JBUR-4456; No.

of Pages 22

burns xxx (2014) xxxxxx

Available online at www.sciencedirect.com

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Review

Clinical and forensic signs related to chemical

burns: A mechanistic approach

Ricardo Jorge Dinis-Oliveira a,b,c,d,e,*, Felix Carvalho c, Roxana Moreira b,e,

Jorge Brandao Proenca b, Agostinho Santos a,d,f, Jose Alberto Duarte g,
Maria de Lourdes Bastos c, Teresa Magalhaes a,d,f
a
Department of Legal Medicine and Forensic Sciences, Faculty of Medicine, University of Porto, Porto, Portugal
b
IINFACTS Institute of Research and Advanced Training in Health Sciences and Technologies, Department of
Sciences, Advanced Institute of Health Sciences North (ISCS-N), CESPU, CRL, Gandra, Portugal
c
REQUIMTE, Laboratory of Toxicology, Department of Biological Sciences, Faculty of Pharmacy, University of Porto,
Porto, Portugal
d
Center of Forensic Sciences (CENCIFOR), Portugal
e
CBMA Centre of Molecular and Environmental Biology, Department of Biology, University of Minho, Braga, Portugal
f
National Institute of Legal Medicine and Forensic Sciences, North Branch, I.P., Portugal
g
CIAFEL, Faculty of Sport, University of Porto, Porto, Portugal

article info abstract

Article history: This manuscript highlights and critically analyses clinical and forensic signs related to
Accepted 8 September 2014 chemical burns. Signs that may lead to suspicion of a particular chemical are thoroughly
discussed regarding its underlying mechanisms. Burns due to sulfuric, hydrofluoric, nitric,
Keywords: hydrochloric (muriatic) and acetic (including derivatives) acids, hydrogen sulphide, sodium
Chemical burns (caustic soda) and calcium (cement) hydroxides, paraquat, burns after inflation and rupture
Sulfuric acid of airbags, povidoneiodine, chlorhexidine/alcohol (in preterm infants), laxatives, and
Hydrofluoric acid vesicants (warfare agents), will be reviewed since these are the most common agents found
Nitric acid in daily practice, for which relevant and timed information may be helpful in formulating an
Hydrochloric acid (muriatic acid) emergency treatment protocols and toxicological analysis.
Acetic acid and derivatives # 2014 Elsevier Ltd and ISBI. All rights reserved.
Hydrogen sulphide
Sodium hydoxide (caustic soda)
Calcium hydroxide (cement)
Paraquat
Inflation and rupture of airbags
Povidoneiodine
Chlorhexidine/alcohol
Laxatives
Vesicants

* Corresponding author at: Department of Legal Medicine and Forensic Sciences, Faculty of Medicine, University of Porto, Jardim Carrilho
Videira, 4050-167 Porto, Portugal. Tel.: +351 222073850.
E-mail address: ricardinis@sapo.pt (R.J. Dinis-Oliveira).
http://dx.doi.org/10.1016/j.burns.2014.09.002
0305-4179/# 2014 Elsevier Ltd and ISBI. All rights reserved.

Please cite this article in press as: Dinis-Oliveira RJ, et al. Clinical and forensic signs related to chemical burns: A mechanistic approach. Burns
(2014), http://dx.doi.org/10.1016/j.burns.2014.09.002
JBUR-4456; No. of Pages 22

2 burns xxx (2014) xxxxxx

Contents

1. Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .... . . . . . . . . . . . . . . . 000

2. Methods . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .... . . . . . . . . . . . . . . . 000
3. Classification of chemicals involved in burns. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .... . . . . . . . . . . . . . . . 000
4. Sulfuric acid (H2SO4) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .... . . . . . . . . . . . . . . . 000
5. Hydrofluoric acid (HF) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .... . . . . . . . . . . . . . . . 000
6. Acetic acid (CH3COOH) and its derivatives glacial acetic acid, trifluoroacetic acid (C2HF3O2) and
monochloroacetic acid (ClCH2CO2H) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .... . . . . . . . . . . . . . . . 000
7. Nitric acid (HNO3) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .... . . . . . . . . . . . . . . . 000
8. Hydrochloric (muriatic) acid (HCl) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .... . . . . . . . . . . . . . . . 000
9. Hydrogen sulphide (H2S) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .... . . . . . . . . . . . . . . . 000
10. Sodium hydroxide (NaOH; caustic soda) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .... . . . . . . . . . . . . . . . 000
11. Calcium hydroxide (Ca(OH)2; cement) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .... . . . . . . . . . . . . . . . 000
12. Burns after inflation and rupture of airbags . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .... . . . . . . . . . . . . . . . 000
13. Paraquat. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .... . . . . . . . . . . . . . . . 000
14. Povidoneiodine. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .... . . . . . . . . . . . . . . . 000
15. Chlorhexidine/alcohol in preterm infants. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .... . . . . . . . . . . . . . . . 000
16. Laxative . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .... . . . . . . . . . . . . . . . 000
17. Vesicants . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .... . . . . . . . . . . . . . . . 000
17.1. Sulfur mustard . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .... . . . . . . . . . . . . . . . 000
17.2. Lewisite . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .... . . . . . . . . . . . . . . . 000
17.3. Phosgene oxime. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .... . . . . . . . . . . . . . . . 000
17.4. Differential diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .... . . . . . . . . . . . . . . . 000
18. White phosphorus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .... . . . . . . . . . . . . . . . 000
19. Concluding remarks . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .... . . . . . . . . . . . . . . . 000
Acknowledgements . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .... . . . . . . . . . . . . . . . 000
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .... . . . . . . . . . . . . . . . 000

forensic toxicological analysis, the suspicion based on signs

1. Introduction
Physical, biological, or chemical agents can cause burns,
leading to a local or generalized reaction, whose severity is
related to its length and depth. Physical agents include
thermal (heated object, flame, boiling liquid, vapor, etc.),
electricity (electrocution/fulguration), hypothermia and hy-
perthermia, and radiation. Biological agents comprise sub-
stances produced by insects, jellyfish, fish, frogs and some
plants. Concerning chemical agents, the focus of the present
review, a large number of compounds (estimated at around
25,000) are capable of causing cutaneous, mucosas and ocular
chemical burns (producing more or less depth disorganiza-
tion, including its complete destruction) as consequence of
their caustic or irritant effects. Additionally, after absorption,
several systemic manifestations in different organs and
systems can be observed [1,2].
Potentially dangerous chemical products are ubiquitous in
daily life particularly in industry, scientific laboratories, at
home (e.g. cleaning products) and in agriculture settings [35].
In spite of this widespread use, chemical burns are uncom-
monly observed in daily practice in comparison to thermal/
electric burns [6]. The extension of the burn lesion depends on
several factors [710], which are highlighted in Table 1.
Accordingly previous studies [1022] chemical burns exhibit
some general characterizes, which were resumed in Table 2.
The present review appears as a natural sequence of
previous reports, in which signs and symptoms related to
xenobiotic exposure have been highlighted [2330]. Indeed, in
and symptoms is an extremely important pre-analytical step
since it allows the clinician to rapidly implement an
appropriate therapy until toxicological results become avail-
able to corroborate (or not) the initial suspicion. In addition, for
the toxicologist, the suspicion also acquires importance for the
correct selection of biological matrices to be analyzed since
when erroneously done it can introduce bias to the obtained
analytical result [24,25,27]. In this manuscript, we highlight
and discuss suggestive clinical and forensic images related to
chemical burns that can further orientate toxicological
analysis. Burns due to sulfuric, hydrofluoric, nitric, hydro-
chloric (muriatic) and acetic (including derivatives) acids,
hydrogen sulfide, sodium (caustic soda) and calcium (cement)
hydroxides, paraquat, inflation and rupture of airbags,
Table 1 Factors that influence the extension of the burn
lesion.
-Physical state (i.e. liquid, solid, gas)
-Mechanism of action of the chemical (e.g. acids, bases and
other chemicals)
-Concentration of chemical in contact/ingested
-Amount of chemical in contact/ingested
-Intent
-Strength (e.g. extreme pH solutions with pH < 2 or pH > 12 have
more serious corrosive effects)
-Duration of exposure (most relevant)
-Regional skin properties (e.g. pre-existing conditions such as
dermatitis; plantar epidermis is less permeable due to thick
stratum corneum)
-Skin differences between ages and races

Please cite this article in press as: Dinis-Oliveira RJ, et al. Clinical and forensic signs related to chemical burns: A mechanistic approach. Burns
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JBUR-4456; No. of Pages 22
burns xxx (2014) xxxxxx
Table 2 General characteristics of chemical burns
lesions.
-Hands, upper limbs, neck and face are typically exposed areas
-Rarely have regular shape (e.g. in the case of liquids, often spilled
by projection, a characteristic run-off grooves is formed
accordingly to gravity)
-Are uniform and do not differ in intensity throughout its surface
(i.e. similar caustic injuries are observed at all points that the
chemical contacts). On the other hand, distinguishable concentric
zones lesions with differences degrees are typical for all thermal
agents
-Discoloration and contractures
-Perforation of the gastrointestinal tract
-Alkalis typically cause severe injuries to the esophagus without
significant injury to the stomach due to neutralization by gastric
secretion
-Acids typically leave the esophagus relatively spared, but cause
significant trauma to the stomach, namely in the pyloric end (e.g.
natural area of stagnation or pooling of liquid) often resulting in
strictures in this region
-Full stomach tends to minimize injury due to dilution and buffer
effect for the ingested acid
-The respiratory system may be affected when aerosolized
chemicals or smoke is inhaled
-With prolonged exposure, damage to proximal and distal airways
develops followed by noncardiogenic pulmonary edema, bron-
chial obliteration, pulmonary hemorrhage and adult respiratory
distress syndrome
-Ocular damage, namely blindness, corneal opacity (i.e. due to
protein coagulation cause by acids), ectropion, keratitis and
cataracts
-Ocular damage by alkali is much more severe and irreversible,
and within 515 min can reach the anterior chamber and damage
the iris, lens, iridocorneal angle and ciliar body
-Severe systemic toxicity may occur, if large body surface areas are
injured
-Death may occurs from circulatory collapse or from secondary
destructive changes in the gastro-intestinal tract, lung, liver and
kidneys
povidoneiodine and chlorhexidine/alcohol (in preterm
infants), laxatives, and vesicants (warfare agents), will be
reviewed since these are the most common agents found in
daily practice, for which relevant and timed information may
be helpful in formulating emergency treatment protocols and
toxicological analysis. Table 3 resumes most relevant signs
and symptoms resulting from exposure to the different
chemicals discussed in this review.
2. Methods
Besides contributions with personal forensic cases, articles
written in English, German, French, Spanish and Portuguese
were searched for macroscopic signs and symptoms related to
chemical burns, using the National Library of Medicines
PubMed MedLine database and the Web of Knowledge (WOK).
3. Classification of chemicals involved in
burns
One useful classification organizes burning chemicals in six
groups according to how they damage protein [1,31]:
Please cite this article in press as: Dinis-Oliveira RJ, et al. Clinical and forensic signs related to chemical burns: A mechanistic approach. Burns
(2014), http://dx.doi.org/10.1016/j.burns.2014.09.002
3
(a) Oxidative agents cause protein denaturation by inserting
oxygen, sulfur, or halogen atoms to viable body proteins
(e.g. sodium hypochlorite, hydrogen peroxide, potassium
permanganate, potassium dichromate and chromic acid);
(b) Reducing agents they bind to free electrons in tissue
proteins, causing reduction of the amide link and protein
denaturation. Heat produced in the chemical reaction can
cause a mixed picture [e.g. nitric and muriatic (concentrat-
ed hydrochloric) acids, ferrous ion and sulfite compounds];
(c) Corrosive agents cause protein denaturation on contact
and tend to produce a soft scar, which may progress to
shallow ulceration (e.g. sulfuric and muriatic acids, and
white phosphorus);
(d) Protoplasmic agents produce their effects by forming
esters with proteins (e.g. formic and acetic acids) or by
chelating calcium or other ions necessary for tissue viability
and function (e.g. oxalic, hydrazoic and hydrofluoric acids);
(e) Vesicant agents produce ischemia with anoxic necrosis
at the site of contact. These agents are characterized by
producing cutaneous blisters (e.g. mustard gas, dimethyl
sulfoxide and Lewisite);
(f) Desiccant agents cause damage by tissues dehydration (e.g.
calcium sulfate, sulfuric and muriatic acids, and silica gel).
Although less accurate, another useful classification is
based on the chemical reactions that the agent initiates. Four
classes are considered [1]:
(a) Acids, donor of protons, release hydrogen ions and reduce
pH to values as low as 0. The free hydrogen ions facilitate
amide bond hydrolysis causing protein structures to
collapse. Acids with a pKa less than 2 (i.e. strong acids)
can produce coagulation necrosis with scars formation on
necrotic tissue, a fact that may limit further tissue
penetration. Coagulation necrosis produces rapid tissue
changes that include consolidation of the loose connective
tissue, thrombosis of intramural vessels, ulceration,
fibrosis, and hemolysis of erythrocytes. The inability of
gastric juices to neutralize these substances contributes to
the onset of lesions in the stomach and intestine, in
addition to the mouth and the esophagus [32]. Without
gastric lavage within 30 min, full-thickness coagulative
necrosis may occur [33]. In severe burns, the microvascular
thrombosis may be full thickness, which may predispose
the stomach or other organ to perforation, namely in a
fasting state and within 24 h of ingestion [33,34]. The
primary mechanism of chemical burns injuries is the
direct chemical reaction, rather than actual thermal
injury. However, several chemicals (e.g. sulfuric acid and
muriatic acid) produce extreme heat when combined with
water, thus necessitating chemical neutralization or
removal prior to lavage with water for therapeutic
purposes [35]. Acids can be highly irritative and unpleasant
to taste. This can lead to choking and gagging upon
ingestion. Choking and gagging lead to the acid coming
into contact with glottis and epiglottitis with airway
compromise [36]. Typically they produce dry scar with
color varying from one substance to another (e.g. black and
yellow for sulfuric and nitric acid, respectively);
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4 burns xxx (2014) xxxxxx

Table 3 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 derivatives Cough, tachypnea, wheezing, headache, nausea, vomiting, impaired vision, abdominal pain, diarrhea, eye,
(glacial acetic, trifluoroacetic nose and throat irritation, tooth erosion, conjunctivitis, pharyngeal and pulmonary edema, whitish
and monochloroacetic acids) discoloration of the skin (exposure to trifluoroacetic acid)
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
Vesicant sulfur mustard Skin burn, pruritus, erythema, xerosis, purpura, hypopigmentation, 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

(b) Alkali compounds have been implicated in injuries by
three main mechanisms [32]: (i) they combine with fats to
form soap (saponification of fat) through an exothermic
reaction, producing a significant amount of heat, which
causes severe tissue damage. Destruction of fat allows an
increase in water penetration of the alkali burn scar,
annulling the natural water barrier that lipid provides [37];
(ii) they extract considerable water from cells causing
damage due to the hygroscopic nature of alkalis; (iii) they
accept hydrogen ions (protons) from the amide bonds of
the protein backbone by hydroxylation, which leads to
protein hydrolysis and therefore tissue dissolution to form
alkaline proteinates, which contain hydroxyl ions (OH)
that can cause further chemical reaction and initiate
deeper injury of the tissue. This penetrating injury induces
liquefaction necrosis and occurs especially if pH is higher
than 11 [38,39]. The products formed favor the penetration
of the remaining alkali into the tissue by increasing the
solubility, causing the alkalis to reach deeper tissue layers,
including muscular, therefore resulting in very serious
injuries [40]. Indeed, damaged tissue has limited capacity
to buffer alkalis and no scar is usually formed. If they exist
are of soft, translucent and moist consistency, passing
to fat saponification (aspect soap) and with ill-defined
margins. Therefore, alkali injuries are commonly regarded
as having the potential to be more severe than acid injuries
(and even more that thermal burns), which are usually
self-limiting and more superficial [2,41];
(c) Organic solutions act by dissolving the cells lipid mem-
branes and disrupting the cellular protein structure;
(d) Inorganic solutions damage by salt formation (e.g. zinc
chloride, potassium chloride, calcium chloride, potassium
oxalate). It should be noted that all of these reactions may
be exothermic, which contributes to tissue injury. Lesions
are usually dry and white.
4. Sulfuric acid (H2SO4)
Sulfuric acid is a very cheap and easy-to-get liquid, being
commonly used for restoring exhausted car batteries and in
the leather industry. Concentrated H2SO4 (52100%, mixed in
water) is also commonly used as a drain cleaner, and is easily
available from various retail outlets. Consequently, it is one
of the chemical agents more often involved in acid burns [42].
It is highly corrosive (also its precursor sulfur trioxide)
and causes damage by tissue dehydration and heat produc-
tion. Dark-brownish colored burns are usually observed
(Fig. 1AD). Sulfuric acid vapor is also strongly irritant to the
respiratory tract and can cause sore throat, coughing,
shortness of breath and potentially fatal severe pulmonary
edema [43].

Please cite this article in press as: Dinis-Oliveira RJ, et al. Clinical and forensic signs related to chemical burns: A mechanistic approach. Burns
(2014), http://dx.doi.org/10.1016/j.burns.2014.09.002
JBUR-4456; No. of Pages 22
burns xxx (2014) xxxxxx
Fig. 1 Dark-brownish colored sulfuric acid skin and mucosal burns.
Reproduced from [42] (A), [44] (B) and [189] (C), with permission.
The internal examination may reveal mural perforation of
the gastroesophageal junction and cardia, and fundus of the
stomach, with complete separation of the stomach from the
esophagus at the level of the gastroesophageal junction (Fig. 1D
F) [44]. Death may be rapid following ingestion as consequence of
cardiovascular collapse or shock secondary to gastrointestinal
tract rupture-related chemical peritonitis [45,46].
The phenomenon of throwing H2SO4 at someone (e.g. for
assault) is relatively common especially in Africa or Asia
[42,47] due to its extremely destructive action, bad scarring,
mainly as hypertrophic and keloid scars, of dark skinned
people [48]. There is a predominance of female victims in the
case of aggression, mainly after domestic disputes [49]. The
face, head, and neck are predominantly injured but extension
to the trunk and upper limbs is not rare. The physical and
psychological outcomes are usually poor, with permanent
disfigurement or loss of vision (Fig. 2A and B).
5. Hydrofluoric acid (HF)
Hydrofluoric acid is widely used in glass etching and cleaning,
the production of semiconductors, fluorocarbon, plastics,
products for rust removal, germicides, insecticides, tile-
cleaning agent, aluminum brighteners, automobile wheel
cleaners, air conditioner cleaners, and other industrial and
domestic processes [50,51]. Since the aqueous HF solution is a
weak acid due to high electronegativity of the fluoride ion
(dilute concentrations remain relatively non-ionized; 1000
times less ionized than hydrochloric acid), dermal burns
significantly depend on its concentration [52], the although
other factors described before may of course influence the
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5
outcome. Solutions of up to 20% may not produce pain or
erythema for up to 24 h. Burns from acid concentrations of 20
50% usually became apparent within 18 h, whereas concentra-
tions of over 50% produce the typical picture (i.e. whitish tissue
with surrounding erythema and immediate pain). Due to its high
electronegativity it acts by two distinct mechanisms [50]:
(a) Fluoride ions are highly lipophilic and penetrate the
tissues deeply, accumulating in cells, leading to painful
liquefactive necrosis with progressive evolution despite
surface decontamination, unless neutralized (by salt
formation) with calcium and/or magnesium drugs [53];
(b) Free hydrogen ions (H+) cause hydration and corrosive
superficial burn of tissues similarly to HCl and H2SO4 [54].
Dermal exposures often cause local injury with signs and
symptoms developing over time, and the patient may not seek
urgent medical evaluation, resulting in a potentially worse
clinical outcome. Systemic toxicity may occur and it is
characterized by consequences of electrolyte imbalance (i.e.
fluoride ions bind to several intra- and extra-cellular ions
resulting in hyperkalemia, hypocalcaemia and hypomagnese-
mia), such as tetany, seizure, corrected QT interval prolonga-
tion, ventricular dysrhythmias, cardiac arrest and death
[50,51,55,56]. The consequent decrease of extracellular calci-
um and magnesium concentrations can transiently be
buffered by protein-bound and bone ion storage. If intense
intravenously, topical and subcutaneous intra- and parale-
sional instillation of calcium (e.g. calcium gluconate) therapy is
performed, cutaneous calcification may developed (Fig. 3A
and B) [57].
JBUR-4456; No. of Pages 22
6 burns xxx (2014) xxxxxx
Fig. 2 Permanent squeals of the esthetic appearance with
retraction and impaired of the movements.
Reproduced [190], with permission.
Fluoride also inhibits intracellular enzymes, including
those of the Krebs cycle and the Na/K+ ATPase pump, which
contributes to cellular energy failure, efflux of potassium and
therefore to cell death [51,58]. These electrolyte shifts at nerve
endings are thought to be source of the extreme pain
associated with hydrofluoric acid burns [59].
Common dermal signs are maceration, erythema, edema,
ulcers, necrosis, progressing to whitish (silvery-gray) discol-
oration and blistering (Fig. 3AC). Gray areas indicate severely
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Fig. 3 Silvery-gray or blue-grayish necrosis due to
hydrofluoric acid.
Reproduced from [57] (A), [191] (B), and [192] (C), with
permission.
damaged tissue and may proceed to deep ulceration and skin
necrosis [52]. If is not removed, tissue destruction may
continue and result in alkali-like liquefactive necrosis,
tendosynovitis, and even osteolysis [50,51,58,60,61]. Subun-
gueal tissue is particularly susceptible [51].
6. Acetic acid (CH3COOH) and its derivatives
glacial acetic acid, trifluoroacetic acid (C2HF3O2)
and monochloroacetic acid (ClCH2CO2H)
Acetic acid has been used for centuries for medical purposes to
reduce infections and to support other means of treatment. It
is also used to manufacture medicines, spices and dyes, as
well as certain pickled foods and synthetic vinegar, and used
JBUR-4456; No. of Pages 22
burns xxx (2014) xxxxxx
as a folk medicine to cure Tinea pedis and to remove nevus or
warts [62].
Glacial acetic acid is a strong acid and the purest form of
acetic acid commercially available (>99.85%). Its name derives
from the solid crystals that form below room temperature
(17 8C) when undiluted (anhydrous) [63]. It can cause severe
inflammation and chemical burns if directly contacts with
mucosa or skin. Yoo et al. [63] described a patient with deep
second-degree chemical burns on the face caused by the
application of a mixture of glacial acetic acid and flour for
chemical peeling. During a 6-month follow-up, hypertrophic
scarring developed on the both nasolabial folds despite scar
management.
Vinegar is produced from various fruits such as grapes,
apples, and lemons and contains 45% acetic acid (gives
Fig. 4 Acetic acid and its derivatives glacial acetic acid,
monochloroacetic acid (A) and trifluoroacetic acid (B)
related burns. (A) Joint deformity after monochloroacetic
acid exposure.
Reproduced from [65] (A) and [69] (B), with permission.
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7
vinegar its sour taste and smell). Although this is a weak acid,
it can produce a chemical skin burn when used under
occlusion or compression for a long time as an antipyretic
(alternative medicine) [64].
Monochloroacetic acid is used in low or high concentra-
tions in most European countries for topical treatment of
warts. It is a strong organic acid, irritating and corrosive to the
skin, leading to burns, and has a high systemic toxicity [65,66].
In addition to wart treatment, it is used for industrial
purposes, such as the synthesis of certain organic chemicals
[67,68]. Tan Baser et al. [65] presented a case of joint deformity
manifesting after the use of a preparation containing
ClCH2CO2H (in very low concentration 0.08%) for topical wart
treatment (Fig. 4A).
Trifluoroacetic acid is used industrially in peptides pro-
duction. In the laboratory, C2HF3O2 is also widely used in low
concentrations in eluents for liquid chromatography [69]. It is
one of the strongest carboxylic acids (i.e. pKa = 0.3) and easily
soluble in both water and organic solvents, which favors the
skin penetration and difficult healing [69]. It is structurally
similar to acetic acid (pKa = 4.8), but the electron-withdrawing
effect of three fluorine atoms in the molecule strongly favors
the release of the proton. It has been suspected that C2HF3O2
could have a similar toxic effect as HF, since it also releases
fluoride ions, resulting in whitish discoloration of the skin
(Fig. 4B), hyperkalemia, hypocalcaemia, hypomagnesaemia.
Cases have been reported where trifluoroacetic anhydride
was the cause of severe chemical burns [70]. This anhydride is
often used as a derivatizing agent for amine groups before
chromatographic analysis. Upon hydrolysis, this anhydride
forms C2HF3O2. Injuries are probably a combination of the
corrosive effect of the acid formed upon hydrolysis and the
high reactivity of the anhydride.
7. Nitric acid (HNO3)
Nitric acid (aqua fortis (strong water), spirit of nitre or
engravers acid) is an important chemical for industrial
and domestic purposes [6,71]. Unlike H2SO4 and HCl, even
when concentrated HNO3 formulations are ingested, the
tendency to produce tissues charring and then perforation is
a rare event, mucosal irritation being commonly observed
[6,72]. A yellowish discoloration of the skin and mucosas
(Fig. 5AC) due to a reaction with keratin (xanthoproteic
reaction nitration of the benzene ring of aromatic amino
acids) as well as whitish tinge of teeth, are usually observed
[6,72]. In high concentration and volume, HNO3 reacts with
blood, forming acid hematin, which is the cause for charring
(black discoloration) of the skin and mucosas. Methemoglo-
binaemia with subsequent hemolysis can also occur due to
the formation of nitric gas (NOx) [73]. In addition, the resulting
hemolytic products and metabolic acidosis can lead to renal
tubular necrosis and acute renal failure [73]. When ocular
contact with nitric acid or its vapors ocuurs, ocular damage
ranges from severe ulceration and necrosis of the cornea and
lens, from resulting ablepsia to increased lacrimation [72].
Nitric acid does not accumulate in the body as it is rapidly
broken down into its constituent ions, which are excreted in
the urine [72].
JBUR-4456; No. of Pages 22
8 burns xxx (2014) xxxxxx
Fig. 5 Yellowish discoloration of the oral (A) and esophageal (B) mucosa and skin (C) due to nitric acid burn.
Reproduced from [6] (A and B) and [72] (C), with permission.
8. Hydrochloric (muriatic) acid (HCl)
Burns caused by this HCl are less frequently observed
comparatively to H2SO4. In contact with the skin, HCl
denatures the proteins into chloride salts [1]. Its bleaching
action causes the damaged surface to be white or grayish in
color (Fig. 6). Even in second-degree chemical burns, the
absence of bulla formation and the white pigmentation,
makes diagnosis less accurate, and unexpectedly severe tissue
damage may be present [74]. Pulmonary damage (upper
airway edema, pulmonary inflammation) can be produced if
HCl fumes are inhaled [1].
9. Hydrogen sulphide (H2S)
Hydrogen sulfide is a colorless and water-soluble gas (flamma-
ble and explosive) that has a pungent odor likened to the smell
of rotten eggs easily noticeable at 0.1 ppm [75,76]. These low
levels that give an olfactory warning are generally not fatal. It is
attenuated and becomes sickly sweet with increasing concen-
trations; above 100 ppm, olfactory saturation occurs and
individuals can no longer detect the presence of this lethal
gas. It is produced during anaerobic bacterial decomposition of
sulfur-containing organic matter [77] and is used in some
manufacturing processes either as raw material or as a waste
product [76]. It is heavier than air and therefore accumulates in
the lower levels of cavities, depressions or hollows.
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Hydrogen sulfide poisoning is infrequently encountered in
medical practice. Most of the cases are related to accidents
from workplace exposure to sewer gas (H2S is released
during the cleaning out of sewers or descaling of pipes) or
during commercial manufacturing [76,78]. Toxicological
analysis for thiosulfate in blood and urine confirm the
diagnosis. Inhalation is the main mode of human exposure.
At low levels, H2S acts primarily as a severe local irritant of
conjunctivae, sclera and the upper respiratory tract [78]. At
higher concentrations (10002000 ppm), systemic toxicity
and rapid death may occur, which is thought to be related
to inhibition of cytochrome oxidase (anoxic effect) of the
electron transport chain, similarly to cyanide [79]. Brain and
heart, which have the highest oxygen requirements, are
particularly sensitive to this disturbance of oxidative metab-
olism [80].
Autopsy findings include an accentuation of the greenish
color of gray matter (Fig. 7A and C) of the brain, cherry-
red or pink lividity (mimicking other intoxications such
carbon monoxide [29]) and green patches in the skin (Fig. 7E)
[76,81]. Although it is hypothesized that sulfhemoglobin
may be responsible for the discoloration, acute H2S
poisoning does not result in high levels of sulfhemoglobin
before the onset of putrefactive changes [82]. Less com-
monly observed are the serous and hemorrhagic pulmonary
edema, visceral congestion, bronchial secretions, and
scattered petechiae [80,83]. Christia-Lotter et al. [77] pre-
sented a fatal case of massive myocardial necrosis after H2S
exposure (Fig. 7F).
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burns xxx (2014) xxxxxx 9

Fig. 6 Grayish-black discoloration of the esophagus, larynx and spleen due to hydrochloric acid ingestion.

10. Sodium hydroxide (NaOH; caustic soda)
Sodium hydroxide presents as white crystals without odor and
takes the form of flakes, granules, tablets or solutions. It is very
hazardous, especially in the liquid form [5]. It is used to
manufacture soap, rayon, paper, explosives, paint, cotton,
bleach, laundry, and beauty products and oil byproducts.
Solutions are easily swallowed, being tasteless and
odorless [36], and is most likely to damage the esophagus
and stomach. Burns typically occur at regions of anatomic
narrowing, such as the cricopharyngeus, the aortic arch, the
left main stem bronchus and the diaphragmatic hiatus [36].
Organs adjacent to the upper gastrointestinal tract such as the
larynx, trachea, aorta, colon, and even pancreas may also be
injured [4]. When at 1.83% (frequently found in commercial-
ized cleaning products), signs of necrosis were observed in the
epithelium and less aggressive injuries in the submucosa and
the muscle layer. Submucosal necrosis becomes visible at
7.33% [84]. Solids produce deep burns where they adhere to the
oral mucosa and are usually spit out. If more than 60 g of the
solid form are ingested, it is almost always fatal [32].
Signs on early presentation include skin burns (Fig. 8A),
oropharyngeal pain, dysphagia, vomiting, drooling and excessive
salivation, ulcerative mucosal burns, dyspnea, stridor [85]. The
strong corrosive action of NaOH is confirmed by the endoscopic
findings of patients, who frequently show multiple tortuous
strictures, often in the upper esophagus [40]. In addition, can
cause severe ocular injury because of the quick corneal
penetration, leaving the victim with significant visual im-
pairment, namely opacification of the cornea and perforation [1].
The pathophysiology process after ingestion occurs in
stages. First stage is characterized by eosinophilic necrosis
with edema and intense hemorrhagic congestion [86], the
tissues ranging from white, to sloughy gray, to black (Fig. 8A).
Ten days later, granulation tissue begins to replace the
necrotic slough, and by 3rd week there is fibroblastic

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10 burns xxx (2014) xxxxxx

Fig. 7 Hydrogen sulfide poisoning. Greenish discoloration of the brain (A), gray matter and nuclei (C) in comparison to
normal appearance (B and D), respectively. E-green patches in the skin. F-Heart showed gross changes and a generally
heterogeneous appearance.
Reproduced from [80] (AD), [81] (E), [77] (F), with permission.

proliferation and scarring, and formation of strictures initiates
[85]. Mortality is low, but morbidity is high, with up to 33% of
patients developing long-term squeal secondary to stricture
formation, such as stenosis of the oral musculature and extra-
articular ankylosis, leading to microstomia (Fig. 8B) and
contracture of tongue and trismus [87,88]. This may lead to
obliteration of the lingual and buccal sulci and failure of
normal tongue movement with resultant difficulty in oral
hygiene, speech, and mastication. Severe fibrosis of the
alveolar mucosa and soft tissue envelope may lead to
abnormal development of the secondary dentition and
subsequent problems with facial growth [85]. Another long-
term complication of ingestion is the high incidence of
malignant transformation at the stricture site [32,89].
11. Calcium hydroxide (Ca(OH)2; cement)
Cement is a solid material obtained by calcinations, widely
used throughout the world in the construction sector to bind

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JBUR-4456; No. of Pages 22
burns xxx (2014) xxxxxx
Fig. 8 Signs of sodium hydroxide exposure. (A) Necrosis
with edema and intense hemorrhagic congestion, the
tissues ranging from white, to sloughy gray, to black. (B)
Severe microstomia secondary to scarring.
Reproduced from [85], with permission.
sand and stones into a matrix of concrete [90]. Employers and
builders do not realize that it as a chemical mixture of silicates
and calcium aluminates. Lime (general term for calcium-
containing inorganic materials, in which carbonates, oxides
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11
and hydroxides predominate; strictly speaking it is calcium
oxide) is the largest constituent of cement and accounts for
65% by weight. The calcium oxide (CaO) in cement reacts with
water to form the highly alkaline product, Ca(OH)2. Within
2 min, the pH reaches 1213 and increases over the next
30 min. Therefore, wet cement can cause serious corrosive
damage through abrasion and prolonged contact with the
skin. This mixture remains alkaline for 814 h until carbon
dioxide in the air converts it to the chemically inert calcium
carbonate [91,92]. Wet cement is the leading cause of
occupational skin disease in the construction industry,
namely causing contact dermatitis, which is favored by
occlusion due to wet clothes or shoes. It damages the skin
by 4 different mechanisms ranging from mild irritation to full
thickness burns [93,94]:
(a) Allergic dermatitis develops as reaction to hexavalent
chromate and cobalt ions to which the patient has
previously become sensitized. In some countries, ferrous
sulfate has been added to cement since it reduces
hexavalent chromium to trivalent chromium, which is less
soluble, has a lower skin penetration rate, and, therefore,
rarely causes sensitization. Indirectly, the predisposition to
cobalt allergy has been decreasing after reduction of the
cases of severe chromate related-dermatitis [93];
(b) Abrasions caused by prolonged rubbing by clothing, boots
or gloves impregnated with alkali, and fine and persistent
abrasive aggregates of cement;
(c) Thermal burns as consequence of the exothermic reaction
with sweat. Even when not exposed to moisture, the dry
powder is very hygroscopic and results in desiccation
injury [95];
(d) Alkali burns (liquefaction necrosis) due to cement high pH.
These burns are more rarely seen in routine dermatologi-
cal practice.
Dermal cement burns (Fig. 9A and B) have an insidious
onset and the patient may be initially unaware of a problem
until several hours later [96]. Indeed, symptoms may begin
15 min to 48 h after exposure and duration until presentation
may range from several hours to 10 days (average 38 h) [97].
Mild irritation, burning sensations, pain, erythema and
vesicles occur as the initial symptoms. After 1248 h, partial
to full thickness burns may occur [97]. Erythema around ulcers
covered with black necrosis is usually observed [98,99].
Exposure to wet cement for a period of 1 h was reported to
produce third-degree burns [100].
Burns can be particularly devastating if they involve the eyes
and are most commonly caused by a splash of thick and moist
plaster, cement, in an individual not wearing protective goggles.
In severe cases, blindness may be permanent [101]. Rarely,
calcium oxide dust may aerosolize and become an irritant to the
respiratory tract. Ulceration and perforation of the nasal
septum as well as pneumonia have been reported [102].
Cement burns usually affect only a limited body surface
area (rarely greater than 5%), namely the lower extremities
[90,97,103,104]. Injury to the upper extremity is less common,
but case reports of hand injury exist from both mixing cement
as well as high-pressure injection [105,106].
JBUR-4456; No. of Pages 22
12 burns xxx (2014) xxxxxx
Fig. 9 Burns following cement exposure with edema, minimal hemorrhage, necrosis, and erythema of the skin.
Reproduced from [193] (A), with permission and B was courtesy of Professor Alena Machovcova [99].
Besides construction workers, unusual cases have been
reported in athletes who have sustained injuries after coming
into contact with the chalked lines of sporting fields in wet
conditions [107]. Santos-Pinto et al. [108] presented an unusual
case of burn in buccal mucosa and on the anterior faucet pillar
caused by calcium Ca(OH)2 used in a pulp therapy.
12. Burns after inflation and rupture of
airbags
Airbags are inflatable rubber-lined woven nylon bags,
designed to inflate upon the detection of rapid deceleration,
even in the case of low-impact collisions, in order to minimize
injury to the driver and passengers [109]. Burns after airbags
inflation are extensively described (Fig. 10A and B) and the
following factors have been implicated [110,111]:
(a) Thermal effect from high-temperature gases (direct) and
due to melting of clothing (indirect);
(b) Chemical effect from alkaline corrosives and particulate
materials (effect yet unknown). Indeed, during this
inflation, approximately 70 g of sodium azide (NaN3) are
ignited, releasing at a great speed from a storage
compartment, nitrogen (96%), carbon dioxide (3%) and
miscellaneous gases and particulates (1%), as well as a
small amount of alkaline aerosol containing NaOH,
sodium carbonate and metallic oxides [111,112]. These
appear to happen when the gases come into contact with
body fluids such as sweat or tears [113,114];
(c) Friction from the nylon covering the airbag may result in
skin abrasions and erythema (most of the cases).
The release of irritant gases and particulates during
deployment can lead to or exacerbate respiratory problems,
especially in asthmatic patients [115]. Burns secondary to
airbag deployment are known to occur primarily on the face
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and neck, but have also been shown to occur on the upper
extremity and chest [37,112,116119]. Although rare (due to
skins scarce capacity to counter alkalinity), scar-formation
after airbag burns has been described [112,118,120]. Since the
contribution of friction and chemical components versus
thermal cannot be separated, certainly the scar formation
may be viewed as being multifactorial.
13. Paraquat
Although deliberate ingestion is responsible for most cases of
serious paraquat toxicity, morbidity and mortality can result
from other routes of exposure, namely dermal by accidental
exposure during spraying [121123]. Due to corrosive effects,
paraquat may cause skin burn (blistering), nails white
discoloration, and ulcerated lesions in the lips, tongue,
oropharynx, esophagus (including perforation), stomach,
scrotum and trachea [124127] (Fig. 11A). Scrotal burns have
also been reported due to contact with cloths soaked in
paraquat formulation (Fig. 11B) [128]. The extent and severity
of such damage is mainly dependent on the concentration of
paraquat in the formulation rather than the dose (as for
gastrointestinal lesions). In general, systemic toxicity in
humans, after percutaneous exposure, seems unusual as
reported by Hoffer and Taitelman [125] whom described 15
consecutive cases of single exposures of the skin or eyes
during contact with paraquat at working places. From these
data it is apparent that a single exposure of healthy skin to
paraquat solutions only causes local lesions. However,
patients with repeated dermal exposures to paraquat may
have significant skin irritation or can even die due to dermal
absorption. In all of these cases, one or more of the following
factors were present: previous skin damage, caused either by
paraquat itself or by mechanical or other chemical means, and
prolonged skin contact to clothes soaked in concentrated
paraquat, or less concentrated solutions if the skin is not
JBUR-4456; No. of Pages 22
burns xxx (2014) xxxxxx
Fig. 10 Airbag skin burns.
Reprinted from [116] (A) and [194] (B), with permission.
washed immediately after exposure [122,129]. At autopsy, the
findings are well described in paraquat poisoning such as
pulmonary fibrosis, intra-alveolar hemorrhage, kidney edema,
cholestasis and hemorrhage, and jaundice liver [121].
14. Povidoneiodine
The antiseptic properties of iodine to cure or prevent infection
in wounds has been recognized for over 150 years [130].
Nevertheless, aqueous or alcoholic (tincture) solutions of
iodine were associated with skin irritation and excessive
staining [131] and therefore have been substituted by poly-
vinylpyrrolidone-iodine (PVP-I or povidoneiodine), which
was firstly introduced as a water-soluble compound by
Shelanski and Shelanski in 1956 [132]. Povidoneiodine is an
example of an iodophor, a complex of molecular iodine and a
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Fig. 11 Burns and ulceration due to paraquat exposure.
Reproduced from [127] (A) and [195] (B), with permission.
solubilizing carrier (polyvinylpyrrolidone), which acts as a
reservoir of free active iodine that is constantly released and
remains in dynamic equilibrium with the complex [131,133].
Povidoneiodine is available in a range of antiseptic formula-
tions (solution, scrub, ointment, tincture, and foam) [134], the
aqueous solution being (10% PVP-I) the most commonly used.
Although uncommon, iatrogenic chemical burns (Fig. 12)
have been reported with povidoneiodine solutions [134,135].
The chemical burn resulting from tourniquet application may
even cause more in-depth injury to the skin than the abrasion
wound because there is a longer exposure and the anesthesia
prevents the patient pain reaction [136138]. The basic
mechanism of tourniquet-induced chemical burn is related
to increased permeability of the skin to povidoneiodine as
consequence of irritation by antiseptics coupled with macer-
ation of the skin, compression pressure and its duration, and
wetness underneath the tourniquet [135,139141]. The bony
prominences, pressure or shearing points under constricted
tourniquet dressings or bandages are the typical locations.
Alcohol (70%), which is used for draping, may also cause
hypersensitivity [134,135]. By using alcohol, the epidermal
lipid barrier may be decreased by de-esterification leading skin
more prone to chemical burn.
JBUR-4456; No. of Pages 22
14 burns xxx (2014) xxxxxx
Fig. 12 Superficial partial thickness burn due to povidone
iodine exposure.
Reproduced from [196], with permission.
15. Chlorhexidine/alcohol in preterm infants
Chlorhexidine is a topical antiseptic agent with well-known
activity against gram-positive bacteria, viruses, and fungi [142].
Its favorable activity, associated with few adverse effects
comparatively to other antiseptics such as mercury or iodine
derivatives, make it a first-line choice for antisepsis in most
neonatal units. Although 0.5% chlorhexidine is considered safe
in neonates, the same is not true when used in combination
with alcohols such ethanol and methanol [143]. Reports of local
reactions with use of chlorhexidine in alcohol-based solutions
have been published in the past (Fig. 13), especially in extremely
low birth weight infants (<28 weeks of gestation) [144,145]. It is
the alcohol content in any skin cleansing solution that is known
to cause skin burns. Skin of extremely low birth weight infants
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Fig. 13 Burns related to chlorhexidine used in
combination with alcohol in extremely low birth weight
infants.
Courtesy of Professor Mannan [145].
is more susceptible to damage by topical application of
chemical cleansing solutions as compared to term infants
[146]. Their stratum corneum is thin and loosely bound to dermis
that can also lead to increased percutaneous absorption of
drugs [143]. In these cases, chemical burns due to alcoholic
solutions may cause important local squeal and impairment of
neurodevelopmental outcome [145,147].
16. Laxative
Senna-containing laxative has been found to induce a range of
skin lesions from severe diaper rash to partial thickness burns
[148,149]. Senna is an anthraquinone laxative and causes
excessive secretion of water into the colon and accelerates
colonic transport by stimulating smooth muscle contraction.
The lesions often occur in situations where there has been
prolonged contact of the skin with diarrhea induced by
children overdose ingestion of Senna-containing laxatives
[148], but cases of therapeutic doses are also described [150].
Indeed, children are more prone to this type of injury, since the
presentation of the product as chocolate tablet formulation is
attractive [151]. Additionally, children are more likely to wear
diapers or overnight pull-ups that expose the skin to
diarrhea for prolonged periods of time [152]. The mechanism
of skin breakdown and length of exposure time needed to
cause lesions is unknown. However, plausible hypotheses
include the irritant effect of digestive enzymes in the diarrheal
stool and the irritant effect of Senna within stool [149,153]. The
location and severity of lesions may lead to suspect of abusive
thermal injury. Diamond-shaped lesion on the buttocks, linear
borders aligning with the diaper edge, and usually sparing of
the perianal tissue and gluteal cleft has been described to help
in the differential diagnosis (Fig. 14A and B) [150,153].
17. Vesicants
The vesicants or blister agents are so called because
they produce blisters. They include the synthetic and
JBUR-4456; No. of Pages 22
burns xxx (2014) xxxxxx
Fig. 14 Laxative-induced thickness burns of the buttocks
incorrectly suspected to be abusive thermal burns.
Reproduced from [153] (A) and [150] (B), with permission.
structural-related nitrogen and sulfur mustard gases, the
organic arsenicals such as Lewisite and phosgene oxime [154].
17.1. Sulfur mustard
Sulfur mustard ([bis-(2-chloroethyl)sulfide]; 2,20 -dichloro-
diethyl sulfide) was firstly used during the First World War
(1917) by the Germany army in Ypres (and since then has been
named yperite; Belgium) resulting in approximately 1,200,000
soldiers exposed [155]. The name mustard was given to the
compound by soldiers, apparently because of the smell
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perceived during gas attacks [155]. Since that time, the odor
has been described as similar to that of garlic, mustard,
horseradish and leeks [155]. More recently, sulfur mustard was
used in the IranIraq (19801988) conflict against Kurdish
civilians and Iranian troops [156]. It is an oily, lipophilic liquid
(color ranges from light yellow to dark brown) with poor
aqueous solubility and highly soluble in organic solvents,
fuels, and lubricants [157,158]. It is a liquid at standard
temperature and pressure (low volatility), and persists in the
environment in this physical state, particularly in cold and
damp climates [157,159]. Warmer climates promote increased
vapor production and shift the exposure from liquid to gas,
with alterations in clinical presentation. If temperature
remains high even at night (as in the southern parts of Iran)
the gas phase is removed by wind, decreasing the persistence
of sulfur mustard in the environment and therefore lessening
the possibility of adverse effects [160]. If night is too cold as in
high altitudes such as in northwestern Iran (Kurdistan), again
it is converted to the liquid form. Recurrence of this cycle
provokes development of cutaneous features from close
contact with the liquid form and also respiratory and ocular
complications after inhalation of sulfur mustard vapor [160].
Sulfur mustard is heavier than air and will concentrate in low
lying areas [154].
The destructive properties of sulfur mustard on the skin,
eyes, and respiratory system, in combination with the lack of
an antidote, significant environmental persistence, and
relative ease production in large amounts, make it a potential
agent of terrorism and to be used on the battlefield. The degree
and onset of injury depends on multiple factors such as dose,
mode of exposure, environmental conditions (temperature
and humidity), skin pH and moisture, mustard formula (liquid,
vapor), friction and occlusion and use of protective equipment
(mask, clothing). Immediate burning is often described if
sulfur mustard is combined with Lewisite to decrease the
freezing point to improve its efficacy in cold weather [161,162].
Food, porous materials, paint, and rubber readily absorb sulfur
mustard and may remain contaminated for prolonged periods
[158].
Once absorbed, sulfur mustard forms a reactive cyclic
structure, the episulfonium ion; this is an alkylating ion
capable of reacting with DNA, RNA, proteins, glutathione
carbohydrates, and lipids [163166]. Sulfur mustard also
triggers a cascade of inflammatory processes resulting in
massive tissue damage, mainly blistering and necrosis of any
organ coming into contact or penetrated [164]. It primarily
affects the skin (with blistering; Fig. 15A), respiratory tract, and
eyes, though as an alkylating agent it can be toxic to rapidly
proliferating cells, such as bone marrow and lymphoid tissue
[157,167,168]. Fatalities are rare but when they occur, blistering
formation are normally present [169,170].
Dermal exposure is characterized by a latent period of 2
24 h without symptoms (depending on the dose of the
inflicting agent), followed by pruritus and burning sensation,
erythema, xerosis, purpura, hypopigmentation, hyperpigmen-
tation (Fig. 15B) and the formation of small vesicles (filled with
an amber colored fluid) by 18 h that coalesce into large bullae
by 48 h [171,172]. Between 48 and 72 h post exposure, new
blisters may appear and those subsisting may rupture,
resulting in full-thickness skin loss, ulcers and scar formation
JBUR-4456; No. of Pages 22

16 burns xxx (2014) xxxxxx

[157]. Sloughing of the scar occurs by days 46 and results in a

pigmented scar by 19 days after exposure [173,174]. The groin
and axilla (flexor surfaces) are more commonly affected
because of moisture due to profuse sweating and occlusion
effects that enhanced absorption [175]. Large dermal expo-
sures can lead to significant systemic absorption and bone
barrow suppression with leukopenia occurring 34 days after
exposure, reaching a nadir approximately 9 days post
exposure [168]. Emadi et al. [176] described a very unusual
case of genitalia contact with sulfur mustard (Fig. 15C). Late
complications were registered, namely hypo- and hyperpig-
mentation on the glans (due to destruction of melanocyte),
extensive depigmentation of the external meatus and pro-
gressive obstruction of the urethral canal.
Contrary to sulfur mustard, nitrogen mustard has been
utilized as a chemotherapeutic agent [154] and has never been
used for chemical warfare [177].

17.2. Lewisite

Lewisite (dichloro (2-chlorovinyl) arsine) was first synthesized

by Wilford Lee Lewis (give the name Lewisite) in the United
States in 1918 but too late for use during World War I [154,166].
It is persistent oily and colorless substance, arsenical vesicant
chemical warfare with the odor of germaniums [154]. There
are no industrial or commercial uses for Lewisite. Although it
is highly toxic to airway tissue, skin and eyes, it is normally
used to lower the freezing point of sulfur mustard (when both
compounds are mixed) in cold weather military operations.
Skin lesions produced differ from those of sulfur mustard in
their pathology and development. Topical exposure is accom-
panied by immediate pain (seconds to minutes), compared to
the delayed symptoms caused by sulfur mustard. Since the
victim experiences pain immediately, they are likely to seek
for protection and treatment rapidly. In addition, although the
blisters produced by Lewisite tend to be much more severe
than those produced by sulfur mustard, they heal faster [161].
Thus, use of the mustard/Lewisite mixture would undoubtedly
produce immediate fatalities with painful and debilitating
injuries that would only heal slowly. The toxicity of Lewisite is
inter alia caused by the high affinity for the vicinal dithiol
system present in dihydrolipoic acid, a component of the
pyruvate dehydrogenase complex, as is also the case for other
arsenicals [178]. This prevents the formation of acetyl
coenzyme A from pyruvate.

17.3. Phosgene oxime

Phosgene oxime (different of plain phosgene) is often

classified as vesicant, but it does not cause the development
of blisters [154]. It is indeed a nettle agent that causes a
corrosive skin or tissue injury. Like phosgene, phosgene oxime
can also cause pulmonary edema. Skin blanching surrounded
by an erythematous ring can be observed within 30 s after

Fig. 15 Signs after sulfur mustard exposure. (A) Vesicant

(blistering) effect. Tense bullous lesion with straw-colored and extensive depigmentation of the external meatus and
fluid and surrounding erythema. (B) Hypo and obstruction of the urethral canal.
hyperpigmentation macules and bright red, dome-shape Reproduced from [197] (A), [198] (B) and [176] (C), with
papules. (C) Hypo- and hyperpigmentation on the glans permission.

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(2014), http://dx.doi.org/10.1016/j.burns.2014.09.002
JBUR-4456; No. of Pages 22
burns xxx (2014) xxxxxx
exposure. A wheal then develops within 30 min. The original
blanched area acquires a brown pigmentation by 24 h. A scar
forms in the pigmented area by 1 week and sloughs after
approximately 3 weeks. Initially, the effects of phosgene oxime
can easily be misidentified as mustard gas exposure. However,
the onset of skin irritation resulting from phosgene oxime
exposure is a great deal faster than mustard gas, which typically
takes several hours or more to cause skin irritation [179].
17.4. Differential diagnosis
When a patient presents with the complaints of blister
formation or exposure to a chemical with a garlic like odor,
several compounds must be considered in the differential
diagnosis besides the vesicant agents described above. Indeed,
Fig. 16 White phosphorus burns. (A) Total left peripheral
facial paralysis. (B) Fluorescent wounds under ultraviolet
light (i.e., Woods lamp). A waxy and yellow appearance is
observed under natural light.
Reproduced from [183] (A) and [199] (B), with permission.
Please cite this article in press as: Dinis-Oliveira RJ, et al. Clinical and forensic signs related to chemical burns: A mechanistic approach. Burns
(2014), http://dx.doi.org/10.1016/j.burns.2014.09.002
17
several toxic agents emit a garlic like odor, including arsenic,
selenium, thallium, and organophosphates [180]. Toxicity
from these metals generally involves gastrointestinal symp-
toms of nausea, vomiting, and diarrhea and can progress to
profound volume loss, metabolic acidosis, and coma. Al-
though arsenic intoxication can lead to skin lesions such as
desquamation and pigmentation changes, vesicles are not
observed [180]. Organophosphates cause muscarinic (vomit-
ing, diarrhea, abdominal cramping, bronchospasm, miosis,
salivation, sweating, and bradycardia) and nicotinic (tremor,
weakness, fasciculations) manifestations [180].
18. White phosphorus
White phosphorus is a smoke-producing, waxy, yellow transpar-
ent combustible solid [181] used in the civilian population in
fireworks and as fertilizers in agricultural plants but also in
military field as a component of munitions such as shell and hand
grenade [182,183]. It is highly flammable and spontaneously
ignites in the presence of oxygen and heat (e.g. body heat) to burn
(producing a yellow flame at a temperature up to 1300 8C) until the
entire agent is oxidized or oxygen is removed [184]. Therefore,
removal of macroscopic clusters of phosphorus in contact with
victim is mandatory. The application of a 0.5% copper sulfate
solution impedes oxidation and turns the particles with a blue-
black cupric phosphite covering, making identification and
removal easier. Burns are very painful and typically appear as
waxy, yellowish (Fig. 16A and B), necrotic, full-thickness lesions
due to both chemical (owing to the corrosive effects of phosphoric
acids) and thermal components [2,185,186]. The diagnosis of
white phosphorus exposure should be hypothesized in presence
of burns with progressive necrosis. Since it is highly lipolytic, the
injuries often extend deep into underlying tissues with resultant
delayed wound healing and potentially important systemic
effects, namely hepatic and renal failure and death due to
electrolyte abnormalities [184186]. Indeed, a reversal of the
calcium/phosphorus ratio (i.e. hypocalcemia and hyperpho-
sphatemia) in the serum, with consequent electrocardiogram
abnormalities, including prolongation of QT interval, bradycar-
dia, and ST-T wave changes, have been described. White
phosphorus fume can cause severe eye irritation with blepha-
rospasm, photophobia, and lacrimation. Malignant lesions may
rarely occur as a long-term consequence [187].
19. Concluding remarks
According to a recent systematic review, the annual incidence
of severe burns in Europe was 0.22.9/10,000 inhabitants, with
a predominance of male patients younger than 16 years [188].
Suicide and accidental ethiologies were much more frequent
than homicide cases. Chemical burns have been related to
several characteristic symptoms and signs (of diverse in
etiology), some of which were resumed and discussed due to
their prevalence in daily practice or individual characteristics
that can help in the differential diagnosis. Comparatively
thermal/electrical burn repair initiates nearly instantaneously
as soon as the physical irritant is removed, whereas the repair
process for chemical burns only begin after the compound is
JBUR-4456; No. of Pages 22
18 burns xxx (2014) xxxxxx
either inactivated by chemical reaction with the tissues,
removed, or neutralized [11]. Therefore, chemical injuries are
more prone to be sustained (lasting minutes and may still
continuing in an emergency room) than thermal/electrical
injuries, which are typically produced by very short-term
exposure (seconds) [1].
Finally, this work may provide appropriate counseling and
education for preventive measures to be taken by victims and
also to implement new emergency treatment protocols when
the mentioned clinical and forensic signs develop upon
chemical exposure [24,27,30].
Conflict of interest statement
Authors declare that there are no conflicts of interest,
particularly any financial and personal relationships with
other people or organizations that could inappropriately
influence (bias) this work.
Acknowledgement
Ricardo Dinis-Oliveira acknowledges Fundacao para a Ciencia
e a Tecnologia (FCT) for his Investigator Grant (IF/01147/2013).
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