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H. B. Huson and H. A. Phelan
cally fatal due to systemic effects. As with other chemical
burns, copious irrigation is the initial treatment of choice, yet
a more specific antidote consists of rinsing with a dilute solution of sodium hyposulfite followed by additional rinsing in a
buffered phosphate solution. Early excision of a chromic acid
burn has also been shown to potentially help avoid the systemic effects [10, 11]. In order to treat the systemic effects,
dimercaprol may be used for 7days (4 mg/kg IM Q4H for
2days, followed by 2–4mg/kg/day). Early dialysis (defined as
initiation within 24h of the exposure) for the removal of any
circulating chromium may be of benefit. In addition, exchange
transfusion may be necessary.
Formic Acid
Formic acid is an agent used extensively in the glue and tanning industries. After skin contact, eschar formation occurs
but systemic circulation is still possible resulting in metabolic
acidosis, intravascular hemolysis, renal failure, pulmonary
complications, and necrotizing pancreatitis. All formic acid
injuries should mandate hospitalization due to the possibility
of these systemic complications.
Epichlorohydrin Acid
Epichlorohydrin acid is rare, colorless, and known for its garliclike odor. It is an agent typically found in glue, plastic, glycerol,
and resin production as well as paper and water purification
processes and the creation of explosives. As with other chemical burns, initial management involves copious irrigation.
Hydrochloric Acid/Muriatic Acid/Sulfuric Acid
Hydrochloric acid can be found diluted within many household cleaners. It causes local coagulation necrosis and ulceration leading to connective tissue consolidation and
Chapter 13. Chemical Burns
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intramural vessel thrombosis, fibrosis, and hemolysis.
Management consists of quick and continuous irrigation. The
fumes from hydrochloric acid, if inhaled, can lead to upper
airway edema and pulmonary inflammation.
Muriatic acid is an industrial-grade version of concentrated hydrochloric acid. Upon skin contact, it denatures
proteins to form chloride salts. Similar to its less-concentrated counterpart, copious irrigation is the treatment of
choice but with the addition of consideration for early
excision.
Sulfuric acid is one of the more common agents responsible for chemical burns, typically seen in the occupational
environment but also found in the domestic setting as it is
found within household drain cleaners. Sulfuric acid and its
precursor, sulfur trioxide, are strong acids, causing dehydration damage in addition to creating a thermal effect within
the tissues. This leads to a coagulation necrosis and necrotic
eschars with microvascular thrombus formation. Immediate
irrigation with excision of any deep burns are the mainstays
of treatment.
Hydrofluoric Acid
Hydrofluoric acid is typically found within the petroleum
industry, as well as in materials for glass etching, germicides, dyes, tanning, and fireproofing materials. This agent is
particularly lethal as it causes severe burns with tremendous systemic toxicity. Hydrogen ions produce superficial
burns, while the fluoride ion penetrates the tissues resulting
in the chelation of calcium and magnesium. This in turn
causes cell death and liquefaction necrosis of the soft tissues. In addition, the free fluoride ions inhibit the Na–K
ATPase allowing the loss of cellular potassium. This is
thought to be the cause of the extreme pain associated with
hydrofluoric acid injuries.
Hydrofluoric acid burns are classified based on the concentration of the exposure. At concentrations less than 20%,
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H. B. Huson and H. A. Phelan
injuries may take up to 24 h to fully manifest. At 20–50%
concentration, the injury becomes apparent within several
hours. At over 50% concentration, immediate tissue destruction and pain occur.
The clinical presentation of a hydrofluoric acid burn
depends on the route of exposure, concentration, duration of
exposure, and the resistance of the tissue affected. Fingers are
the most commonly injured structures. Death, however, is
typically secondary to the systemic toxicity, with symptoms
such as acidemia, hypocalcemia, hypomagnesemia, and
hyperkalemia resulting in cardiac dysrhythmias. Due to the
difficulty in the restoration of normal cardiac rhythm, hemodialysis may be necessary to eliminate fluoride ions and
restore electrolyte imbalances.
Initial treatment consists of copious irrigation for a minimum of 30min. With higher concentration exposures, calcium gluconate can be used. Topically, 3.5g of 2.5% calcium
gluconate mixed with a water-soluble lubricant can be
applied to the wound 4–6 times daily over the course of
3–4days. Alternatively, 0.5 mL/cm2 of 10% calcium gluconate can be injected subcutaneously or intradermally in the
area of the injury. Finally, 10mL of 10% calcium gluconate
and 40 mL of D5W can be infused intra-arterially but
should occur within 6 h of the exposure to minimize the
tissue necrosis and pain. Treatment should continue until
the patient is symptom free.
Nitric Acid
Nitric acid is typically found in fertilizer, the iron and steel
industries, and engraving products. It acts via oxidation, combining with proteins to form organonitrates, which are metabolic poisons. Upon skin contact, a yellow/brown stain will
develop followed by eschar. Burn depth is difficult to assess
due to the slow progression of the injury. Irrigation and topical treatments are the initial management.
Chapter 13. Chemical Burns
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Oxalic Acid
Oxalic acid is typically found within bleaching products and
rust removers. It acts via combination with calcium which
limits its bioavailability and thus limits muscle contraction. In
addition to irrigation, treatment consists of intravenous calcium as well as the inclusion of cardiac monitoring and the
frequent measurement of renal function and serum
electrolytes.
Phosphoric Acid/Phosphorus
Phosphorus is an incendiary agent typically found within
fireworks and fertilizers as well as in hand grenades and artillery shells. White phosphorus ignites upon contact with air
and continues to burn until the oxygen source is removed,
therefore copious irrigation and the removal of any macroscopic particles is the mainstay of treatment. Soaked dressings should be used during any transportation. In addition,
ultraviolet light can be used to help identify embedded particles. Additionally, a 0.5% copper sulfate topical solution can
be applied which will turn the particulates black, thus aiding
in their identification and removal. Systemic effects include
hypocalcemia, and hyperphosphatemia as well as cardiac
arrythmias.
Alkalis
Alkalis, typically found in household cleaners in the form
of lime, sodium hydroxide and potassium hydroxide, are
commonly ingested as a means of suicide. Typically burns
may appear superficial, but tissue destruction occurs long
after exposure and thus may become full thickness over
2–3days. Alkalis bind lipids and proteins, allowing passage
of hydroxyl ions into the tissue, allowing deep penetration
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H. B. Huson and H. A. Phelan
of the chemical and systemic absorption. Alkali injuries to
the eyes are of specific concern as quick corneal penetration leads to scarring, opacification of the cornea, and perforation. Initial management requires prompt removal of
any contaminated clothing, the removal of any dry residue
and prompt large volume irrigation until the alkali is completely removed from the wound. As water cannot eliminate the alkali from the deeper layers of the wounds,
excision of deep burns with immediate coverage should be
considered.
Cement
Cement is one of the most commonly used chemical agents in
the world. Calcium oxide accounts for 65% of the weight of
cement, which when exposed to water becomes calcium
hydroxide. Injury is the result of this hydroxyl ion and acts as
both an alkali and a desiccant. Injury might not be noticed
until several hours after exposure, and most commonly
involves the lower extremities. Treatment consists of removal
of cement-covered clothing and shoes. The practitioner must
keep in mind that cement burns can be quite dangerous when
ocular exposure occurs from a lack of proper safety eyewear.
Similarly, the respiratory tract may become injured as a result
of aerosolized calcium oxide dust.
Metals
Metals are typically involved with occupational injuries
when molten metals are in use, most commonly involving
sodium, lithium, potassium, magnesium, aluminum, and
calcium. For chemical burns related to metals, water is contraindicated as it can lead to an explosive exothermic reaction. As such, sand and Class D fire extinguishers are
treatments of choice. Mineral oil has also been shown to be
effective [12].
Chapter 13. Chemical Burns
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Hydrocarbons
Hydrocarbons are typically found within plants, animal fats,
and fuel oils. With prolonged contact, they act as corrosives
causing the dissolution of the lipid cell membrane and thus
cell death. The chemical burn associated is typically superficial. Early use of soap and water is most effective. Respiratory
depression is a common systemic toxicity.
Hypochlorite Solutions
Hypochlorite solutions typically are found within household
cleaners as well as bleaches. Systemic toxicity can lead to
confusion, airway edema, vomiting, cyanosis, cardiovascular
collapse, and coma. As little as 30mL of a 15% solution can
be fatal. Similar to other compounds, initial treatment is copious irrigation.
Alkyl Mercuric Compounds
Alkyl mercuric compounds react upon contact with skin, creating blisters in which free mercury can be found within the blister fluid. Over time, mercury can be absorbed leading to
systemic toxicity. Initial treatment involves debridement of the
blisters followed by repeat irrigation to remove the blister fluid.
Tar
Tar is a mineral product created from petroleum and coal.
Also known as crude oil or asphalt, upon cooling it will produce a liquefaction injury that may require debridement.
Hence immediate removal should be undertaken. Antibiotic
ointments in addition to some household products such as
mayonnaise, butter, or mineral oil have been shown to assist
in the agent’s removal [12, 13].
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H. B. Huson and H. A. Phelan
Vesicant Chemical Warfare Agents (Mustard,
Lewisite, Nitrogen)
Historically used during trench warfare in World War I, these
agents affect all of the epithelial layers. Exposure to mustard
gas leads to burning of the eyes and throat as well as a feeling
of suffocation. Depending on the dosage, symptoms may not
arise until 24h after exposure. Erythema of the skin occurs
followed by blister formation and pruritus. The blisters then
rupture, leaving shallow ulcerations. Owing to its disruption
of cell replication, cutaneous lesions may take several months
to heal. Lewisite is more powerful than mustard gas, and
symptoms tend to appear sooner.
Clothing must be removed immediately followed by large
volume irrigation. Benzodiazepines, antihistamines, and phenothiazines may be used to aid with pruritus. Blisters must be
debrided/deroofed with topical antimicrobial and sterile
dressing application. Dimercaprol has been used as an antidote in Lewisite poisoning, while sodium thiosulfate and
N-acetylcysteine can help with mustard gas if administered
early [14]. Keep in mind that most patients exposed to these
agents have multiple sites of injury and these agents may also
cause agranulocytosis or aplastic anemia. As such, bone marrow transplantation may be required.
Conclusion
While chemical burns account for only a small proportion of
total burn injuries, their lethal implications mandate a special
attention. While the prevention of such injuries is of the
utmost importance, the gold standard of treatment remains
copious irrigation with removal of the offending agents.
Wound care for chemical burns can be carried out in a similar
manner to that of thermal injuries, keeping in mind that
chemical burns tend to be deeper than initially appear.
Patients should be treated by specialized practitioners with
referral to a Burn Center as soon as possible.
Chapter 13. Chemical Burns
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299
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Chapter 14
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ICU Care ofBurn
Patients
MollyHunter andDavidT.Harrington
Introduction
As burn care has improved, patients with severe burn injury
have had improved survival [1]. However, severe burn injury
requires care in specialized intensive care unit (ICU) due to
the profound impact of burn injury on the body. Patients with
burns >20% total body surface area (TBSA) require admission to a burn ICU because they are at risk for complications
such as resuscitation failure, infection, sepsis, and multi-organ
failure due to their injury [2]. Some patients with smaller
burns also require ICU care because of significant medical
comorbidities or either very young or advanced age. This
chapter will address some of the special concerns in caring for
severe burns in the ICU.Many topics discussed in this chapter are reviewed in more extensive detail in other chapters.
M. Hunter · D. T. Harrington (*)
Department of Surgery, Warren Alpert Medical School of Brown
University, Providence, RI, USA
e-mail: david.harrington@brownphysicians.org
© 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_14
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