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Chapter 12. Electrical Injuries
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Chapter 12. Electrical Injuries
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Chapter 13
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Chemical Burns
HenryB.Huson andHerbA.Phelan
Background
There are a wide variety of compounds that have the potential to cause cutaneous and ocular burns, as well as systemic
side effects requiring the need for medical care. These compounds can be found in the occupational environment or the
home, with an estimated 25,000 chemicals identified as
potential sources of burns [1]. According to the American
Association of Poison Control Centers, in 2019 alone, 7.1% of
all exposures were due to household cleaning substances with
an additional 6.2% of cases being related to cosmetics or
personal care products, which is consistent with prior years [1,
2]. For pediatric exposures, 11.4% of exposures are related to
cosmetic/personal care products, and 10.5% related to household cleaning substances with 43% of cases being children
under the age of 5 [1]. While the rate of exposure within the
H. B. Huson
Department of Surgery, LSUHSC-New Orleans,
New Orleans, LA, USA
e-mail: hhuson@lsuhsc.edu
H. A. Phelan (*)
University Medical Center-New Orleans Burn Unit,
New Orleans, LA, USA
e-mail: hphel1@lsuhsc.edu
© The Author(s), under exclusive license to Springer Nature
Switzerland AG 2023
J. O. Lee (ed.), Essential Burn Care for Non-Burn Specialists,
https://doi.org/10.1007/978-3-031-28898-2_13
285
286
H. B. Huson and H. A. Phelan
pediatric population is concerning, a more pressing matter is
that the rate of serious complications such as major injury or
death has increased by almost 5% each year since 2000 [1–3].
While these domestic exposures have a variety of causes,
ranging from mislabeling and improper storage to intentional
harm of others or suicide attempts, this growing threat is present with most products readily available to the general
population.
According to data gathered by the American Burn
Association, chemical burns account for 3% of hospital
admissions but are related to approximately 30% of burn
deaths [4]. Chemical burns carry a high morbidity, with 55%
requiring surgical intervention, and most commonly involve
the cosmetic areas of the body such as the face, neck, and
hands [4]. Chemical burns present a dilemma to physicians
given the difficulty in assessing the depth of burn as well as
the timing of surgical excision. While the variety of chemical
agents and their treatments is too vast to be covered in total,
we will provide general principles for the treatment of chemical injuries, the most common agents, and an overview of the
complications that may arise from exposure.
Pathophysiology
Burn injuries, whether as a result of a thermal or chemical
insult, have a common pathophysiologic pathway: they result
in the denaturation of proteins. A protein’s three-dimensional
structure is responsible for its biological activity and is dependent on forces such as hydrogen bonding or Van der Waal’s
forces. While thermal energy breaks these bonds causing the
protein to unfold, chemical influences such as changes in pH
or the dissolution of surrounding lipids may stabilize a protein resulting in a change in its biologic activity. These mechanisms continue as long as the offending agent is present,
which is particularly important in chemical injuries where
exposures are typically longer than those seen with thermal
injuries. In addition, chemical agents may act systemically if
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287
their components, with their potential toxicity, end up in the
circulation.
Several factors determine the severity of a chemical burn
injury. The concentration and quantity of the offending agent
determine the scope of injury, as do the manner and the duration of contact. The depth to which the chemical is capable of
penetrating tissues has an obvious impact as does the agent’s
phase, as many chemicals behave differently as solids, liquids,
or gases. Finally, the chemical’s mechanism of action has a
significant influence on tissue damage. Generally speaking,
chemical agents in biological systems can be broken down
into six mechanisms of action:
1. Reduction: Reducing agents denature proteins via the
binding of free electrons within the tissue proteins. This
chemical reaction may also produce a thermal effect caus-
ing a mixed picture. The most common agents encountered
include hydrochloric acid, nitric acid, ferrous iron, alkyl
mercuric compounds, and sulte compounds.
2. Corrosion: Corrosive agents denature proteins via contact.
They produce a soft eschar, typically progressing to shal-
low ulceration. The most common agents encountered
include phenols, cresols, white phosphorus, sodium metals,
lyes, sulfuric acid, dichromate salts, and hydrochloric acid.
3. Oxidation: Oxidizing agents denature proteins via the
insertion of an oxygen, sulfur, or halogen atom to a viable
body protein. The by-products produced are toxic and can
continue to cause a reaction on the surrounding tissues.
The most common agents encountered include sodium
hypochloride, chromic acid, peroxide, and potassium
permanganate.
4. Vesication: Vesicant agents act via the induction of tissue
ischemia with anoxic necrosis at the site of contact. This
results in a cytokine release with resultant cutaneous blis-
ter formation. The most common agents encountered
include cantharides, mustard gas (nitrogen and sulfur),
Lewisite, and dimethyl sulfoxide (DMSO).
5. Desiccation: Desiccant agents act via the dehydration of
tissues resulting in an exothermic reaction causing the
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H. B. Huson and H. A. Phelan
release of heat within the tissues, exacerbating the tissue
damage. The most common agents encountered include
sulfuric acid, calcium sulfate, silica gel, and muriatic acid.
6. Protoplasmic poisons: These agents act via the formation
of esters with proteins or via the binding/inhibiting of cal-
cium or other organic ions that are necessary for tissue
function and viability. The most common agents encoun-
tered include ester formers such as “alkaloidal” acids, ace-
tic acid, and formic acid as well as the metabolic
competitors/inhibitors such as hydrouoric acid, oxalic
acid, and hydrazoic acid.
The chemical agents can be classified by the chemical reaction they produce. The chemical agent’s most important characteristic is that of its influence on pH, while its concentration
will also affect its reactivity. Chemical burns can be described
as either acidic or alkaline and while individual acids and
alkali differ, the resultant injuries are similar enough to be
broken down into groups as a whole.
Acids act as proton donors, releasing hydrogen ions and
reducing the pH.Acids with a pH below 2 are regarded as
strong acids and produce coagulation necrosis and precipitation of protein on skin contact. A better reflection of the
strength of the acid than pH alone is the needed amount of
alkali to restore a neutral pH.
Bases, on the other hand, are proton acceptors, removing
hydrogen ions from the protonated amine groups and carboxylic groups, with the potential of injuring tissue at a pH
above 11.5. Typically, alkali cause more injury than their
acidic counterparts through liquefaction necrosis, allowing
the alkali deeper penetration into the tissues. The hydroxyl
ions within the tissues increase the solubility, allowing alkali
proteinates to be formed after alkali dissolves the tissue
proteins.
Organic solutions act via the dissolution of the lipid membrane within the cell walls, thus causing disruption of the cellular protein architecture.
Finally, inorganic solutions damage tissue by directly bind-
ing to the exterior of the cell wall, acting as a transporter for
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289
the previously mentioned agents, as well as forming salts with
the proteins themselves. These reactions can also be associated with an exothermic reaction, resulting in additional tissue injury.
General Management
When treating the chemical burn patient, the principles of the
primary and secondary assessments of trauma care are applicable. Beyond that generality, however, chemical burns also
mandate removing the offending agent from the skin surface
as quickly as possible, and tailoring subsequent care to the
individual agent.
The clinician should elicit a thorough history in order to
identify the offending agent and expedite appropriate treatment to minimize tissue damage. A valuable resource in this
endeavor is the Material Safety Data Sheets (MSDS) required
by law to be available for all chemicals present in the occupational setting. The MSDS sheets provide information on
agent hazardous effects as well as systemic toxicities.
Additional assistance can be acquired through the regional
poison control centers for household chemicals or unidentified agents.
The importance of the duration of a chemical’s contact
and its direct correlation to the severity of injury cannot be
overstated. As long as the inciting agent is present on the skin
surface, tissue damage/destruction will be ongoing. The
immediate removal of the offending agent is vital. This
requires removal of any potentially contaminated clothing,
copious irrigation at the scene of injury, and repeat irrigation
upon arrival to the hospital. Irrigation of chemical burns
should be carried out with large volumes of fluid and should
occur in an environment that allows runoff of the irrigant.
Tubs and tanks should be avoided as these can contain the
chemical and spread the injurious material to previously
unaffected tissues. Irrigation should be carried out with the
safety of the healthcare provider in mind. For chemical burns,
290
H. B. Huson and H. A. Phelan
immediate copious irrigation has been shown to reduce the
extent and depth of the injury and shorten hospital stay [5].
While there is currently no measure to grade the efficacy of
the irrigation, the monitoring of the effluent’s pH can provide
a quantitative measure for adequacy. Irrigation ranging from
30min to 2h may be necessary to attain a normal pH.While
copious irrigation is a mainstay in the treatment of virtually
all chemical burns, there are some exceptions such as phenol,
dry lime, and muriatic acid as these chemicals create a significant exothermic reaction when combined with water.
A point of contention within chemical burn care is the use
of neutralizing agents. Theoretically, a neutralizing solution
should eliminate the active chemical compound from the
wound bed and prevent any further injury. As such, when the
identity of an injurious agent is known as one that has a specific antidote, some benefit to the use of neutralization has
been demonstrated [6]. However, the control over the quantity of the neutralizing agent is problematic as use may provoke an exothermic reaction, thus exacerbating the thermal
injury in addition to creating a potential delay in the initiation of hydrotherapy. One must also take into account the
fact that neutralizing agents may themselves cause toxicities.
Due to these complicating factors, the use of neutralizing
agents is discouraged as no single agent has been shown to be
more efficacious than plain water irrigation [7].
Conventional burn formulas for resuscitation are used
when appropriate, and urine output should be monitored to
assess end organ perfusion and thus resuscitation. Due to the
effects on systemic pH, blood gas and electrolyte analysis
should be obtained,. In addition, the room should be maintained between 28 and 31 °C as the large volume lavage
typically required for chemical burns puts the patient at risk
for hypothermia. This risk is exacerbated by the use of
unwarmed fluids and thus the irrigation water should be as
near to body temperature as possible.
Principles in wound care for chemical burns are usually
the same as those of thermal injuries. Following irrigation and
debridement of blisters, chemical burns can be treated via
Chapter 13. Chemical Burns
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coverage with antibiotic agents, creams, and/or dressings. The
clinical assessment of the depth and extent of a chemical burn
is difficult due to the unusual tanning and local anesthetic
properties of some agents, resulting in some deep burns
appearing to be more superficial. Due to this, chemical burns
also tend to heal slower than their thermal counterparts.
291
Special Agents forConsideration
Acetic Acid
Acetic acid is a mild chelating agent that is usually found
diluted to concentrations less than 40% (such as in products
like table vinegar or hair products). At this concentration, it is
usually harmless, however, if used inappropriately it may cause
partial thickness burns. Some other names for acetic acid are
ethanoic acid, ethylic acid, and methane carboxylic acid.
Carbolic Acid
Carbolic acid (otherwise known as phenol) is derived from
coal tar. When concentrated, it acts as a caustic agent, causing
partial or full thickness burns based off duration of skin contact. Ingestion of carbolic acid is also dangerous, as ingested
amounts as small as 1 g can be lethal due to systemic effects
such as ventricular arrhythmias and pulmonary edema.
Prompt irrigation is required. In addition, polyethylene glycol
as well as intravenous sodium bicarbonate has been shown to
have some benefit [8, 9] but should not delay irrigation.
Chromic Acid
Chromic acid is responsible for corrosive ulcerations upon
skin contact. Blood levels peak within 5h of exposure and
can be symptomatic with only 1% total body surface area
(TBSA) burns, while burns greater than 10% TBSA are typi-
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