Topical chemical burns: Initial evaluation and management

INTRODUCTION — Chemical burns are unique injuries that require individualized evaluation and management depending upon the causative agent. They are often occupational exposures and account for 4 percent and up to 14 percent of admissions to burn units in resource-abundant and resource-limited settings, respectively [1,2].

Many chemicals are manufactured for household, agricultural, industrial, and military use, with an estimated 60,000 new chemicals produced each year [3]. Management is guided by organizing these chemicals into general categories, although some have overlapping properties or incompletely understood pathophysiology.

The evaluation and management of common topical chemical burns will be reviewed here, with a focus on the basic principles of management. Thermal burns, caustic ingestions, eye injuries, chemical warfare, and an overview of common occupational exposures are discussed elsewhere.

●(See "Emergency care of moderate and severe thermal burns in adults".)

●(See "Caustic esophageal injury in adults" and "Caustic esophageal injury in children".)

●(See "Overview of eye injuries in the emergency department" and "Approach to diagnosis and initial treatment of eye injuries in the emergency department" and "Corneal abrasions and corneal foreign bodies: Clinical manifestations and diagnosis".)

●(See "Chemical terrorism: Rapid recognition and initial medical management".)

●(See "Common occupational chemical exposures: General approach and management of selected exposures".)

ALL PATIENTS

Overview of approach — Chemical burns require immediate treatment because the duration of contact, in addition to the potency and concentration of the toxic agent, determines the degree of tissue destruction. In most cases, the management of topical chemical burns consists of the following:

●Ensure protection of rescuers and health care workers from exposure

●Remove the patient from the exposure scene

●Remove all clothing and jewelry

●Brush off any dry chemicals (any suitable instrument such as dry brush or towel can be used)

●Copious water irrigation

The most important component of active therapy is thorough irrigation of all wounds and areas of exposure with copious amounts of water [4]. We recommend that clinicians err on the side of copious irrigation even if a burn appears superficial. Skin decontamination typically occurs after airway, breathing, and circulation are addressed, but may need to be performed during the initial resuscitation in the critically ill-patient.

Ideally, water irrigation is started immediately at the scene of exposure since pre-hospital irrigation reduces burn severity and the length of hospitalization [5]. Many first responder systems (eg, emergency medical personnel, fire departments) will decontaminate and irrigate the patient using portable decontamination units prior to entering the hospital. Decontamination can also be performed by hospital-based decontamination teams and/or emergency department staff. Hazardous substance decontamination plans are generally determined by the hospital's disaster planning committee and local and state emergency management agencies.

The principles of management of chemical burns are similar to those for thermal injuries (with the addition of clinician protection, immediate decontamination, and extensive irrigation). These include airway stabilization as needed, fluid resuscitation, tetanus prophylaxis, and analgesia. 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 non-superficial burns. The management of thermal burns is presented in the algorithm (algorithm 1) and discussed separately. (See "Emergency care of moderate and severe thermal burns in adults".)

Protection of clinicians — Before irrigating a patient with chemical burns, first responders and clinicians must don appropriate protective gear to prevent contamination or injury. The necessary clothing and equipment depends upon the type of threat and the duration of exposure. Available equipment varies considerably among first responder systems and hospitals. In the United States, the Occupational Safety and Health Administration (OSHA) classification system is often used to describe the levels of personal protection [6,7]:

●Level A: Maximal protection that 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

For most hospital decontaminations of an unknown substance, OSHA believes the following protection is adequate for those working in the decontamination zone [8]:

●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 (with openings 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 decontaminated 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).

Assess for inhalational injury or systemic toxicity — Some chemicals are absorbed through the skin or produce vapors absorbed through the lungs and cause systemic toxicity and/or cause airway/lung injury from inhaled caustic vapors. 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.)

The presence of dyspnea, cough, hoarseness, drooling, stridor, tachypnea, decreased breath sounds, wheezing, rales, rhonchi, or use of accessory respiratory muscles suggests a caustic chemical inhalation with upper airway or lung parenchymal edema or injury. Tracheal intubation and/or direct airway examination are frequently required, which is discussed separately. (See "Inhalation injury from heat, smoke, or chemical irritants" and "Common occupational chemical exposures: General approach and management of selected exposures", section on 'Dyspnea, cough, or wheezing'.)

Crowd-control agents (eg, oleoresin capsicum, pepper spray, mace) can also cause respiratory symptoms such as stridor, drooling, hoarseness, laryngospasm, or wheezing, which often resolve with removal from the exposure and fresh air. Further management and other pulmonary complications are discussed separately. (See "Chemical terrorism: Rapid recognition and initial medical management", section on 'Crowd-control agents'.)

Examples of systemic toxicity from selected agents include the following and are discussed below:

●Hydrofluoric acid: QTc prolongation, ventricular dysrhythmia, hypocalcemia, hyperkalemia, hypomagnesemia (see 'Hydrofluoric (HF) acid' below)

●Phenols: agitation, seizures, coma, hypotension, dysrhythmia (see 'Phenol (carbolic acid) and derivatives' below)

●White phosphorous: hypocalcemia, hyperphosphatemia, hepatic necrosis (see 'White phosphorus' below)

●Hydrocarbons: pulmonary, neurologic, kidney, cardiovascular, gastrointestinal injuries (see 'Hydrocarbons' below)

Skin 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 chemicals and may permit systemic absorption.

Prior to irrigation — Remove all clothing (including footwear and jewelry) and brush off all dry agents. Any suitable instrument can be used, such as a dry brush or towel. A small number of chemicals (eg, dry lime, phenols, elemental metals) should not be immediately irrigated with water. (See 'Chemicals NOT treated with immediate water irrigation' below.)

Water irrigation — Continue water irrigation if already started at the scene of exposure, otherwise immediately begin irrigation with copious amounts of water. Copious irrigation with water dilutes and removes the large majority of chemicals (a common mnemonic is: "the solution to pollution is dilution") [4].

●Irrigation technique – Moderately warm water in high volumes but at low pressures should be used for irrigation. Either a shower or a hose can be used. During cold weather, warmer water is needed to prevent hypothermia. High pressure irrigation should be avoided as it can splash chemicals on to unexposed areas and drive them deeper into tissue [9].

Irrigation should begin at the site of contamination and the eyes and face, if they are involved, followed by adjacent to the exposed area. Decontamination of the face prevents further inhalation or ingestion of any toxin.

A patient with an exposure to a strong acid should also 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. 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, the most important factor in mitigating tissue damage is early decontamination [11].

●Duration of irrigation – For acid or alkali skin exposure, we suggest continuous water irrigation until the pH of any exposed tissue becomes neutral. Compared with acid burns, alkali burns may require a much longer period of irrigation; two hours or more of continuous irrigation may be required before the pH of tissue exposed to a strong alkali returns to neutral. However, evidence is insufficient to guide the method and duration of water irrigation.

●Alternatives to water for acid or alkali exposure – Some experts prefer the following irrigation fluids:

•Diphoterine – This amphoteric, hypertonic, polyvalent, chelating solution is used in Europe as a first-line irrigation solution for both alkaline and acidic exposures, primarily in industrial settings. Studies suggest that it is well tolerated, free of harmful effects, and potentially a good first-line decontaminating agent [12-16]. However, evidence is insufficient that Diphoterine (and similar buffered solutions such as Cederroth) are substantially superior to water irrigation, and concerns have been raised about bias stemming from industry-sponsored research [12,17,18]. The delivery system uses a pressurized canister that physically removes substances in addition to Diphoterine's chemical effects and thus, the US Food and Drug Administration (FDA) and the European Union classify it as a medical device.

•Acetic acid – Neutralization of alkali burns using a weak acid, such as 5 percent acetic acid (household vinegar), may be a useful treatment, but evidence is insufficient to recommend routine use [19].

●Following irrigation – Measure the pH approximately 5 to 10 minutes after stopping irrigation to ensure the immediate post-irrigation measurement accurately excludes any residual chemical rather than reflecting the water used for irrigation [9]. Some experts suggest cleaning the exposed area with a mild soap following irrigation.

Once imminent threats to human health and life are addressed, make reasonable efforts to contain and mitigate environmental damage. 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.

Chemicals NOT treated with immediate water irrigation — Do not immediately perform water irrigation for exposure to chemicals that causes a harmful exothermic (heat-producing) reaction or releases hazardous byproducts. Examples include dry lime, phenol, and metals such as elemental potassium and sodium; selected chemicals requiring specific decontamination are presented in the table (table 1).

●Dry lime – This should be brushed off the skin prior to irrigation. It contains calcium oxide, which reacts with water to form calcium hydroxide, a strong alkali. If water irrigation is begun inadvertently, stop irrigation as soon as the presence of dry lime is recognized, brush off any remaining particles, and then restart water irrigation; intravenous pain medication will also likely be needed.

●Elemental metals – Elemental sodium, potassium, magnesium, phosphorous, lithium, cesium, and certain reactive metal compounds (eg, titanium tetrachloride) combust or release hazardous byproducts when exposed to water. All fragments of such materials should be carefully removed with dry forceps and placed in a non-aqueous solution (eg, mineral oil). Afterwards, 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 – Removal requires wiping off the skin with sponges soaked in 50 percent polyethylene glycol (PEG) since phenol is not readily soluble in water. 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.)

Burn assessment — Similar to thermal burns, assess the extent and depth of burn injury. The Lund-Browder chart (figure 1), the "Rule of Nines", and the palm method are discussed separately. (See "Assessment and classification of burn injury", section on 'Extent of burn injury'.)

However, the extent of injury from a topical chemical burn is often underestimated, and can lead to insufficient irrigation [20]. 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].

Burns that appear superficial may be associated with severe deep tissue injury. Frequent reexamination of the patient and all wounds should be performed with any chemical burn. Occasionally, wounds may need to be reassessed for days to weeks to truly determine the extent and depth of injury. 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].

A table summarizing the signs and symptoms of some common chemical burns is provided (table 2). Wounds can have various discoloration depending on the agent involved.

Limited role for antidotes — Antidotes do not play a major role in the treatment of most chemical burns. Water irrigation is of primary importance and should not be delayed while an antidote is sought. (See 'Water 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 (HF) acid' below.)

PATIENT WITH EYE EXPOSURE — Eye contact with a caustic chemical requires immediate evaluation and treatment to prevent permanent vision loss. Immediate water irrigation reduces the risk for chronic conjunctivitis and sight-threatening corneal ulceration. However, for ocular exposure to dry lime, wet plaster/cement, phenol, or metals such as elemental potassium and sodium, the fornices should be inspected and swabbed prior to irrigation. (See 'Chemicals NOT treated with immediate water irrigation' above.)

Chemicals commonly associated with ocular burns and their typical uses are presented in the table (table 3) [21,22]. In the United States, chemical ocular burns occur most often in residential settings, with children age 1 to 2 years the most common victims [23].

Clinical manifestations — Chemical eye burns cause decreased vision, moderate to severe eye pain, blepharospasm (inability to open the eyelids), conjunctival redness, and photophobia. In severe cases (as may occur with alkali exposure), the eye may appear white due to ischemia of the conjunctiva and scleral vessels (picture 1).

Burn severity depends upon the chemical involved, duration of exposure, and depth of penetration:

●Acids – These cause coagulation necrosis that may result in sight-threatening corneal ulceration and scarring but tend to be self-limited. (See 'Acids' below.)

●Alkali – These usually cause more severe damage than acids because they saponify phospholipid membranes, which causes a liquefactive necrosis, 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 and irreversible blindness within three to five minutes [21]. Glaucoma is a potential long-term sequelae from the internal damage caused by alkaline exposure. (See 'Alkali' below.)

Initial irrigation — Irrigation initiated at the scene is continued at the emergency department. Prior to performing an exhaustive eye examination, grossly inspect the eye, remove contact lenses, measure the pH, and perform initial irrigation continuously for 15 to 30 minutes.

●Ocular pH measurement – Ocular pH is generally taken at the fornix using litmus paper. Urine dipsticks, which contain litmus paper, can also be used safely to measure the ocular pH [24]. We recommend measuring the pH before irrigation at the hospital but not at the exposure scene. Ideally, the pH should be measured before instillation of topic anesthetic, but if not feasible, we wait five minutes before checking pH to prevent measuring the pH of the anesthetic itself. The pH measurement takes seconds to perform, establishes a baseline, and helps to prognosticate on the clinical course.

●Analgesia – We apply a topical anesthetic agent 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.

●Irrigation technique and fluid – In general, water or isotonic saline can be used for irrigation. The irrigation technique and optimal fluid depend on available equipment, agent of exposure, and suspicion for concomitant injury:

•Scleral lens (Morgan lens) if available – Prolonged irrigation using intravenous tubing and a polymethylmethacrylate scleral lens (Morgan lens) (figure 2 and picture 2 and picture 3 and picture 4) is simple, convenient, and effective. However, the Morgan lens causes discomfort and may leave some material trapped in the fornices, and thus requires careful forniceal exploration. (See 'Subsequent decontamination, irrigation, and pH interpretation' below.)

•Scleral lens not available or exposure likely to leave retained material (eg, cement, wet plaster) – In these situations, we prefer direct manual irrigation, which is more labor intensive compared with the Morgan lens. It is important to keep the eyelids retracted for maximal exposure of the conjunctiva and cornea. In a young child who cannot cooperate, physical restraint using a sheet wrap or procedural sedation (for prolonged irrigation) may be needed.

•Suspected/confirmed concomitant globe rupture or penetrating injury – Do not use a Morgan lens and only careful and gently irrigate to avoid exacerbating the injury [25]. (See "Open globe injuries: Emergency evaluation and initial management".)

•Significant ocular alkali or acid exposure – We suggest irrigation with a buffered eye wash solution (eg, Cederroth, Diphoterine), if available. Observational evidence suggests that the use of these solutions reduces the severity of eye injury [16,26-28]. If not available, use water or isotonic saline.

Subsequent decontamination, irrigation, and pH interpretation

●Forniceal exploration – After initial irrigation, evert the eyelids and remove any particulate matter by gentle swabbing the fornices (region between the conjunctiva and the lower eyelid) with a moistened cotton or synthetic fiber swab. Irrigation alone is insufficient to normalize pH if there is caustic particulate matter embedded in the globe or sequestered in the fornices. Facial exposure to cement, wet plaster, 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.

●Duration of irrigation and pH interpretation – A patient with significant ocular alkali or acid exposure requires continuous irrigation until a neutral pH is achieved in the eye [21,29-31]. Eye pH should be remeasured every 15 to 30 minutes during irrigation.

Many solvents only minimally penetrate the cornea or eye and irrigation longer than 15 to 30 minutes may not be necessary. Weak acids do not readily penetrate into the anterior chamber.

•Ocular pH interpretation – 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 litmus paper. If only one eye is affected, the uninvolved eye should be used to determine the normal pH.

•Persistent pH abnormality – Occasionally, more than two hours may be required to achieve a neutral pH at the eye surface. If the pH measurements continue to be abnormal after two hours, reevaluate the fornices for any particulate matter before irrigation is continued.

•Alkali burns – Irrigation should be continued for at least two to three hours regardless of the eye surface pH in order to normalize the pH of the anterior chamber. Severe burns occasionally require prolonged continuous irrigation, which may exceed 12 hours, and should be managed in consultation with an ophthalmologist [24].

●After irrigation completed (pH in neutral range) – Remeasure the pH at 5 and 30 minutes after the completion of irrigation to confirm that a neutral pH has been maintained. The measurement following 30 minutes is to exclude a change in ocular surface pH from the slow release of ions from inside the eye; the internal ocular pH is responsible for long-term damage. Perform a complete eye examination, which is discussed in detail separately. (See "Approach to diagnosis and initial treatment of eye injuries in the emergency department", section on 'Sequential eye examination'.)

We apply a broad spectrum topical ophthalmic antibiotic (eg, erythromycin ointment; polymyxin/trimethoprim drops) following any alkali or other severe exposure. Management of corneal injuries, including antibiotic selection, is discussed separately. (See "Corneal abrasions and corneal foreign bodies: Management", section on 'Management'.)

A significant eye injury (eg, anything beyond superficial scleral or corneal abrasion) requires immediate ophthalmologic consultation. Otherwise, follow-up with an ophthalmologist should be arranged for the next day.

SPECIFIC CONSIDERATIONS FOR SELECTED AGENTS

Acids — These 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 (table 2). Initial treatment in the majority of cases consists of extensive irrigation with water. (See 'Water irrigation' above.)

Hydrofluoric (HF) acid

●Sources and chemical properties – Hydrofluoric acid (HF) is a highly corrosive inorganic acid with numerous applications. It is widely used in a variety of industries that include etching, semiconductors, electronics, laboratories, and cleaning solutions.

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 [32,33]. Hypocalcemia may stimulate an efflux of potassium ions from cells resulting in hyperkalemia, and predisposing to cardiotoxicity [34,35].

●Clinical manifestations – When hydrofluoric acid contacts skin, it causes both local injury and a potentially fatal systemic reaction [36]. 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 [37]. HF burns are very painful and often cause blanching and/or blistering with surrounding erythema. Initial skin changes may underestimate the degree and extent of the final burn due to ongoing deep tissue injury from free fluoride ions. Many HF injuries occur on the hands and upper extremities.

Electrolyte abnormalities and the direct cardiotoxic effects of fluoride ions contribute to the development of cardiac dysrhythmias, which are the primary cause of death in HF burns [38,39]. QTc interval prolongation or ventricular dysrhythmia, due to hypocalcemia, hypomagnesemia, and/or hyperkalemia may be seen. (See "Acquired long QT syndrome: Definitions, pathophysiology, and causes", section on 'Metabolic abnormalities'.)

Inhalation of HF vapor can cause severe pulmonary injury [40]. Ophthalmic injury from topical HF exposure can be severe [41].

●Initial evaluation and management – In addition to above (see 'All patients' above), we obtain IV access, serum electrolyte (including calcium and magnesium) concentrations, an electrocardiogram, and cardiac monitoring in most patients exposed to HF. An exception is a patient with isolated fingertip burns (thus <1 percent total body surface area) following low-concentration exposure (symptom onset delayed by at least four hours and concentration <10 percent) since systemic toxicity would be extremely unlikely.

The airway of any patient with an inhalational HF vapor 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. (See "Inhalation injury from heat, smoke, or chemical irritants" and "Rapid sequence intubation in adults for emergency medicine and critical care", section on 'Neuromuscular blocking agents'.)

Immediate treatment using intraarterial calcium 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 'Regional poison control centers' below.)

●Management of HF dermal burns — In a patient with a symptomatic HF burn, we recommend treatment with a fluoride neutralizer (eg, calcium) in addition to copious water irrigation. Calcium ions complex free fluoride ions; the inactivation of free fluoride ions results in pain relief, prevents further cellular injury, helps to correct cellular hypocalcemia, and potentially prevents systemic hypocalcemia.

•Use and preparation of topical calcium gel – Initial treatment consists of topically applying calcium gluconate gel (2.5 percent) to burned areas, which is most effective within the first three hours following the exposure [42-44].

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. The patient or clinician performing the massage should wear two pairs of surgical gloves. Topical calcium gel treatment may be repeated as necessary.

•Finger or hand burns – The calcium 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. If there is evidence of nailbed burn, removing the nail to apply topical calcium may prevent need for subsequent debridement [44].

•Alternative to calcium gel – If calcium gel is unavailable or cannot be made, topical magnesium hydroxide antacid is an alternative but may be less effective [45].

•Persistent pain despite topical calcium – If pain persists despite initial topical 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 to 50 mL of Ringer's lactate or normal saline may be given via an arterial line proximal to the burn in the affected extremity over three hours [37,46]. 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 units of heparin may be added to 40 mL of Ringer's lactate and instilled intravenously using a Bier block [1,20,37,47]. Pediatric dosing for intraarterial or Bier block has not been established.

●Management of systemic HF toxicity – In a patient with suspected systemic toxicity due to HF (eg, QTc prolongation, ventricular dysrhythmia, hypocalcemia, hyperkalemia, hypomagnesemia, or other obvious systemic illness), calcium IV administration is required. We have a low threshold for administering calcium since ongoing calcium depletion can be occurring in the presence of free fluoride ions. Calcium gluconate can be given as 1000 mg (10 mL of a 10 percent solution) infused slowly over two to three minutes (children: 60 mg/kg or 0.6 mL/kg of 10 percent calcium gluconate; maximum single dose 1 g or 10 mL of a 10 percent solution); several repeat doses may be necessary if profound hypocalcemia is present. In cases of systemic toxicity, we also give magnesium replacement (adults: magnesium sulfate 4 g IV over 20 minutes; children: magnesium sulfate 25 to 50 mg/kg IV over 20 minutes, maximum dose 2 g).

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 [48]. 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

●Sources and chemical properties – 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 lungs (if vapor is inhaled).

●Clinical manifestations – Phenol causes dermal burns. Severe dermal burns can cause systemic toxicity, such as central nervous system (CNS) and cardiac abnormalities, and death [49]. CNS dysfunction can manifest as agitation, seizures, or coma. Cardiac dysfunction generally manifests as hypotension or dysrhythmia. Phenol also demyelinates peripheral nerves and lyses erythrocytes.

●Evaluation and management – Swab the skin thoroughly with a 50 percent polyethylene glycol (PEG) 400 solution to remove phenol from the skin [20]. PEG can generally be found in hospital pharmacies or areas where phenol is used. After swabbing, irrigate exposed areas with copious amounts of water. Phenol is only moderately soluble in water; swabbing with water prior to PEG merely spreads the chemical, increasing the area of absorption and toxicity. (See 'Skin decontamination' above.)

If PEG is unavailable, isopropanol or glycerol may be substituted. If there will be a delay to obtaining PEG, decontamination may be started with large amounts of water, followed by swabbing with PEG. It is important to use copious amounts of water because dilute solutions of phenol are more rapidly absorbed through the skin.

The systemic toxicity of phenol depends upon the free plasma concentration. Even though assays for phenol concentrations are offered by some laboratories, the results are typically not available in a timeframe to be useful for acute management.

White phosphorus

●Sources and chemical properties – 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 [50]. The corrosive action of phosphoric acids and the heat from their chemical reactions contribute to tissue damage.

●Clinical manifestations – White phosphorus produces a combined chemical and thermal burn. Particles of white phosphorus that become embedded in wounds can continue to oxidize and cause tissue damage until debrided, treated, or consumed. Systemic toxicity can include severe hypocalcemia or hyperphosphatemia and hepatic necrosis. Burns covering a total body surface area of only 10 to 15 percent can be fatal.

●Evaluation and management – Following the removal of all clothing, the initial management of white phosphorus injuries consists of copious water irrigation. (See 'Skin decontamination' above.)

Cover wounds with saline-soaked gauze to prevent drying. White phosphorus particles embedded in wounds must be kept wet; particles will reignite if allowed to dry. Immediate surgical debridement is often necessary, and repeated debridement may be needed to remove all phosphorus particles.

Monitor serum calcium and phosphorus concentrations for 48 to 72 hours. A reliable method does not exist that predicts which patients will develop severe metabolic abnormalities.

We recommend not treating with copper sulfate. Copper sulfate solution is potentially dangerous since it is readily absorbed from wounds and can cause acute renal failure, cardiovascular collapse, and death [51]. In the past, some toxicologists recommended treating white phosphorus burns with 1 or 2 percent copper sulfate solution along with copious water irrigation [20]. Animal studies have found 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 [50].

Alkali — These dissolve proteins and collagen forming soluble protein complexes and causing extensive tissue damage (picture 5). The soluble protein complexes permit the alkali agent to penetrate deeper into tissues creating further damage and complicating irrigation. 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. (See 'Water irrigation' above.)

Anhydrous ammonia

●Sources and chemical properties – Anhydrous ammonia is a colorless, pungent gas usually stored as a pressurized liquid at -33º Celsius (-28º Fahrenheit). It is very soluble in water. Anhydrous ammonia is used extensively as a fertilizer and in the manufacturing of synthetic fibers and methamphetamine (ie, illicit "meth labs"). 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].

●Clinical manifestations – Exposure often causes a combination of cold injury (since stored as a cold liquid) and alkali burn [53]. 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.

Injuries to eyes and lungs are common. Acute contact with high concentrations of ammonia causes laryngospasm and glottic edema and lung parenchymal damage via collagen degradation and other means. Mild pulmonary insults produce coughing, laryngitis, pharyngitis, or tracheobronchitis. Severe pulmonary injury can cause pulmonary edema and bronchiectasis.

●Evaluation and management – Immediate treatment consists of removing clothing and copiously irrigating with water. Repeat irrigation should be performed every four to six hours for the first 24 hours. (See 'Skin decontamination' above.)

Eye exposures are treated with topical analgesics (eg, proparacaine) and copious water irrigation. (See 'Patient with eye exposure' above.)

A patient with significant facial or pharyngeal burns or signs of upper airway exposure (eg, dyspnea, stridor, hoarseness, hemoptysis) requires early tracheal intubation. Inhalational injury is managed with supportive care; there is no specific treatment. (See "Inhalation injury from heat, smoke, or chemical irritants", section on 'Management overview'.)

Cement burns

●Sources and chemical properties – Wet cement is an under-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. Many patients are unaware of the potential hazards of cement and fail to take preventive measures, such as wearing appropriate skin protection [54].

●Clinical manifestations – Cement burn injuries occur most often on the lower legs and knees [55]. Signs and symptoms generally develop several hours after exposure and include burning sensations, erythema, pain, and vesicle formation. Partial to full thickness burns become evident 12 to 48 hours after exposure [56].

●Evaluation and management – Treatment consists of copious water irrigation. (See 'Skin decontamination' above.)

An ocular exposure requires inspection and swabbing of the fornices. (See 'Subsequent decontamination, irrigation, and pH interpretation' above.)

Automobile airbag burns

●Sources and chemical properties – Airbags may occasionally perforate during deployment and release sodium azide (reacts with water to form hydrazoic acid) or sodium hydroxide (an alkali) [57].

●Clinical manifestations – Damaged, deployed airbags may cause both chemical (acid or alkali) and thermal injury. Full-thickness burns have been reported [58].

●Evaluation and management – In a patient with burns following airbag deployment, ask the patient and paramedics whether the airbag was perforated. Such exposures require aggressive irrigation and may require advanced burn care. The degree of injury from such wounds may be underestimated [58]. (See 'Skin decontamination' above.)

If the eyes are involved, swab and irrigate the fornices in case there is embedded or sequestered particulate matter. (See 'Subsequent decontamination, irrigation, and pH interpretation' above.)

Hydrocarbons

●Sources and chemical properties – Hydrocarbons are found ubiquitously, including kitchen cleaning products, chemical solvents, and automobile products. Hydrocarbons cause lipid dissolution and cell membrane injury, and with prolonged exposure, this results in skin necrosis [59]. Hydrocarbons are readily absorbed through damaged skin.

●Clinical manifestations – Contact with gasoline and other hydrocarbons may cause dermatitis, itching, and inflammation. Most burns are superficial or partial thickness. However, prolonged exposure or significant trauma (eg, industrial or motor vehicle accidents) may cause full thickness burns and systemic absorption, resulting in severe pulmonary, neurologic, kidney, cardiovascular, and gastrointestinal systemic toxicity [60].

●Evaluation and management – Treatment of dermal exposure consists of removal from the scene and decontamination, including copious water irrigation. (See 'Skin decontamination' above.)

The management of systemic hydrocarbon toxicity is discussed separately and should be undertaken with the assistance of a toxicologist. (See "Acute hydrocarbon exposure: Management" and 'Regional poison control centers' below.)

Tar and asphalt

●Sources and chemical properties – Tar and asphalt are used for paving and roofing. Tar is obtained from bituminous coal; asphalt is produced from crude petroleum. Both substances must be heated to high temperatures for use in construction (approximately 140ºC for paving; approximately 245ºC for roofing), but both also cool rapidly.

●Clinical manifestations – Heated tar or asphalt cause both thermal and caustic chemical burns upon skin contact [61].

●Evaluation and management – Initial management at the exposure scene consists of accelerating cooling by immediately applying cold water. In the emergency department, tar and asphalt that is adherent to blistered skin should be removed with blister epithelium. Tar and asphalt that is adherent to intact skin can be removed by applying any of the following organic solvents: polymyxin-neomycin-bacitracin ointment (which has the added benefit of infection prophylaxis), polyoxyethylene sorbitan, petrolatum, sunflower oil, olive oil, butter, or baby oil [62-65].

Reapplications of the solvent hourly may be required for complete remove of the tar or asphalt. For minor exposures without complications, this may be done as an outpatient with a follow-up visit the next day. Once the wound is clean, the remaining burn is managed as a thermal burn. (See "Emergency care of moderate and severe thermal burns in adults" and "Treatment of minor thermal burns".)

Vaping devices (e-cigarettes) — Several case reports describe burns sustained by users of vaping devices [66,67]. Explosions of lithium batteries have resulted in significant thermal burns, including a case of systemic absorption of chemicals (cobalt, manganese) found in the devices, although lithium serum concentrations were not elevated. (See "Vaping and e-cigarettes", section on 'Adverse health effects'.)

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".)

Guidebook and databases — 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 5^th to 6^th 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 10^th to 12^th 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

●General principles of evaluation and management – Chemical burns require immediate treatment because the duration of contact, in addition to the potency and concentration of the toxic agent, determines the degree of tissue destruction. In most cases, the management of topical chemical burns consists of the following (see 'Overview of approach' above):

•Ensure protection of rescuers and health care workers from exposure (see 'Protection of clinicians' above)

•Remove the patient from the exposure scene

•Remove all clothing and jewelry

•Brush off any dry chemicals (any suitable instrument such as dry brush or towel can be used

•Copious water irrigation

A table summarizing the signs and symptoms of some common chemical burns is provided (table 2). The extent of injury from a topical chemical burn is often underestimated, and burns that appear superficial may be associated with severe deep tissue injury. Frequent reexamination of the patient and all wounds is required. (See 'Burn assessment' above.)

Antidotes do not play a major role in the treatment of most chemical burns, with the important exception of hydrofluoric acid. (See 'Limited role for antidotes' above.)

●Skin irrigation – Moderately warm water in high volumes but at low pressures (eg, from either a shower or hose) should be used for irrigation and continued until the pH of any exposed tissue becomes neutral. (See 'Skin decontamination' above.)

Some chemicals, such as dry lime, phenol, and elemental metals (table 1), should not be treated with immediate water irrigation. (See 'Chemicals NOT treated with immediate water irrigation' above.)

●Eye exposure – Eye contact with a caustic chemical (table 3) requires irrigation until a neutral surface eye pH is achieved. Some exposures are likely to leave retained material (eg, cement, wet plaster) and require forniceal exploration and swabbing. In a patient with significant ocular acid or alkali exposure, we suggest irrigation with a buffered eye wash solution (eg, Cederroth, Diphoterine) (Grade 2C). If not available, use water or isotonic saline. (See 'Patient with eye exposure' above.)

●Potential for inhalational injury or systemic toxicity – Some chemicals are absorbed through the skin or produce vapors absorbed through the lungs and cause systemic toxicity and/or cause airway/lung injury from inhaled caustic vapors, such as the following (see 'Assess for inhalational injury or systemic toxicity' above):

•Hydrofluoric acid: QTc prolongation, ventricular dysrhythmia, hypocalcemia, hyperkalemia, hypomagnesemia (see 'Hydrofluoric (HF) acid' above)

•Phenols: agitation, seizures, coma, hypotension, dysrhythmia (see 'Phenol (carbolic acid) and derivatives' above)

•White phosphorous: hypocalcemia, hyperphosphatemia, hepatic necrosis (see 'White phosphorus' above)

•Hydrocarbons: pulmonary, neurologic, kidney, cardiovascular, gastrointestinal injuries (see 'Hydrocarbons' above)

●Hydrofluoric (HF) acid – This corrosive inorganic acid can cause both local injury (can be delayed if exposure to low-concentration solution) and potentially fatal systemic toxicity from hypocalcemia, hypomagnesemia, and cardiac dysrhythmias. (See 'Hydrofluoric (HF) acid' above.)

•Dermal burns – Initial skin changes may underestimate the degree and extent of the final burn due to ongoing deep tissue injury from free fluoride ions. Thus, in a patient with a symptomatic HF burn, we recommend treatment with a fluoride neutralizer (eg, calcium) in addition to copious water irrigation (Grade 1C). We initially apply calcium gluconate gel (2.5 percent) to burned areas; resolution of pain suggests that treatment is successful and ongoing injury from free fluoride ions has ceased.

•Systemic toxicity – A patient with suspected systemic toxicity due to HF (eg, QTc prolongation, cardiac dysrhythmia, hypocalcemia, hypomagnesemia, or other obvious systemic illness) requires IV calcium. We have a low threshold for administering calcium since ongoing calcium depletion can be occurring in the presence of free fluoride ions. For adults, 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).