Emergency care of moderate and severe thermal burns in adults" and "Treatment of minor thermal burns".)
ADDITIONAL RESOURCES
Regional poison control centers — Management of chemical exposures can be complex and we recommend clinicians consult with a medical toxicologist or poison control center about specific exposures. Regional poison control centers in the United States are available at all times for consultation on patients with known or suspected poisoning, and who may be critically ill, require admission, or have clinical pictures that are unclear (1-800-222-1222). In addition, some hospitals have medical toxicologists available for bedside consultation. Contact information for poison centers around the world is provided separately. (See "Society guideline links: Regional poison control centers".)
The United States Department of Transportation publishes an Emergency Response Guidebook to help first responders managing a chemical spill or exposure to identify specific agents, protect themselves, and protect the general public during the initial response (www.phmsa.dot.gov/hazmat/library/erg). The handbook includes concise descriptions and tables for the initial management of many toxic chemicals.
PubChem, available through the United States National Library of Medicine, provides a searchable database with detailed information about a wide range of chemicals. The table of contents for each chemical includes sections on safety (including medical care of exposures) and toxicity.
The Unites States National Institute for Occupational Safety and Health (NIOSH) website includes a searchable database with information about a wide range of chemicals and management of toxic exposures.
Society guideline links — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Care of the patient with burn injury".)
INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, “The Basics” and “Beyond the Basics.” The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on “patient info” and the keyword(s) of interest.)
●Basics topic (see "Patient education: Chemical eye injury (The Basics)")
SUMMARY AND RECOMMENDATIONS
●Initial care – The potency and concentration of the toxic agent and the duration of contact primarily determine the degree of tissue destruction. (See 'General approach' above.) In the great majority of cases, the management of topical chemical burns consists of the following general steps:
•Ensure protection of rescuers and health care workers from exposure. (See 'Protection of providers' above.)
•Remove the patient from the area of exposure.
•Remove all clothing and jewelry.
•Brush any dry chemicals off the patient; any suitable instrument may be used (eg, dry brush, towel).
•Irrigate exposed tissue with copious amounts of water. The details of skin and eye irrigation are discussed in the text. (See 'Irrigation' above.)
●Importance of thorough decontamination – Complete removal of the toxic chemical is essential. Tissue damage continues for as long as the chemical remains in contact with skin. Furthermore, destruction of the epidermis allows substances to reach the dermis, which is more permeable to chemical toxins and may permit systemic absorption. A table summarizing the signs and symptoms of some common chemical burns is provided (table 1).
●Rare chemicals not initially irrigated with water – A small number of chemicals should not be treated with immediate water irrigation. These include dry lime, phenol, and metals such as elemental potassium and sodium (table 3). (See 'Chemicals NOT treated with immediate water irrigation' above.)
●Difficulty of burn assessment – Chemical burns can be difficult to assess, and burns that appear superficial may be associated with severe deep tissue injury. As a result, the extent of injury is often underestimated, leading to insufficient irrigation. We recommend that clinicians err on the side of treating with copious water irrigation. Frequent re-examination of the patient and all wounds is crucial. (See 'Burn assessment' above.)
●Burn care – Other than the importance of immediate decontamination, the principles of management for chemical burns are similar to those for thermal injuries. These include rapid airway assessment and stabilization as indicated, fluid resuscitation, tetanus prophylaxis, topical antibiotics, and analgesia. (See "Emergency care of moderate and severe thermal burns in adults".)
●Antidotes – Antidotes do not play a major role in the treatment of most chemical burns. Hydrofluoric acid is an important exception. (See 'Management of hydrofluoric acid burns' above.)
●Systemic toxicity and clinical resources – Toxic chemicals absorbed through the skin can cause systemic toxicity, and inhaled chemical vapors can cause both systemic toxicity and lung injury. Management of such exposures can be complex, and we recommend that clinicians consult with a medical toxicologist or poison control center. (See 'Additional resources' above.)
●Alkali and specific chemical injuries – Alkali burns cause greater tissue destruction than comparable acid burns. The management of common chemical burns is described in the text. (See 'Specific agents and treatments' above.)
