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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.
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Contents
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Table 2 General characteristics of chemical burns (a) Oxidative agents cause protein denaturation by inserting
lesions. oxygen, sulfur, or halogen atoms to viable body proteins
-Hands, upper limbs, neck and face are typically exposed areas (e.g. sodium hypochlorite, hydrogen peroxide, potassium
-Rarely have regular shape (e.g. in the case of liquids, often spilled permanganate, potassium dichromate and chromic acid);
by projection, a characteristic run-off grooves is formed (b) Reducing agents they bind to free electrons in tissue
accordingly to gravity)
proteins, causing reduction of the amide link and protein
-Are uniform and do not differ in intensity throughout its surface
(i.e. similar caustic injuries are observed at all points that the
denaturation. Heat produced in the chemical reaction can
chemical contacts). On the other hand, distinguishable concentric cause a mixed picture [e.g. nitric and muriatic (concentrat-
zones lesions with differences degrees are typical for all thermal ed hydrochloric) acids, ferrous ion and sulfite compounds];
agents (c) Corrosive agents cause protein denaturation on contact
-Discoloration and contractures and tend to produce a soft scar, which may progress to
-Perforation of the gastrointestinal tract
shallow ulceration (e.g. sulfuric and muriatic acids, and
-Alkalis typically cause severe injuries to the esophagus without
white phosphorus);
significant injury to the stomach due to neutralization by gastric
secretion (d) Protoplasmic agents produce their effects by forming
-Acids typically leave the esophagus relatively spared, but cause esters with proteins (e.g. formic and acetic acids) or by
significant trauma to the stomach, namely in the pyloric end (e.g. chelating calcium or other ions necessary for tissue viability
natural area of stagnation or pooling of liquid) often resulting in and function (e.g. oxalic, hydrazoic and hydrofluoric acids);
strictures in this region (e) Vesicant agents produce ischemia with anoxic necrosis
-Full stomach tends to minimize injury due to dilution and buffer
at the site of contact. These agents are characterized by
effect for the ingested acid
producing cutaneous blisters (e.g. mustard gas, dimethyl
-The respiratory system may be affected when aerosolized
chemicals or smoke is inhaled sulfoxide and Lewisite);
-With prolonged exposure, damage to proximal and distal airways (f) Desiccant agents cause damage by tissues dehydration (e.g.
develops followed by noncardiogenic pulmonary edema, bron- calcium sulfate, sulfuric and muriatic acids, and silica gel).
chial obliteration, pulmonary hemorrhage and adult respiratory
distress syndrome Although less accurate, another useful classification is
-Ocular damage, namely blindness, corneal opacity (i.e. due to
based on the chemical reactions that the agent initiates. Four
protein coagulation cause by acids), ectropion, keratitis and
cataracts
classes are considered [1]:
-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 (a) Acids, donor of protons, release hydrogen ions and reduce
-Severe systemic toxicity may occur, if large body surface areas are pH to values as low as 0. The free hydrogen ions facilitate
injured
amide bond hydrolysis causing protein structures to
-Death may occurs from circulatory collapse or from secondary
collapse. Acids with a pKa less than 2 (i.e. strong acids)
destructive changes in the gastro-intestinal tract, lung, liver and
kidneys can produce coagulation necrosis with scars formation on
necrotic tissue, a fact that may limit further tissue
penetration. Coagulation necrosis produces rapid tissue
povidoneiodine and chlorhexidine/alcohol (in preterm changes that include consolidation of the loose connective
infants), laxatives, and vesicants (warfare agents), will be tissue, thrombosis of intramural vessels, ulceration,
reviewed since these are the most common agents found in fibrosis, and hemolysis of erythrocytes. The inability of
daily practice, for which relevant and timed information may gastric juices to neutralize these substances contributes to
be helpful in formulating emergency treatment protocols and the onset of lesions in the stomach and intestine, in
toxicological analysis. Table 3 resumes most relevant signs addition to the mouth and the esophagus [32]. Without
and symptoms resulting from exposure to the different gastric lavage within 30 min, full-thickness coagulative
chemicals discussed in this review. 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
2. Methods fasting state and within 24 h of ingestion [33,34]. The
primary mechanism of chemical burns injuries is the
Besides contributions with personal forensic cases, articles direct chemical reaction, rather than actual thermal
written in English, German, French, Spanish and Portuguese injury. However, several chemicals (e.g. sulfuric acid and
were searched for macroscopic signs and symptoms related to muriatic acid) produce extreme heat when combined with
chemical burns, using the National Library of Medicines water, thus necessitating chemical neutralization or
PubMed MedLine database and the Web of Knowledge (WOK). 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
3. Classification of chemicals involved in ingestion. Choking and gagging lead to the acid coming
burns into contact with glottis and epiglottitis with airway
compromise [36]. Typically they produce dry scar with
One useful classification organizes burning chemicals in six color varying from one substance to another (e.g. black and
groups according to how they damage protein [1,31]: yellow for sulfuric and nitric acid, respectively);
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(b) Alkali compounds have been implicated in injuries by (and even more that thermal burns), which are usually
three main mechanisms [32]: (i) they combine with fats to self-limiting and more superficial [2,41];
form soap (saponification of fat) through an exothermic (c) Organic solutions act by dissolving the cells lipid mem-
reaction, producing a significant amount of heat, which branes and disrupting the cellular protein structure;
causes severe tissue damage. Destruction of fat allows an (d) Inorganic solutions damage by salt formation (e.g. zinc
increase in water penetration of the alkali burn scar, chloride, potassium chloride, calcium chloride, potassium
annulling the natural water barrier that lipid provides [37]; oxalate). It should be noted that all of these reactions may
(ii) they extract considerable water from cells causing be exothermic, which contributes to tissue injury. Lesions
damage due to the hygroscopic nature of alkalis; (iii) they are usually dry and white.
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 4. Sulfuric acid (H2SO4)
alkaline proteinates, which contain hydroxyl ions (OH)
that can cause further chemical reaction and initiate Sulfuric acid is a very cheap and easy-to-get liquid, being
deeper injury of the tissue. This penetrating injury induces commonly used for restoring exhausted car batteries and in
liquefaction necrosis and occurs especially if pH is higher the leather industry. Concentrated H2SO4 (52100%, mixed in
than 11 [38,39]. The products formed favor the penetration water) is also commonly used as a drain cleaner, and is easily
of the remaining alkali into the tissue by increasing the available from various retail outlets. Consequently, it is one
solubility, causing the alkalis to reach deeper tissue layers, of the chemical agents more often involved in acid burns [42].
including muscular, therefore resulting in very serious It is highly corrosive (also its precursor sulfur trioxide)
injuries [40]. Indeed, damaged tissue has limited capacity and causes damage by tissue dehydration and heat produc-
to buffer alkalis and no scar is usually formed. If they exist tion. Dark-brownish colored burns are usually observed
are of soft, translucent and moist consistency, passing (Fig. 1AD). Sulfuric acid vapor is also strongly irritant to the
to fat saponification (aspect soap) and with ill-defined respiratory tract and can cause sore throat, coughing,
margins. Therefore, alkali injuries are commonly regarded shortness of breath and potentially fatal severe pulmonary
as having the potential to be more severe than acid injuries edema [43].
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The internal examination may reveal mural perforation of outcome. Solutions of up to 20% may not produce pain or
the gastroesophageal junction and cardia, and fundus of the erythema for up to 24 h. Burns from acid concentrations of 20
stomach, with complete separation of the stomach from the 50% usually became apparent within 18 h, whereas concentra-
esophagus at the level of the gastroesophageal junction (Fig. 1D tions of over 50% produce the typical picture (i.e. whitish tissue
F) [44]. Death may be rapid following ingestion as consequence of with surrounding erythema and immediate pain). Due to its high
cardiovascular collapse or shock secondary to gastrointestinal electronegativity it acts by two distinct mechanisms [50]:
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 (a) Fluoride ions are highly lipophilic and penetrate the
[42,47] due to its extremely destructive action, bad scarring, tissues deeply, accumulating in cells, leading to painful
mainly as hypertrophic and keloid scars, of dark skinned liquefactive necrosis with progressive evolution despite
people [48]. There is a predominance of female victims in the surface decontamination, unless neutralized (by salt
case of aggression, mainly after domestic disputes [49]. The formation) with calcium and/or magnesium drugs [53];
face, head, and neck are predominantly injured but extension (b) Free hydrogen ions (H+) cause hydration and corrosive
to the trunk and upper limbs is not rare. The physical and superficial burn of tissues similarly to HCl and H2SO4 [54].
psychological outcomes are usually poor, with permanent
disfigurement or loss of vision (Fig. 2A and B). 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
5. Hydrofluoric acid (HF) clinical outcome. Systemic toxicity may occur and it is
characterized by consequences of electrolyte imbalance (i.e.
Hydrofluoric acid is widely used in glass etching and cleaning, fluoride ions bind to several intra- and extra-cellular ions
the production of semiconductors, fluorocarbon, plastics, resulting in hyperkalemia, hypocalcaemia and hypomagnese-
products for rust removal, germicides, insecticides, tile- mia), such as tetany, seizure, corrected QT interval prolonga-
cleaning agent, aluminum brighteners, automobile wheel tion, ventricular dysrhythmias, cardiac arrest and death
cleaners, air conditioner cleaners, and other industrial and [50,51,55,56]. The consequent decrease of extracellular calci-
domestic processes [50,51]. Since the aqueous HF solution is a um and magnesium concentrations can transiently be
weak acid due to high electronegativity of the fluoride ion buffered by protein-bound and bone ion storage. If intense
(dilute concentrations remain relatively non-ionized; 1000 intravenously, topical and subcutaneous intra- and parale-
times less ionized than hydrochloric acid), dermal burns sional instillation of calcium (e.g. calcium gluconate) therapy is
significantly depend on its concentration [52], the although performed, cutaneous calcification may developed (Fig. 3A
other factors described before may of course influence the and B) [57].
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as a folk medicine to cure Tinea pedis and to remove nevus or vinegar its sour taste and smell). Although this is a weak acid,
warts [62]. it can produce a chemical skin burn when used under
Glacial acetic acid is a strong acid and the purest form of occlusion or compression for a long time as an antipyretic
acetic acid commercially available (>99.85%). Its name derives (alternative medicine) [64].
from the solid crystals that form below room temperature Monochloroacetic acid is used in low or high concentra-
(17 8C) when undiluted (anhydrous) [63]. It can cause severe tions in most European countries for topical treatment of
inflammation and chemical burns if directly contacts with warts. It is a strong organic acid, irritating and corrosive to the
mucosa or skin. Yoo et al. [63] described a patient with deep skin, leading to burns, and has a high systemic toxicity [65,66].
second-degree chemical burns on the face caused by the In addition to wart treatment, it is used for industrial
application of a mixture of glacial acetic acid and flour for purposes, such as the synthesis of certain organic chemicals
chemical peeling. During a 6-month follow-up, hypertrophic [67,68]. Tan Baser et al. [65] presented a case of joint deformity
scarring developed on the both nasolabial folds despite scar manifesting after the use of a preparation containing
management. ClCH2CO2H (in very low concentration 0.08%) for topical wart
Vinegar is produced from various fruits such as grapes, treatment (Fig. 4A).
apples, and lemons and contains 45% acetic acid (gives 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.
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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.
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Fig. 6 Grayish-black discoloration of the esophagus, larynx and spleen due to hydrochloric acid ingestion.
10. Sodium hydroxide (NaOH; caustic soda) 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
Sodium hydroxide presents as white crystals without odor and solid form are ingested, it is almost always fatal [32].
takes the form of flakes, granules, tablets or solutions. It is very Signs on early presentation include skin burns (Fig. 8A),
hazardous, especially in the liquid form [5]. It is used to oropharyngeal pain, dysphagia, vomiting, drooling and excessive
manufacture soap, rayon, paper, explosives, paint, cotton, salivation, ulcerative mucosal burns, dyspnea, stridor [85]. The
bleach, laundry, and beauty products and oil byproducts. strong corrosive action of NaOH is confirmed by the endoscopic
Solutions are easily swallowed, being tasteless and findings of patients, who frequently show multiple tortuous
odorless [36], and is most likely to damage the esophagus strictures, often in the upper esophagus [40]. In addition, can
and stomach. Burns typically occur at regions of anatomic cause severe ocular injury because of the quick corneal
narrowing, such as the cricopharyngeus, the aortic arch, the penetration, leaving the victim with significant visual im-
left main stem bronchus and the diaphragmatic hiatus [36]. pairment, namely opacification of the cornea and perforation [1].
Organs adjacent to the upper gastrointestinal tract such as the The pathophysiology process after ingestion occurs in
larynx, trachea, aorta, colon, and even pancreas may also be stages. First stage is characterized by eosinophilic necrosis
injured [4]. When at 1.83% (frequently found in commercial- with edema and intense hemorrhagic congestion [86], the
ized cleaning products), signs of necrosis were observed in the tissues ranging from white, to sloughy gray, to black (Fig. 8A).
epithelium and less aggressive injuries in the submucosa and Ten days later, granulation tissue begins to replace the
the muscle layer. Submucosal necrosis becomes visible at necrotic slough, and by 3rd week there is fibroblastic
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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 abnormal development of the secondary dentition and
[85]. Mortality is low, but morbidity is high, with up to 33% of subsequent problems with facial growth [85]. Another long-
patients developing long-term squeal secondary to stricture term complication of ingestion is the high incidence of
formation, such as stenosis of the oral musculature and extra- malignant transformation at the stricture site [32,89].
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 11. Calcium hydroxide (Ca(OH)2; cement)
normal tongue movement with resultant difficulty in oral
hygiene, speech, and mastication. Severe fibrosis of the Cement is a solid material obtained by calcinations, widely
alveolar mucosa and soft tissue envelope may lead to used throughout the world in the construction sector to bind
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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 and neck, but have also been shown to occur on the upper
reported in athletes who have sustained injuries after coming extremity and chest [37,112,116119]. Although rare (due to
into contact with the chalked lines of sporting fields in wet skins scarce capacity to counter alkalinity), scar-formation
conditions [107]. Santos-Pinto et al. [108] presented an unusual after airbag burns has been described [112,118,120]. Since the
case of burn in buccal mucosa and on the anterior faucet pillar contribution of friction and chemical components versus
caused by calcium Ca(OH)2 used in a pulp therapy. thermal cannot be separated, certainly the scar formation
may be viewed as being multifactorial.
Airbags are inflatable rubber-lined woven nylon bags, Although deliberate ingestion is responsible for most cases of
designed to inflate upon the detection of rapid deceleration, serious paraquat toxicity, morbidity and mortality can result
even in the case of low-impact collisions, in order to minimize from other routes of exposure, namely dermal by accidental
injury to the driver and passengers [109]. Burns after airbags exposure during spraying [121123]. Due to corrosive effects,
inflation are extensively described (Fig. 10A and B) and the paraquat may cause skin burn (blistering), nails white
following factors have been implicated [110,111]: discoloration, and ulcerated lesions in the lips, tongue,
oropharynx, esophagus (including perforation), stomach,
(a) Thermal effect from high-temperature gases (direct) and scrotum and trachea [124127] (Fig. 11A). Scrotal burns have
due to melting of clothing (indirect); also been reported due to contact with cloths soaked in
(b) Chemical effect from alkaline corrosives and particulate paraquat formulation (Fig. 11B) [128]. The extent and severity
materials (effect yet unknown). Indeed, during this of such damage is mainly dependent on the concentration of
inflation, approximately 70 g of sodium azide (NaN3) are paraquat in the formulation rather than the dose (as for
ignited, releasing at a great speed from a storage gastrointestinal lesions). In general, systemic toxicity in
compartment, nitrogen (96%), carbon dioxide (3%) and humans, after percutaneous exposure, seems unusual as
miscellaneous gases and particulates (1%), as well as a reported by Hoffer and Taitelman [125] whom described 15
small amount of alkaline aerosol containing NaOH, consecutive cases of single exposures of the skin or eyes
sodium carbonate and metallic oxides [111,112]. These during contact with paraquat at working places. From these
appear to happen when the gases come into contact with data it is apparent that a single exposure of healthy skin to
body fluids such as sweat or tears [113,114]; paraquat solutions only causes local lesions. However,
(c) Friction from the nylon covering the airbag may result in patients with repeated dermal exposures to paraquat may
skin abrasions and erythema (most of the cases). have significant skin irritation or can even die due to dermal
absorption. In all of these cases, one or more of the following
The release of irritant gases and particulates during factors were present: previous skin damage, caused either by
deployment can lead to or exacerbate respiratory problems, paraquat itself or by mechanical or other chemical means, and
especially in asthmatic patients [115]. Burns secondary to prolonged skin contact to clothes soaked in concentrated
airbag deployment are known to occur primarily on the face paraquat, or less concentrated solutions if the skin is not
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16. Laxative
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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
Fig. 14 Laxative-induced thickness burns of the buttocks massive tissue damage, mainly blistering and necrosis of any
incorrectly suspected to be abusive thermal burns. organ coming into contact or penetrated [164]. It primarily
Reproduced from [153] (A) and [150] (B), with permission. 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
structural-related nitrogen and sulfur mustard gases, the [157,167,168]. Fatalities are rare but when they occur, blistering
organic arsenicals such as Lewisite and phosgene oxime [154]. formation are normally present [169,170].
Dermal exposure is characterized by a latent period of 2
17.1. Sulfur mustard 24 h without symptoms (depending on the dose of the
inflicting agent), followed by pruritus and burning sensation,
Sulfur mustard ([bis-(2-chloroethyl)sulfide]; 2,20 -dichloro- erythema, xerosis, purpura, hypopigmentation, hyperpigmen-
diethyl sulfide) was firstly used during the First World War tation (Fig. 15B) and the formation of small vesicles (filled with
(1917) by the Germany army in Ypres (and since then has been an amber colored fluid) by 18 h that coalesce into large bullae
named yperite; Belgium) resulting in approximately 1,200,000 by 48 h [171,172]. Between 48 and 72 h post exposure, new
soldiers exposed [155]. The name mustard was given to the blisters may appear and those subsisting may rupture,
compound by soldiers, apparently because of the smell resulting in full-thickness skin loss, ulcers and scar formation
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17.2. Lewisite
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exposure. A wheal then develops within 30 min. The original several toxic agents emit a garlic like odor, including arsenic,
blanched area acquires a brown pigmentation by 24 h. A scar selenium, thallium, and organophosphates [180]. Toxicity
forms in the pigmented area by 1 week and sloughs after from these metals generally involves gastrointestinal symp-
approximately 3 weeks. Initially, the effects of phosgene oxime toms of nausea, vomiting, and diarrhea and can progress to
can easily be misidentified as mustard gas exposure. However, profound volume loss, metabolic acidosis, and coma. Al-
the onset of skin irritation resulting from phosgene oxime though arsenic intoxication can lead to skin lesions such as
exposure is a great deal faster than mustard gas, which typically desquamation and pigmentation changes, vesicles are not
takes several hours or more to cause skin irritation [179]. observed [180]. Organophosphates cause muscarinic (vomit-
ing, diarrhea, abdominal cramping, bronchospasm, miosis,
17.4. Differential diagnosis salivation, sweating, and bradycardia) and nicotinic (tremor,
weakness, fasciculations) manifestations [180].
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 18. White phosphorus
diagnosis besides the vesicant agents described above. Indeed,
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].
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
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Conflict of interest statement [20] Ho WS, Ying SY, Chan HH, Chow CM. Assault by burning
a reappraisal. Burns 2001;27:4714.
[21] Pfister D, Pfister R. Acid injuries of the eye. Fundam Cornea
Authors declare that there are no conflicts of interest,
Extern Dis Cornea 2005;127784.
particularly any financial and personal relationships with
[22] Pfister R, Pfister D. Alkali injuries of the eye. In: Krachmer
other people or organizations that could inappropriately J, Mannis M, Holland E, editors. Fundamentals of cornea
influence (bias) this work. and external disease cornea. Philadelphia: Elsevier Mosby;
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[23] Dinis-Oliveira RJ, Caldas I, Carvalho F, Magalhaes T.
Acknowledgement Bruxism after 3,4-methylenedioxymethamphetamine
(ecstasy) abuse. Clin Toxicol (Phila) 2010;48:8634.
[24] Dinis-Oliveira RJ, Carvalho F, Duarte JA, Proenca JB, Santos
Ricardo Dinis-Oliveira acknowledges Fundacao para a Ciencia
A, Magalhaes T. Clinical and forensic signs related to
e a Tecnologia (FCT) for his Investigator Grant (IF/01147/2013). cocaine abuse. Curr Drug Abuse Rev 2012;5:6483.
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