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Topical chemical burns: Initial evaluation and

management
��: Sangeeta Kaushik, MD, Steven Bird, MD, FACEP
�� : Richard G Bachur, MD, Maria E Moreira, MD, Matthew F Gardiner, MD, Michelle Ruha, MD
�� : Michael Ganetsky, MD
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Feb 2024.

This topic last updated: Oct 27, 2023.
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".)
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● (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.
2 of 40 3/19/24, 20:36
(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
3 of 40 3/19/24, 20:36
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
4 of 40 3/19/24, 20:36
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
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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
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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
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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.
8 of 40 3/19/24, 20:36
● 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.
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● 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.
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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)
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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,
12 of 40 3/19/24, 20:36
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
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● 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
14 of 40 3/19/24, 20:36
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
15 of 40 3/19/24, 20:36
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.)
16 of 40 3/19/24, 20:36
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
17 of 40 3/19/24, 20:36
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
18 of 40 3/19/24, 20:36
(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 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)")
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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
20 of 40 3/19/24, 20:36
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).
Use of UpToDate is subject to the Terms of Use.
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Topic 345 Version 40.0
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GRAPHICS
Initial burn management
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* ABCDE: Airway, Breathing, Circulation, Disability (neurologic evaluation), Exposure.
¶ Refer to UpToDate topics on the emergency care of moderate to severe burns.
Δ Useful for small or patchy burns. The entire palm surface including fingers is 1% in children and
adults, and approximately 0.5% excluding fingers.
Graphic 51484 Version 6.0
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Selected chemicals requiring specific decontamination
Toxin Classification Treatment
Bitumen (Tar) Caustic ▪ Copious irrigation with cold water until bitumen cools
and hardens.
▪ Bitumen that is adherent to blistered skin should be
removed with blister epithelium. Bitumen adherent to
unblistered skin should be covered liberally with a
hydrocarbon solvent (eg, mineral oil).
Hydrofluoric acid Caustic with ▪ Standard decontamination followed by application of

systemic toxicity 10% calcium gluconate gel. Parenteral calcium
administration by injection or venous or arterial
infusion may be required.
▪ Patient at risk for hypocalcemia.
Lime (calcium Caustic ▪ Brush off as much as possible prior to contact with
oxide) water.
Phenol Caustic with ▪ Irrigate with polyethylene glycol (PEG) 400.

systemic toxicity
Phosphorus Caustic ▪ Avoid exposure to air.

(elemental yellow ▪ Copious water irrigation, and keep covered with water.
phosphorus)
Radiation Acute radiation ▪ Obtain radiation monitoring device.

syndrome ▪ Protect personnel if patient is radioactive.
▪ Decontaminate from periphery to center of area of
exposure. Avoid creating new breaks in the skin. Allow
wounds to bleed freely. Collect urine and feces for signs
of internal decontamination.
Reactive metals Caustic ▪ Apply mineral oil and remove visible particles with
(eg, elemental forceps, gauze, or towels, then store removed particles
sodium, in mineral oil.
potassium,
lithium)
NOTE: The treatment protocols given here are theoretically optimal, but decontamination efforts
should not be delayed for a significant time to institute them.
Adapted with permission from: King C, Henretig FM (Eds). Skin decontamination. In: Textbook of Pediatric Emergency
Procedures, 2nd ed, Lippincott Williams & Wilkins 2008. Copyright © 2008 Lippincott Williams & Wilkins. www.lww.com.
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Modified Lund-Browder chart
Numbers refer to the percentage body surface area burned.
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Common signs and symptoms of chemical burns
Sulfuric acid Dark-brownish colored burns, mural perforation of the stomach,

cardiovascular collapse, dyspnea, pneumonia, sialorrhea, fever, rapid
decrease of blood pressure, tachypnea, severe pain in the mouth and
throat, hematemesis, blindness, chest pain (tightness), cough, dizziness.
Hydrofluoric acid Whitish tissue with surrounding erythema, immediate abdominal, mouth
and throat pain, skin edema, ulcers and necrosis, vomiting, fever, dyspnea,
stridor, laryngeal edema, wheezing, tachypnea, vomiting, tetany, cardiac
arrhythmias.
Acetic acid and Cough, tachypnea, wheezing, headache, nausea, vomiting, impaired
derivatives vision, abdominal pain, diarrhea, eye, nose and throat irritation, tooth
(glacial acetic, erosion, conjunctivitis, pharyngeal and pulmonary edema, whitish
trifluoroacetic, discoloration of the skin (exposure to trifluoroacetic acid).
& monochloroacetic
acids)
Nitric acid Yellowish discoloration of the skin and mucosas, whitish tinge of teeth,
eye, mouth, throat and abdominal burns and pain, dyspnea, hematemesis,
dizziness, cough, tachypnea, pneumonia, laryngospasm.
Hydrochloric acid White or grayish discoloration of the skin and mucosas, eye, mouth, throat
and abdominal burns and pain, hematemesis, vomiting, dizziness,
dyspnea, cough, tachypnea, pneumonia, laryngospasm, headache,
respiratory failure.
Hydrogen sulphide Greenish color of gray matter, "cherry-red" or pink lividity, green patches
in the skin, irritant of conjunctivae, sclera and the upper respiratory tract,
serous and hemorrhagic pulmonary edema, visceral congestion, bronchial
secretions, scattered petechiae, anorexia, headache, amnesia, dizziness,
photophobia, tearing, pain and blurred vision.
Sodium hydroxide Skin burns, oropharyngeal pain, dysphagia, vomiting, drooling and
excessive salivation, ulcerative mucosal burns, dyspnea, stridor,
perforation, and strictures can involve the entire gastrointestinal tract,
often in the upper esophagus, severe ocular injury, opacification and
perforation of cornea, microstomia, contracture of tongue and trismus,
diarrhea, severe abdominal pain, hematemesis, laryngeal edema.
Calcium hydroxide Allergic dermatitis, abrasions, eye and skin burns, erythema and vesicles,
ulcers covered with black necrosis, pulmonary edema, cough, nausea,
vomiting or severe abdominal pain.
Airbags inflation Skin abrasions and erythema, respiratory problems, sneezing, sore throat
and rhinorrhea.
Paraquat Skin burn, nails white discoloration, and ulcerated lesions in the lips,
tongue, oropharynx, esophagus (including perforation), stomach, scrotum
and trachea, pulmonary edema and fibrosis, multiorganic failure, seizures,
hematemesis.
30 of 40 3/19/24, 20:36
Vesicant – sulfur Skin burn, pruritus, erythema, xerosis, purpura, hypopigmentation,

mustard hyperpigmentation and blistering, chronic respiratory disease, repeated
respiratory infections, eye pain, swelling, and tearing, abdominal pain,
diarrhea, fever, nausea and vomiting.
White phosphorus Eye and respiratory tract irritation, sensation of a foreign body in the eye,
lacrimation, blepharospasm, photophobia, cornea perforation,
endophthalmitis, blindness, skin partial (second degree) to full thickness
burns.
Reproduced from: Dinis-Oliveira RJ, Carvalho F, Moreira R, et al. Clinical and forensic signs related to chemical burns: a
mechanistic approach. Burns 2015; 41:658. Table used with the permission of Elsevier Inc. All rights reserved.
31 of 40 3/19/24, 20:36
Chemicals commonly associated with ocular burns
Chemical substance Typical use
Alkali
Ammonia hydroxide (anhydrous ammonia) Cleansers
Fertilizer
Hair dyes and tints
Floor strippers
Calcium carbonate or magnesium carbonate Lime soil treatment
Calcium hydroxide Cement, plaster, or mortar
Sodium hydroxide Lye cleansers
Potassium hydroxide Oven or drain cleaners
Sodium hypochlorite (70 percent) Swimming pool cleaner
Calcium hypochlorite (70 percent)
Sodium hypochlorite (3 to 15 percent)* Bleach
Sodium tripolyphosphate Automatic dishwasher detergent
Acids
Acetic acid Permanent hair wave neutralizers
Hydrochloric acid (muriatic acid) Toilet bowl cleaner
Grout cleaner
Rust stain remover
Swimming pool cleaner
Hydrofluoric acid Glass etching
Rust remover
Phosphoric acid Rust remover
Toilet bowel cleaner
Sulfuric acid (30 to 70 percent) Toilet bowl cleaner
Car battery fluid
* Industrial strength bleach is up to 15 percent concentration.
Data from: Farjo AA, Soong HK. Corneal epithelium. In: Ophthalmology, 2nd ed, Yanoﬀ, M, Duker, JS (Eds), Mosby, St. Louis,
MO 2004. p. 413.
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Corneal alkali burn
Alkali burn. Significant corneal, conjunctival, and scleral damage occurred after a severe alkali
injury. Notice the opacified cornea and the conjunctival and scleral blanching, indicating severe
damage to the surrounding blood vessels.
Reproduced with permission from: Tasman W, Jaeger E. The Wills Eye Hospital Atlas of Clinical Ophthalmology, 2e.
Lippincott Williams & Wilkins, 2001. Copyright © 2001 Lippincott Williams & Wilkins.
34 of 40 3/19/24, 20:36
Morgan® lens
The Morgan® lens provides a simple and effective means for irrigating eyes exposed to toxic
chemicals.
Reproduced with permission from: MorTan, Inc. Copyright © 2009.
35 of 40 3/19/24, 20:36
Insertion of Morgan® lens
* Solution acts as a cushion, suspending the Lens above the cornea and protecting injured surfaces
from the eyelids.
36 of 40 3/19/24, 20:36
Morgan® lens flow
Prolonged irrigation is often necessary for alkali burns. Immediate ophthalmologic consultation is
mandatory for all significant eye exposures.
37 of 40 3/19/24, 20:36
Morgan® lens removal
The pH should be rechecked to confirm that a neutral pH has been maintained initially at five
minutes and again at thirty minutes after the completion of irrigation.
38 of 40 3/19/24, 20:36
Full thickness alkali burn of leg
The photo shows a deep (third-degree) alkali burn from cleaning products. Note the leathery, dead
appearance of the dermis and visible thrombosed vessels (which are not always this obvious).
From: Vercruysse GA, Alam HB, Martin MJ, et al. Western Trauma Association critical decisions in trauma: Preferred triage
and initial management of the burned patient. J Trauma Acute Care Surg 2019; 87:1239. DOI: 10.1097/TA.
0000000000002348. Copyright © 2019 American Association for the Surgery of Trauma. Reproduced with permission from
Wolters Kluwer Health. Unauthorized reproduction of this material is prohibited.
39 of 40 3/19/24, 20:36
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Topical Chemical Burns Initial Evaluation and Management - UpToDate

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Official reprint from UpToDate®

Topical chemical burns: Initial evaluation and

Literature review current through: Feb 2024.

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

● (See "Caustic esophageal injury in adults" and "Caustic esophageal injury in

● (See "Overview of eye injuries in the emergency department" and "Approach to

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

● (See "Common occupational chemical exposures: General approach and

Overview of approach — Chemical burns require immediate treatment because the

● Ensure protection of rescuers and health care workers from exposure

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

Protection of clinicians — Before irrigating a patient with chemical burns, first

● Level C: Splash suit and full or half-face respirator

For most hospital decontaminations of an unknown substance, OSHA believes the

● Powered air-purifying respirator (PAPR) that provides a protection factor of 1000

● Double layer protective gloves

● Chemical resistant suit (with openings sealed with tape)

● Chemical protective boots

toxicologist or poison control center. (See 'Additional resources' below.)

The presence of dyspnea, cough, hoarseness, drooling, stridor, tachypnea, decreased

● Hydrofluoric acid: QTc prolongation, ventricular dysrhythmia, hypocalcemia,

● Phenols: agitation, seizures, coma, hypotension, dysrhythmia (see 'Phenol (carbolic

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

● Hydrocarbons: pulmonary, neurologic, kidney, cardiovascular, gastrointestinal

Skin decontamination — Complete removal of the toxic chemical is essential. Tissue

● Irrigation technique – Moderately warm water in high volumes but at low

A patient with an exposure to a strong acid should also be decontaminated as

● Duration of irrigation – For acid or alkali skin exposure, we suggest continuous

• Diphoterine – This amphoteric, hypertonic, polyvalent, chelating solution is used

● Following irrigation – Measure the pH approximately 5 to 10 minutes after stopping

Chemicals NOT treated with immediate water irrigation — Do not immediately

● Elemental metals – Elemental sodium, potassium, magnesium, phosphorous,

polyethylene glycol (PEG) since phenol is not readily soluble in water.

PATIENT WITH EYE EXPOSURE

conjunctivitis and sight-threatening corneal ulceration. However, for ocular exposure to

Clinical manifestations — Chemical eye burns cause decreased vision, moderate to

● Acids – These cause coagulation necrosis that may result in sight-threatening

Initial irrigation — Irrigation initiated at the scene is continued at the emergency

● Ocular pH measurement – Ocular pH is generally taken at the fornix using litmus

● Analgesia – We apply a topical anesthetic agent to permit irrigation and

• Scleral lens (Morgan lens) if available – Prolonged irrigation using intravenous

• Suspected/confirmed concomitant globe rupture or penetrating injury – Do not

• Significant ocular alkali or acid exposure – We suggest irrigation with a buffered

Subsequent decontamination, irrigation, and pH interpretation

● Duration of irrigation and pH interpretation – A patient with significant ocular

• Ocular pH interpretation – A "normal" eye pH depends upon the method of

• Persistent pH abnormality – Occasionally, more than two hours may be required

● After irrigation completed (pH in neutral range) – Remeasure the pH at 5 and 30

We apply a broad spectrum topical ophthalmic antibiotic (eg, erythromycin ointment;

SPECIFIC CONSIDERATIONS FOR SELECTED AGENTS

Hydrofluoric (HF) acid

● Sources and chemical properties – Hydrofluoric acid (HF) is a highly corrosive

concentrations, an electrocardiogram, and cardiac monitoring in most patients

Immediate treatment using intraarterial calcium injection or a Bier block may be

● Management of HF dermal burns — In a patient with a symptomatic HF burn, we

• Alternative to calcium gel – If calcium gel is unavailable or cannot be made,