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CURRENT CONCEPTS

Hand Chemical Burns
Elliot P. Robinson, MD, A. Bobby Chhabra, MD
CME INFORMATION AND DISCLOSURES

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Ghazi M. Rayan, MD, has no relevant conflicts of interest to disclose.
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Learning Objectives
! Elucidate the pathophysiology of chemical burns.
! Clarify the difference between chemical and thermal burns.
! Discuss the characteristics and mechanism of action of different chemical burns.
! Review the clinical presentation and diagnosis of the most common chemical burns.
! Describe the management options for chemical burns.
Deadline: Each examination purchased in 2015 must be completed by January 31, 2016, to
be eligible for CME. A certificate will be issued upon completion of the activity. Estimated
time to complete each JHS CME activity is up to 1 hour.
Copyright ª 2015 by the American Society for Surgery of the Hand. All rights reserved.

There is a vast and ever-expanding variety of potentially harmful chemicals in the military,
industrial, and domestic landscape. Chemical burns make up a small proportion of all skin burns,
yet they can cause substantial morbidity and mortality. Additionally, the hand and upper extremity are the most frequently involved parts of the body in chemical burns, and therefore these
injuries may lead to severe temporary or permanent loss of function. Despite this fact, discussion
of the care of these injuries is sparse in the hand surgery literature. Although most chemical
burns require only first response and wound care, some require the attention of a specialist for
surgical debridement and, occasionally, skin coverage and reconstruction. Exposure to certain
chemicals carries the risk of substantial systemic toxicity and even mortality. Understanding the
difference between thermal and chemical burns, as well as special considerations for specific
compounds, will improve patient treatment outcomes. (J Hand Surg Am. 2015;40(3):605e612.
Copyright ! 2015 by the American Society for Surgery of the Hand. All rights reserved.)
Key words Chemical, burn, hydrofluoric, acid, management.
From the Department of Orthopaedic Surgery, University of Virginia Health System, Charlottesville, VA.
Received for publication May 21, 2014; accepted in revised form July 30, 2014.
No benefits in any form have been received or will be received related directly or indirectly
to the subject of this article.

Corresponding author: A. Bobby Chhabra, MD, Department of Orthopaedic Surgery,
University of Virginia Health System, Box 800159, Charlottesville, VA 22908; e-mail: AC2H@
hscmail.mcc.virginia.edu.
0363-5023/15/4003-0036$36.00/0
http://dx.doi.org/10.1016/j.jhsa.2014.07.056

! 2015 ASSH

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Published by Elsevier, Inc. All rights reserved.

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The Review Section of JHS will contain at least 2 clinically relevant articles selected by the
editor to be offered for CME in each issue. For CME credit, the participant must read the
articles in print or online and correctly answer all related questions through an online
examination. The questions on the test are designed to make the reader think and will
occasionally require the reader to go back and scrutinize the article for details.

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HAND CHEMICAL BURNS

chemical exposure
make up a diverse set of injuries. They may
range from mild erythema to severe tissue
loss and even loss of life. The variation depends on
the specific characteristics of the agent, the concentration, and duration of exposure.
Chemical burns may occur in the domestic,
occupational, or war setting. Each setting presents its
own concerns. In the domestic setting there may be a
lack of knowledge of the potential harm certain
chemicals present and how to perform appropriate
first aid. Non-accidental abusive or self-injurious
behavior such as attempted suicide may also be
involved. The industrial setting has become safer for
chemical burns due to increased governmental regulations. Lastly, exposure to chemicals in warfare may
be associated with other injuries.
Chemical burns occur most commonly in workingaged individuals.1 Additionally, the wrist and hand
are the most common sites of severe burns.2 It has
also been noted that chemical burns often heal more
slowly than thermal burns and require surgery more
frequently.3 When combined, these factors suggest
that chemical burns, despite their relative rarity, are a
considerable source of economic burden.
Most chemical burns do not result in serious longterm sequelae. Nevertheless, the importance of vigilance and prompt treatment cannot be overstated:
Despite only making up 3% of a particular burn
center’s admissions, chemical burns were responsible
for up to 30% of burn-related deaths.4
AND BURNS SECONDARY TO

2.

3.
4.
5.

6.

DIAGNOSIS
Crucial data in the management of chemical burns
are: specific chemical compound and concentration,
mechanism of exposure, time of exposure and timeframe of initiation of decontamination. Trauma protocol consisting of focused assessment of airway,
breathing, and circulation should be followed. Other
areas of exposures such as ocular and inhalational
must be ruled out.
Examination of the burn should identify all
involved locations. Chemical burns may not show the
same early signs of skin damage as thermal burns,4,5
therefore early grading of burns may be difficult.
Serial examination is recommended. An estimation of
TBSA involved will guide fluid resuscitation and
other treatment measures. Systemic complications are
ruled out by obtaining early electrocardiography and
electrolyte analysis.

PATHOPHYSIOLOGY
The crucial difference between a chemical burn and a
thermal burn is that the damage continues until the
chemical is removed or neutralized. Therefore, thorough and prompt decontamination is paramount.
Several factors contribute to the characteristic of a
burn after chemical exposure.

Current Concepts

1. Responsible substance: Chemicals vary in their
physical properties and mechanism of action.
Although there are many chemicals that may
cause burns, we will address only those substances
that are important either because of their ubiquity,
or because of special considerations involved. For
detailed information on any given chemical substance, the U.S. Centers for Disease Control and
Prevention (CDC) compiles material safety data,
which is readily available on-line. The Agency for
Toxic Substances and Disease Registry is a federal
public health agency of the U.S. Department of
Health and Human Services. Their Web site,
J Hand Surg Am.

administered by the CDC, contains medical
management guidelines (available at: http://www.
atsdr.cdc.gov/mmg/index.asp).
Burn percentage: The risk of systemic toxicity
increases with total body surface area (TBSA)
affected. Additionally, a larger area of damage
may make coverage and reconstruction more
difficult.
Chemical concentration: Higher concentration
leads to more rapid and extensive damage.
Time of exposure: The extent of damage is
correlated with time of exposure. Early lavage is
the most important means of limiting damage.
Treatment: Immediate high volume water lavage is
the best early management strategy. The use of
neutralizing compounds and alternative lavage
substances is controversial, but generally discouraged. Certain chemicals have a high risk of systemic toxicity, which requires specific antidotes
and supportive measures.
Skin properties: The palmar skin has thick stratum
corneum, which is more impermeable and therefore resistant to chemical insult than the dorsum.
Laceration or breakdown of the resistant epidermis
exposes the more sensitive underlying dermis.1

INITIAL TREATMENT
Initial treatment involves decontamination, and must
begin immediately after chemical exposure. Industrial
settings are mandated to have procedures in place and
high-flow rinsing stations. Evidence indicates that
when treatment is initiated “in the field”, outcomes
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HAND CHEMICAL BURNS

are improved: pH normalizes faster6 and hospital stay
is decreased.7
First responders and medical center staff should
continue the decontamination process and proceed
along a treatment algorithm to minimize morbidity and
mortality. First, the management team must take precautions not to contaminate themselves. Eyewear,
gloves, and appropriate gowns are a minimum requirement. Although simple chemical burns may be
managed in the community setting by an informed team,
the American College of Surgeons and the American
Burn Association recommend referral of severe burns to
designated centers.8 Table 1 summarizes common
chemicals and their characteristics and primary and
secondary treatment considerations. The following are
initial treatment measures for chemical burns:

There are exceptions to the initial use of water for
lavage. Phenol is insoluble in water, so polyethylene
glycol may be used initially to increase its solubility in
water.11 Elemental metals such as sodium, potassium,
and lithium combust when exposed to water; hence,
burns from these metals should be immersed in
mineral oil, and then the elemental metal with the
mineral oil is then removed. Dry lime becomes caustic
only when dissolved, so it should be thoroughly dusted off. Some authors caution that concentrated
muriatic, sulfuric, and hydrochloric acid may generate
an exothermic reaction when combined with water,1
but high flow cool water can minimize this effect.
3. Neutralization: There is controversy as to whether
neutralizing substances should be used in the
management of chemical injury. Theoretically, a
neutralizing substance would more effectively halt
the activity of the offending chemical agent.
However, neutralization agents may be toxic
themselves, and it is difficult to control the quantity
administered. Reactions between compounds and

DEBRIDEMENT
Decision making for surgical treatment of a chemical
injury may be challenging. Depth is difficult to estimate,
hence the benefits of excision versus observation can be
difficult to weigh.5,11 As in all burns, surgical debridement removes necrotic tissue, which may serve as a
nidus for infection. Another important advantage
of surgical debridement is the removal of residual
chemicals. In severe exposures to chemicals with

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Current Concepts

their neutralizing agent may be exothermic and
cause further thermal injury. Additionally, whereas
water is generally immediately available, it may
take valuable time to identify and locate a specific
neutralizing substance. Scientific evidence is conflicting, with some studies showing no benefit to
the use of neutralizers,12 whereas others have
shown more rapid return of the affected area to
physiologic pH.13 However, it is generally
accepted that hydrotherapy (dilution with
extremely large volumes of water) is the most
appropriate means of eliminating the majority of
chemical contaminants.11
4. Systemic support: The ABCs of trauma apply to
chemical burn management: Inhalational injury
may require intubation, and electrolyte disturbance
may lead to cardiovascular collapse. Conventional
burn fluid resuscitation formulas should be followed
with adequate monitoring of urine output. It is
important to remember that irrigation with large
volumes of cold water may cause hypothermia.11
Inhalational injury should be assumed whenever
clothes are saturated or the injury mechanism
involved an explosion.9 In such cases, evaluation
and prompt treatment is critical. Ocular injury is also
common and should be managed by a specialist.
5. Systemic toxicity: Electrolyte monitoring and
management are important in all major burns.
Remember, however, that seemingly innocuous
chemical burns may cause severe electrolyte
imbalance. The threshold for early and prolonged
electrolyte and cardiac monitoring should be low,
particularly in compounds like hydrofluoric acid
(HF) and phosphorus, which are known to have
high systemic toxicity.
6. Skin care: Wound care of chemical burns is similar to
that of thermal burns. Ointments such as silver sulfadiazine are commonly used to keep the wound from
desiccating and to suppress bacterial growth. Dressings should be changed daily and wounds should
be regularly examined for signs of infection and to
identify nonviable tissue in need of debridement.

1. Removal: Loose dry agent should be dusted off,
and clothing should be removed. This step is
particularly important for dry chemical agents, such
as lime, which may react with water exothermically
and cause additional thermal damage.
2. Dilution: Copious irrigation under high flow
should last at least 20 minutes, but this may be as
long as several hours for concentrated alkali. Hand
or limb submersion should be avoided, as this will
not sufficiently dilute chemical agents and may
spread the chemical to other areas. Similarly,
high-pressure jet lavage may spread concentrated
agent.9 pH testing of the skin with litmus paper
may help determine safe end point for lavage in
the case of basic or acidic burns.10

J Hand Surg Am.

607

Current Concepts
608

TABLE 1.

Common Chemical Burn Treatment Considerations

Chemical

Industrial Use

Domestic Use

Special
Characteristics and
Systemic Effects

Primary Treatment

Secondary
Treatment

Additional Workup

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Fluoride binding leads High flow water
decontamination
to systemic
hypocalcemia;
painful; potentially
fatal

Serial electrolyte, renal
Topical calcium
function, and cardiac
gluconate gel,
monitoring
intravenous or
arterial calcium,
surgical excision
for severe exposure

Corrosion of tissue
due to hydrogen
ions, chromium
binds cations

Chromium toxicity,
renal failure

High flow water
decontamination

Phosphate buffer
soaks, low
threshold for
surgical
debridement and
dialysis in severe
exposure

Serial electrolyte, renal
function, and cardiac
monitoring

Drain cleaner,
lead-acid
car batteries

Corrosion of tissue
due to free
hydrogen ions

Most common cause
of chemical burns

High flow water
decontamination

Supportive, woundspecific

Consider nonaccidental
exposure. Drain
cleaner is often used in
asault and suicide
attempt

None

Corrosion of tissue
due to free
hydrogen ions

Yellow staining
of skin

High flow water
decontamination

Supportive, woundspecific

Chemical peels,
small amounts in
pharmaceuticals

Corossive, cytotoxic

Dilute polyethylene
Painless burn,
glycol wash and
hemolysis, renal
high flow water
injury, CNS toxicity
decontamination

Supportive, woundspecific

Alkaline, corrossive
Household
Industrial
bleaching and
oxidizing
cleaning products
reagent, bleach,
and disinfectant

Commonly associated High flow water
decontamination,
with inhalation
dilute soapy wash
exposure, metabolic
acidosis with
ingestion

Supportive, woundspecific

Delayed presentation
is typical

Supportive, woundspecific

Glass etching,
microchip
manufacture

Chromic acid

None
Production of
alloys, plating,
dye manufacture

Sulfuric acid

Refining and
manufacturing
reagent

Nitric acid

Refining and
manufacturing
reagent

Phenol (carbolic Synthetics
acid)
manufacturing

Cement (calcium Construction
oxide)

Construction

Forms alkaline
calcium hydroxide

High flow water
decontamination

Monitor blood count,
electrolytes, and renal
function

(Continued)

HAND CHEMICAL BURNS

J Hand Surg Am.

Corrosion of tissue
due to hydrogen
ions, free fluoride
binds cations

Rust remover

Hydrofluoric
acid

Bleach (sodium
or calcium
hypochlorite)

Mechanism of
Action

TABLE 1.

Common Chemical Burn Treatment Considerations (Continued)

Chemical

Industrial Use

Domestic Use

Mechanism of
Action
Alkaline, corrossive

Special
Characteristics and
Systemic Effects

Primary Treatment

Secondary
Treatment

Additional Workup

Supportive, woundDust off dry lye, long
Dry lyme causes
specific
duration high flow
exothermic reaction
water decontamination
with water

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Manufacture of
soaps and
petroleum
products, paper
and metal
processing

Drain and oven
cleaners

White
phosphorus

Munitions,
pesticides,
fertilizers

Fireworks, illegal
May be combined
methamphetamine
thermal and
production
chemical corrosive
injury, high lipid
solubility allows
deep pentration

Complete removal with Supportive, woundHypocalcemia and
specific
aid of ultraviolet light,
hyperphosphatemia,
high flow water
renal injury,
decontamination
hemolysis

Anhydrous
ammonia

Fertilizer

Fertilizer

Alkaline when
combined with
water

Often stored as
pressurized gas,
inhalation common

High flow water
decontamination

Supportive, woundspecific, avoid
early ointments

Elemental Na,
K, Li

Laboratory

None

Combustible when
combined with
water

Must be kept under
inert gas or oil

Particles must be
physically removed
(no water)

Supportive, woundspecific

Petroleum
products

Fuel, solvent,
synthetic
manufacturing,
and other uses

Fuel, solvent

Lipid barier
disruption

Potential for systemic Removal from skin with Supportive, woundspecific
mild soap followed by
absorbtion, CNS,
high flow water
liver, lung,
decontamination
endothelial and
hematologic toxicity

Serial electrolyte, renal
function, and cardiac
monitoring

HAND CHEMICAL BURNS

J Hand Surg Am.

Lye (sodium
hydroxide)

CNS, central nervous system.

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Current Concepts

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HAND CHEMICAL BURNS

potentially lethal systemic toxicity (like chromic acid,
HF, and phosphorus acid), this may be the only way to
limit morbidity and mortality.9,14
In a patient in stable condition, timing of debridement, if necessary, is controversial. Delayed debridement of fully demarcated eschar at approximately 1
week post injury followed by split-thickness skin
grafting typically leads to satisfactory results.15 However, by limiting ongoing tissue damage, early
tangential excision may improve functional and
cosmetic results,16,17 though this algorithm will require
more frequent use of skin grafting. After early excision,
skin grafting may be delayed to ensure the adequacy of
the first debridement.9 Versajet (Smith & Nephew,
Memphis, TN) has been reported as a useful adjunctive
tool in debridement. This system creates a high velocity stream of saline. On lower settings, this will
remove devitalized tissues while leaving viable tissue
intact and simultaneously providing copious lavage.18
The hand contains specialized structures that
warrant specific treatment considerations. The impermeable nail plate may prevent thorough decontamination efforts.8 Removal of the nail should be
considered in situations like HF exposure, as this will
allow application of calcium gluconate gel to the
matrix and neutralize the damaging fluoride ion.8
Compartment swelling may occur after chemical
injury, and the need for fasciotomy should always be
considered.8 The management of skin blisters in
thermal burns is not universally agreed upon, but
expert opinion suggests unroofing blisters associated
with chemical injury to ensure removal of any residual chemical within.8,19
In summary, decision making for debridement
should favor emergent surgery for severe burns with
systemic toxicity, and urgent or early surgery for
burns in which progressive local tissue damage will
lead to functional loss. Delayed excision and
coverage of demarcated eschar also generally leads to
satisfactory results.

irrigated and dressed with antibacterial ointment.
Wounds are then observed for possible debridement
and grafting.11
Lye and alkaline drain cleaners
Lye, or dry sodium hydroxide, is a strongly alkaline
compound, which causes a vigorous exothermic reaction when combined with water. Aqueous solutions are
commonly marketed as drain and oven cleaners.
Alkaline substances penetrate tissue deeply, and cause
progressive damage until removed or diluted. They
may cause full-thickness skin loss and saponification of
subcutaneous lipids.20 Very large volumes of irrigation
are required to return the skin to a neutral pH.13,15
Dressing with mafenide acetate has been recommended
for its antibacterial properties and inert byproducts.20
Anhydrous ammonia
Widely used as a nitrogen fertilizer in the farming
industry, this gas is stored and transported as a
pressurized liquid. When combined with enough
oxygen, it becomes combustible.10 Contact with the
liquid, which is stored at e33" C, causes frostbite and
tissue necrosis. When dissolved in water it is strongly
alkaline.21 Ammonia is highly damaging to mucous
membranes, and in its gaseous state can often be
harmful by exposure to eyes and lungs. According to
recent literature, lavage should be continued every
few hours for 24 hours. Additionally, the use of
ointments should be delayed for the first day, as they
can worsen penetration of anhydrous ammonia.21

Current Concepts

Sodium hypochlorite
Also known as bleach, it is chemically similar to
calcium hypochlorite. Both are used as oxidizing,
bleaching, and disinfecting agents. The hypochlorite
anion is strongly basic, and therefore causes tissue
damage by liquefaction necrosis. It is important to
remember that hypochlorite vapors are strongly irritating to eyes and the respiratory tract. Management
is similar to other exposures to alkaline substances,
with immediate high flow irrigation. Diluted soapy
wash can help remove residue.

SPECIAL CONSIDERATIONS FOR SPECIFIC
COMPOUNDS
Cement
Cement is widely used and its ability to cause burns
is underappreciated, particularly outside of industry
circles. The predominant compound is calcium oxide,
which becomes alkaline calcium hydroxide when
exposed to water and the culprit for chemical burns.11
Onset of symptoms is typically insidious and may
result in full-thickness burns. Loose dry agent is dusted off, then contaminated areas should be thoroughly
J Hand Surg Am.

White phosphorus
Barillo et al published an excellent review of phosphorus burns at a referral center.22 White phosphorus
is a component of munitions and explosives, and is a
frequent cause of military burns.22 However, as it is
also used in pesticides, fertilizers, and fireworks, as
well as illegal methamphetamine production, civilian
injuries have become more common. Ignited white
phosphorus creates combined thermal and chemical
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burns. Its lipophilic nature allows it to penetrate
deeply in tissues, which is why outcomes have been
noted to be worse than isolated chemical burns, with
slower recoveries.3
Initial management revolves around irrigation and
removal of remaining residue. White phosphorus can
auto-ignite in contact with oxygen at temperatures as
low as 30" C, so water for burn irrigation should be
cool. Particles may become imbedded in tissue, and
these must be removed to prevent further damage.
Immediate and repeated surgical debridement is
advocated to ensure prompt and complete removal.22
Copper sulfate, which turns phosphorus particles
black, was once used to facilitate identification and
removal. Systemically absorbed copper, however,
can lead to severe toxicity including hemolysis, oliguria, and cardiovascular collapse.3,22 A preferable
alternative is ultraviolet light from a Wood’s lamp,
which causes phosphorus to fluoresce, enabling
identification and removal without risk of copper
toxicity.
It should be noted that systemic toxicity from
phosphorus is a main concern, as life-threatening
hypocalcemia and hyperphosphatemia may occur. An
electrocardiogram must be part of initial evaluation
and electrolytes should be monitored initially and for
several days postinjury.

Systemic hypocalcemia and resultant hyperkalemia
may cause myocardial arrhythmia. Hypocalcemia
may develop with as little as 1% TBSA exposure to
concentrated HF.25 Fluoride is also directly toxic to
many enzymes and organs.24 Although most HF
burns are more painful than dangerous,26 the potential
for mortality has been documented in the literature.
With TBSA exposure of 20%, mortality approaches
100%, and death has been reported with only 2.5%
TBSA exposure to highly concentrated HF.24
Treatment includes the following phases:

Hydrofluoric acid
Hydrofluoric acid is present in a variety of over-thecounter products such as rust removers at concentrations of 6% to 12%. It may also be stored as HF
gas and used in industrial glass and microchip etching
in concentrations exceeding 70%.
Hydrofluoric acid is particularly dangerous
because of its dual mechanism of action: In addition
to acidic corrosive effect, fluoride ions penetrate
deeply into tissues where they react with calcium and
magnesium with multiple local and systemic effects.
One hallmark effect is pain seeming out of proportion
to the injury. This is due to shifts in potassium, which
lead to continued nerve depolarization.24 Other local
effects include slow-healing wounds and osteolysis.

Chromic acid
Chromic acid, like HF, contains an anion that may
cause severe systemic toxicity beyond the local
caustic acid burn. The hexavalent form is most toxic.
Acute renal failure has been reported after burns of
only 1% TBSA, and death after 10% TBSA.14 After
immediate lavage, phosphate buffer soaks are applied
to bind residual ions. Additionally, immediate surgical excision has been recommended as an important

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1. Immediate, copious, and repeated lavage. Recent
recommendations suggest a relatively brief initial
lavage for 20 minutes in order to proceed to the
next step.9
2. Topical treatment with 2.5% calcium gluconate
gel is highly effective at neutralizing free fluoride
ions, limiting further damage and improving
pain.9,24 It is made by mixing 100 mL of watersoluble surgical lubricant with 2.5 mg of calcium
gluconate powder.24 It should be applied for at
least 30 minutes. Relief of pain is an indicator of
its effectiveness.26
3. Local subcutaneous infiltration of calcium gluconate
solution has been advocated as an adjunctive means
of binding fluoride ions and limiting local and systemic toxicity. The recommended dose is 0.5 mL of
5% per square centimeter injected via small-bore
needle. It should not be used in closed spaces such as
the hand due to the risk of compartment syndrome
and pressure necrosis.9,24,26 Intra-arterial infusion
via angiographically placed catheter is an alternative
means of delivering calcium to a selected vascular
bed in the extremities.9,24 Infiltration techniques are
suggested primarily for high concentration and
delayed presentation injuries.9
4. It is important to emphasize the potential for rapid
mortality with this compound, so vigilance must
be high. Electrolyte and cardiac monitoring should
be initiated early and electrolyte replacement may
begin before laboratory results return.25

Sulfuric acid
Sulfuric acid is one of the most common causes of
chemical burns due to its availability in concentrated
form in home-use drain cleaners. It causes dehydration
of tissues and coagulation necrosis.11 As it may often
result in full-thickness burns, excision and closure or
split-thickness grafting of lesions may be needed.23

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means of removing the cutaneous supply of chromium and to limit systemic toxicity.14

4. Luterman A, Curreri P. Chemical burn injury. In: Jurkiewcz M,
Krizek T, Mathes S, eds. Plastic Surgery: Principles and Practice.
St. Louis, MO: CV Mosby; 1990:1355e1440.
5. Kolios L, Striepling E, Kolios G, et al. The nitric acid burn trauma of
the skin. J Plast Reconstr Aesthet Surg. 2010;63(4):358e363.
6. Gruber RP, Laub DR, Vistnes LM. The effect of hydrotherapy on the
clinical course and pH of experimental cutaneous chemical burns.
Plast Reconstr Surg. 1975;55(2):200e204.
7. Leonard LG, Scheulen JJ, Munster AM. Chemical burns: effect of
prompt first aid. J Trauma. 1982;22(5):420e423.
8. Reilly DA, Garner WL. Management of chemical injuries to the
upper extremity. Hand Clin. 2000;16(2):215e224.
9. Kirkpatrick JJ, Burd DA. An algorithmic approach to the treatment of
hydrofluoric acid burns. Burns. 1995;21(7):495e499.
10. Wibbenmeyer LA, Morgan LJ, Robinson BK, et al. Our chemical
burn experience: exposing the dangers of anhydrous ammonia.
J Burn Care Rehabil. 1999;20(3):226e231.
11. Palao R, Monge I, Ruiz M, et al. Chemical burns: pathophysiology
and treatment. Burns. 2010;36(3):295e304.
12. Segal EB. First aid for skin/eye decontamination: are the present
practices effective? J Chemical Health and Safety. 2007;14(4):16e22.
13. Andrews K, Mowlavi A, Milner SM. The treatment of alkaline burns of the
skin by neutralization. Plast Reconstr Surg. 2003;111(6):1918e1921.
14. Matey P, Allison KP, Sheehan TM, et al. Chromic acid burns: early
aggressive excision is the best method to prevent systemic toxicity.
J Burn Care Rehabil. 2000;21(3):241e245.
15. Al-Qattan MM, Pitkanen J. Delayed primary excision and grafting of
full thickness alkali burns of the hand and forearm. Burns.
2001;27(4):398e400.
16. Bhat FA. Early sequential excision of chemical burns—our experience
in Riyadh burns unit. Ann Burns Fire Disasters. 2006;19(2):78e79.
17. Burd A, Ahmed K. The acute management of acid assault burns: a
pragmatic approach. Indian J Plast Surg. 2010;43(1):29e33.
18. Gumus N, Erkilic A, Analay H. Water jet for early treatment of
chemical burn. Burns. 2010;36(3):36e37.
19. Bope ET, Kellerman RD. Chemical burns. In: Conn HF, Rakel RE,
eds. Conn’s Current Therapy. Philadelphia, PA: W.B. Saunders;
1984:1127e1209.
20. Wolfort FG, Nevarre DR, De A. Alkali burns to the hand. Ann Plast
Surg. 2000;44(3):346.
21. Amshel CE, Fealk MH, Phillips BJ, et al. Anhydrous ammonia
burns case report and review of the literature. Burns. 2000;26(5):
493e497.
22. Barillo DJ, Cancio LC, Goodwin CW. Treatment of white phosphorus and other chemical burn injuries at one burn center over a 51year period. Burns. 2004;30(5):448e452.
23. Bond SJ, Schnier GC, Sundine MJ, et al. Cutaneous burns caused by
sulfuric acid drain cleaner. J Trauma. 1998;44(3):523e526.
24. Dunser MW, Ohlbauer M, Rieder J, et al. Critical care management of major hydrofluoric acid burns: a case report, review of the
literature, and recommendations for therapy. Burns. 2004;30(4):
391e398.
25. Dalamaga M, Karmaniolas K, Nikolaidou A, et al. Hypocalcemia,
hypomagnesemia, and hypokalemia following hydrofluoric acid
chemical injury. J Burn Care Res. 2008;29(3):541e543.
26. Burd A. Hydrofluoric acid burns: rational treatment. J Burn Care
Res. 2009;30(5):908.
27. Lin TM, Lee SS, Lai CS, et al. Phenol burn. Burns. 2006;32(4):
517e521.

Phenol
Also known as carbolic acid, it is an isolate of coal tar
used in synthetic manufacturing. Joseph Lister
advocated its use as an antiseptic, but this use has
been curtailed because its toxicity.27 Its contact with
skin can cause a range of effects from dermatitis,
depigmentation, and defatting in low concentration
(1.5%) to severe necrosis at higher concentration
(10% to 40%).27 It has an anesthetic effect, and
because exposure is not painful, presentation may be
delayed. Its lipophilic nature causes deep penetration
and systemic absorption, which may lead to hemolysis and kidney, liver, and central nervous system
toxicity.1
Phenol is much more soluble in polyethylene
glycol than in water. Recommended treatment,
therefore, is dilute polyethylene glycol wash followed
by high-flow water lavage.11
In conclusion, chemical burns can cause severe
local tissue damage and systemic complications.
The effect is not resolved until the chemical is
removed or neutralized. Therefore early and thorough decontamination of these injuries is the
mainstay of treatment. Surgical debridement may be
necessary when systemic complications may
become life threatening, or when further damage
could lead to compromise of functionally important
structures. Because chemical burns frequently affect
the hand and upper extremity, hand surgeons should
be familiar with causative substances and principles
of their surgical and nonsurgical wound management, and recognition and treatment of systemic
complications.
REFERENCES

Current Concepts

1. Ahmadi H, Durrant CT, Sarraf KM, et al. Chemical burns: a review.
Curr Anaesth Crit Care. 2008;19(5):282e286.
2. Islam SS, Nambiar AM, Doyle EJ, et al. Epidemiology of workrelated burn injuries: experience of a state-managed workers’
compensation system. J Trauma. 2000;49(6):1045e1051.
3. Barqouni L, Abu Shaaban N, Elessi K. Interventions for treating
phosphorus burns. Cochrane Database Syst Rev. 2012;3:CD008805.

J Hand Surg Am.

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Vol. 40, March 2015