REVIEW ARTICLE
Deaths Related to Chemical Burns
Joseph J. Pavelites, PhD,* Walter L. Kemp, MD,Þ Jeffrey J. Barnard, MD,þ§
and Joseph A. Prahlow, MD*||
Abstract: The authors present a series of 6 deaths due to the uncom-
mon cause of chemical burns. Of the 6 deaths due to chemical burns,
4 deaths were due to ingestion of a chemical, 1 death was caused by
chemical burns of the skin, and 1 death resulted from rectal insufflation
of a chemical. Seven additional cases where chemical burns may have
been a contributing factor to the death or an incidental finding are also
presented. Four cases are related to an incident involving chemical
exposure during an industrial explosion. Three cases involve motor fuel
burns of the skin. Two cases concern a plane crash incident, and 1 case
involved a vehicular collision. Cases are derived from the records of
the Dallas County Medical Examiner’s Office and those of the authors’
consultation practices. Each of the cases is presented, followed by a
discussion of the various mechanisms of chemical injury.
Key Words: burns, insufflation, chemical, chemical burns, lye,
sodium hydroxide, bleach, gasoline, forensic, death, phosphoric acid,
mercuric chloride
(Am J Forensic Med Pathol 2011;32: 387Y392)
U nlike thermal injury, tissue damage resulting from contact
with caustic substances involves a primary chemical reac-
tion, varying in mechanism based on the inciting agent. Two
prominent routes of contact are by ingestion and cutaneous
exposure. Although chemical burns of the skin are fairly com-
mon, death by chemical burns is rare even under occupational
and mass casualty situations.1,2 This is surprising, considering
the sheer number of chemicals available on the market, the
number of new chemicals produced annually, and the general
dearth of information on the potential injurious effects these
chemicals have on humans.3 Most autopsy cases, including
those in our series, involve ingestion.4 In infants and toddlers,
the manner of ingestion is predominantly accidental. Accidental
ingestion can also occur in adults. However, suicide is a more
likely reason for such an exposure.
Although ingestion and skin contact are the most com-
monly encountered routes of exposure in chemical burn cases,
other forms of exposure can also occur. In this review, we
present 6 deaths due to chemical burns, including 4 deaths
caused by ingestion of a caustic material, 1 death caused by
cutaneous exposure, and 1 death related to rectal insufflation of
a chemical. Seven additional cases where chemical burns may
Manuscript received September 18, 2008; accepted January 9, 2009.
From the *Indiana University School of Medicine-South Bend at the Uni-
versity of Notre Dame, South Bend, IN; †Montana State Department of
Justice, Missoula, MT; ‡Dallas County Medical Examiner’s Office; §The
University of Texas Southwestern Medical Center, Dallas, TX; and
||South Bend Medical Foundation, South Bend, IN.
The authors report no conflicts of interest.
A portion of this article was presented at the 2001 annual meeting of the
National Association of Medical Examiners.
Reprints: Joseph A. Prahlow, MD, Indiana University School of
Medicine-South Bend at the University of Notre Dame, South Bend,
IN. E-mail: jprahlow@sbmf.org.
Copyright * 2011 by Lippincott Williams & Wilkins
ISSN: 0195-7910/11/3204Y0387
DOI: 10.1097/PAF.0b013e31822a6182
Am J Forensic Med Pathol & Volume 32, Number 4, December 2011
Copyright © 2011 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
have been a contributing factor in the victim’s death or simply
an incidental finding are also presented. A discussion of the
mechanism of injury in chemical burn cases follows the case
presentations.
CASE REPORTS
Case 1
A 60-year-old man was found to have ingested a solution
of lye for the purpose of ending his own life. He was brought
to the Veteran’s Administration Hospital shortly after the event
but was unable to be saved. An autopsy revealed multiple irre-
gular chemical burns of the cheeks, chin, nose, and lateral
aspects of the left side of the forehead (Fig. 1). The lips were
swollen. Extending downward from the mouth was a 5.0 
9.0-cm confluent black and brown area of chemical burn (Fig. 2).
A blackened tongue with superficial loss of the mucosa was
noted. The epiglottis, pharynx, esophagus (Fig. 3), stomach
(Fig. 4), and 30 cm of the duodenum possessed swollen, moist,
dark black mucosa. The distal esophagus was ruptured, and
100 mL of black fluid was in the left side of the chest cavity.
The mucosa of the larynx and trachea was unremarkable. Also
noted at the time of autopsy was hypertensive and atheroscle-
rotic cardiovascular disease with severe stenosis (85%) of all
3 major coronary arteries. The cause of death was lye ingestion,
and the manner of death was suicide.
Case 2
A 1.5-year-old male toddler accidentally ingested lye, was
treated (including intubation), observed for 5 days, and released
from the hospital. Two months later, he presented with inter-
mittent periods of apnea and cyanosis lasting 2 to 3 minutes.
Antemortem studies revealed a posterior tracheal mass. Before
diagnosis of the mass, the infant developed seizures and, on
transfer to another hospital, experienced respiratory and car-
diac arrest. Despite resuscitation, the infant developed cerebral
edema with uncontrollable intracranial pressure. He subse-
quently died, almost 4 months after ingesting the lye. An au-
topsy revealed a trachea with generalized fibrosis and moderate
thickening of the wall. The fibrosis was accentuated in 2 areas,
3.0 cm below the vocal cords, and in the distal trachea, 1.7 cm
above the carina. The second area of fibrosis extended to the
left main stem bronchus where it formed a distinct stricture.
The esophageal mucosa was smooth and glistening with no
evidence of fibrosis or stricture formation, although the esoph-
agus was adherent to the posterior trachea by fibrous tissue.
There was no significant amount of fibrosis involving the lar-
ynx. This suggests that the tracheal fibrosis was related more to
the tracheostomy than to the lye ingestion. The cause of death
was ruled as complications of lye ingestion. The manner of
death was accident.
Case 3
A 1-year-old male infant was brought to the emergency
department by his mother with complaints of uncharacteristic
irritability. An evaluation indicated no specific cause, and the
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Pavelites et al
FIGURE 1. Caustic burns of the cheeks, chin, nose, and left side
of the forehead from case 1.
infant was discharged. The mother was instructed to bring him
to the hospital if his condition worsened. After the infant’s
condition deteriorated, the mother returned with him to the
hospital, where he died shortly after arrival. The mother did not
know if the infant ate or drank anything and related that he had
been doing fine before that day. At autopsy, the mucosa of the
larynx, trachea, and major bronchi was found to be pale green-
brown and indurated. Also noted was marked edema of the
lower esophagus and stomach, with black discoloration of the
mucosa that was friable and necrotic. The black discoloration
extended through the pyloric region and duodenum and into the
proximal jejunum. Further investigation revealed that the in-
fant had ingested an unknown quantity of Dun-Rite, a cleaning
solution that contains 25% to 40% phosphoric acid. The cause
of death was chemical (acid) ingestion. The manner of death was
ruled an accident.
Case 4
A 36-year-old woman was reportedly washing dishes when
she knocked over a bottle of Drano (S.C. Johnson & Son, Inc,
Racine, Wis) (dry powder) and inhaled or aspirated an unknown
amount. The Drano spill was extensive, covering shelves and
cans. The woman cleaned the spill with a broom and dustpan.
FIGURE 2. Confluent caustic burn of the left side of the face
from case 1.
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Am J Forensic Med Pathol & Volume 32, Number 4, December 2011
FIGURE 3. Caustic burns of the tongue, epiglottis, pharynx, and
esophagus from case 1. Note blackening of the tongue with
superficial loss of the mucosa and swollen, moist, dark black
mucosa of the esophagus.
She started to vomit 1.5 hours later and told her family about the
accident in the morning. At the time, she had hoarseness and a
sore throat but was feeling better. The woman was taken to the
hospital and found to have gastrointestinal bleeding from alka-
line burns. She underwent surgical repair of the bleeding site,
and her condition stabilized. Several days later, the patient
developed a massive gastrointestinal bleed and was unable to be
resuscitated. Although the accident had not been witnessed, the
woman had not expressed suicidal ideation and was thought to
have a good state of emotional and mental health, with no serious
financial or relationship concerns. An autopsy revealed an oval
well-circumscribed 1.5-cm ulcer in the anterior pharynx, an
irregular 1.5-cm-wide ulcer involving the entire length of the
esophagus, and a 0.2-cm ulcer in the stomach surrounded by 4 cm
of erythema. One thousand milliliters of blood filled the stomach.
The supraglottic region of the larynx was hyperemic. However, the
mucosa of the vocal cords and the trachea were unremarkable. The
cause of death was ingestion of a caustic substance, and the
manner of death was undetermined.
Case 5
A 38-year-old woman with mental handicap and a seizure
disorder was found on the floor of her group home, lying in a
cleaning solution containing Clorox (The Clorox Company, Oak-
land, Calif) bleach, Formula 409 (The Clorox Company, Oakland,
Calif), and Mr. Clean (Procter & Gamble, Cincinnati, Ohio). It
was unknown how long she had laid in the solution. Employees of
the home attempted to shower the combative patient, but washing
of her skin lasted only a few minutes. Petroleum jelly was then
applied to her skin. The next morning, her skin had a red dis-
coloration, and she was taken to a physician. The patient was pre-
scribed pain medication and topical ointment and was sent back to
the home. That evening, she fell from her bed and was found
unresponsive. She was taken to the hospital and admitted into the
intensive care unit with a diagnosis of sepsis. Cultures did not
reveal an infection, and she died 36 hours after admission. An
FIGURE 4. Blackened swollen mucosa produced by caustic burns
of the stomach from case 1.
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Am J Forensic Med Pathol & Volume 32, Number 4, December 2011
FIGURE 5. Confluent lesions of denuded epidermis caused
by a mixture of cleaning solutions from case 5.
autopsy revealed multiple irregular and confluent pink, red, and
yellow-green areas of denuded epidermis, involving most of the
back, arms, and legs (Fig. 5). The cause of death was complica-
tions of chemical burns, and the manner of death was accident.
Case 6
A 38-year-old man with paranoid schizophrenia and 2
previous suicide attempts inserted the contents of a bottle of
mercuric chloride into his rectum. His mother took him to the
emergency department, where he was noted to have explosive
bloody diarrhea. He was admitted and, despite treatment, died
14 days later. An autopsy revealed the mucosa of the rectum to
be edematous, hemorrhagic, and focally necrotic. There was
transmural extension of the necrosis in the rectum. The skin
of the scrotum, inner thighs, anus, and buttocks was ulcerated,
necrotic, and focally inflamed with prominent eschar formation
(Fig. 6). The colonic mucosa was erythematous and focally
ulcerated in the distal portion. The distal jejunum and ileum
were erythematous and edematous. The cause of death was
FIGURE 6. Mercuric chloride burn of the scrotum, inner thighs,
anus, and buttocks from case 6. Note skin ulceration, necrosis, and
focal inflammation with prominent eschar formation.
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Deaths Related to Chemical Burns
FIGURE 7. Whole-body thermal burns with chemical involvement
as described in cases 7 to 10.
intrarectal insufflation of mercuric chloride, and the manner of
death was suicide.
Cases 7 to 10
These 4 cases stem from an incident at a specialty fire
extinguisher factory that manufactured a chimney fire sup-
pressor. Although it was denied by the owners of the factory, it
was speculated but not confirmed by officials at the scene that
fireworks were also being produced illegally on-site. Each of
the bodies was badly burned thermally, with 3 of the individuals
having burns covering virtually 100% of the total body sur-
face area (Fig. 7). Internal examination of the upper airways
and trachea revealed the presence of soot material coating the
mucosal surfaces of the tracheobronchial tree, with the lungs
containing probable bilateral hemorrhages. During sectioning
of the lungs, a faint but evident chemical/metallic odor was
present. In addition, on internal examination, the soft tissues of
the bodies demonstrated marked pink discoloration. One case,
corresponding to the highest cadmium level and other abnormal
toxicologic findings (see later paragraphs), revealed a markedly
green/gray discoloration of the brain during sectioning.
Toxicology tests revealed carboxyhemoglobin levels rang-
ing from 14% to 44% for the 4 individuals. Cadmium levels
ranged from 17.8 to 506.2 Kg/L (reference, G5 Kg/L). The 2
individuals with the highest cadmium levels also had elevated
sulfhemoglobin levels of 6.4% to 16.6% (reference, G1%) and
corresponding methemoglobin levels of 43.5% to 13.1% (refer-
ence, G1.5%). The following chemicals were used at the fac-
tory in the manufacturing of the chimney fire suppressor: sulfur,
potassium chloride, potassium perchlorate, zinc powder, sodium
FIGURE 8. Chemical burns sustained from immersion in airplane
fuel from cases 11 to 12.
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Pavelites et al
bicarbonate, and potassium nitrate. The cause of death for these
individuals was smoke and soot inhalation with thermal inju-
ries due to a chemical explosion, and the manner of death was
accident.
Cases 11 and 12
These 2 cases originate from a plane that crashed into a
lake, killing a minor and his young adult flight instructor at
a summer aviation camp. The crash spilled fuel into the sur-
rounding water and the plane’s cabin. External examination of
the adolescent boy revealed extensive dry, red-yellow apparent
skin burns that were firm and relatively solid compared with
the surrounding skin. These burns were patchy over much of
the body including the chest, abdomen, upper extremities, back
(Fig. 8), front and back of the legs, and anterior and posterior
parts of the neck. Associated pink-red discoloration of the
skin with skin slippage surrounded the dry burns. Less severe
chemical burns involved most of the remainder of the skin sur-
face, with relative sparing of the groin region, buttocks, and
scalp. A subtle abraded contusion ran diagonally from the left
clavicle region across the central chest and onto the right lower
side of the chest. Other rare superficial abrasions were else-
where but were obscured by the chemical burns. Internally, there
were rare subgaleal hemorrhages posteriorly. The brain was
swollen but with no intracranial injuries identified. The cervical
spine and atlanto-occipital junction were intact. Both lungs
demonstrated extensive areas of extravasated blood. There were
no other internal injuries. The man showed similar internal
injuries. Full-thickness-appearing areas of dry, red-yellow skin
burns were evident over the right side of the hip, the anterior
part of the neck, the lower right part of the back, and the posterior
and lateral parts of the thighs bilaterally and focally elsewhere
on the skin. The cause of death for both individuals was a com-
bination of drowning, blunt force injuries, and chemical burns,
and the manner of death was accident.
Case 13
A 23-year-old man was riding a lawn tractor down a rural
road in the early morning with another individual when he
was struck from behind by a semitractor trailer. The decedent
sustained multiple blunt force injuries including craniocerebral
trauma with multiple facial and scalp abrasions, lacerations and
contusions, skull fractures, nasal fracture, mandible fracture, sub-
arachnoid hemorrhage, and subdural hemorrhage. There were
also multiple fractures involving all ribs, the sternum, and the left
FIGURE 9. Postmortem chemical tissue destruction consisting
of skin slippage and red-yellow discoloration scattered over
the back of case 13.
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Am J Forensic Med Pathol & Volume 32, Number 4, December 2011
clavicle, with lacerations of the lungs, heart, aorta, right hemi-
diaphragm, and hemoperitoneum with numerous abrasions and
contusions of the skin. Scattered over the entire back region, as
well as on the dorsal aspect of both arms and posterior aspect of
the left calf, there were multiple areas of irregular superficial
skin slippage with red-yellow discoloration consistent with post-
mortem chemical tissue destruction (Fig. 9). A strong scent of
gasoline was noted in these areas. The cause of death was multiple
blunt force injuries, and the manner of death was accident. The
chemical burns were considered incidental postmortem findings.
DISCUSSION
Many different types of chemicals can damage the human
body and produce a chemical burn. Chemical burns differ from
thermal burns in that the mechanism of action is a chemical
reaction and not just heat. Many chemicals can be categorized
as acids and alkalis. Examples of commonly encountered alka-
lis include lye (sodium and potassium hydroxide), as well as
ammonium, lithium, barium, and calcium hydroxides.5 Exam-
ples of acids commonly encountered include nitric, sulfuric,
chromic, hydrofluoric, acetic, and hydrochloric.5 Alkali and
acids affect the tissues in different manners. Alkalis produce
saponification, which results in liquefactive necrosis of the body
fats. The organic complexes that are formed penetrate further
into the body, carrying loose alkali molecules that continue to
damage tissues. The eye has the most sensitive tissue to alkali
burns. Acids produce more fulminant skin burns than do alkali
solutions. Acids cause tissue damage by precipitating proteins.6
Acids are water soluble, enabling them to quickly penetrate into
subcutaneous tissue. However, the subcutaneous tissue coagu-
lates after contact, forming a tough eschar.5 The appearance of
this eschar can vary with the type of acid. With sulfuric acid, it
is green-black to dark brown, whereas nitric acid produces a
yellow eschar, hydrochloric acid causes a yellow-brown eschar,
and trichloroacetic acid produces a white eschar.5
Although a large number of chemicals can be divided into
acids or alkalis, many chemicals fall outside this simple classi-
fication and can make up a significant number of occupationally
specific injuries. Military chemical burns, as an example, in-
clude injuries from white and red phosphorus,6 sulfur mustard
vesicants,6,7 and inappropriate use of Freon 113 as a degreaser.8
White phosphorus injuries were the most common chemical
burn at 1 particular military US Army installation during a
51-year period producing 146 cutaneous injuries.6 Sixteen
burns were recorded by the US Navy in a 7-year period for
Freon 113, a chemical that is not normally included in lists of
dangerous chemicals found in toxicology texts.8
Other important mechanisms of injury include oxidation
or reduction reactions, salt formation, corrosion, protoplasmic
poisoning, metabolic competition or inhibition, desiccation, and
vesication.9 The amount of damage produced by the chemical
depends on 8 factors: (1) concentration, (2) duration of contact,
(3) amount of substance contacting the skin (or gastrointestinal
or respiratory tract), (4) length of exposure, (5) regional epi-
dermal or mucosal properties, (6) penetrability of the chemical,
and its (7) manner and (8) speed of action.10 It must also be
remembered that, depending on the chemical involved, absorp-
tion of the chemical into the blood with subsequent toxic phys-
iologic effects may also play a contributory role in death. For
example, the systemic toxic effects of mercuric chloride played a
contributory role in case 6.
As previously described, exposure to chemicals can be
generally divided into 2 categories: (1) skin contact and (2)
ingestion. Chemical skin burns most often occur from accidental
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Am J Forensic Med Pathol & Volume 32, Number 4, December 2011
exposure at work. In most cases, the exposure is over a rela-
tively small surface area and does not necessitate hospitaliza-
tion. Larger exposures (15% of total body surface or more) or
exposures to chemicals that have long-term effects (phenol,
gasoline, and hydrofluoric acid) may require hospitalization and
can cause death. There are reports in the literature of chemical
burn deaths resulting from extensive skin contact.11,12 As in
patients with extensive thermal burns, patients with extensive
chemical burns of the skin require fluid and electrolyte support
as well as protection against infection, and they are at risk for
systemic inflammatory response syndrome.13 In this syndrome,
the severity of injury is so great that the normally local response
of the inflammatory system becomes systemic in nature. The
systemic inflammatory response syndrome will result in in-
creased cardiac output, reduced systemic vascular resistance,
and lactic acidemia before hypotension, hypermetabolism, and
multiple-organ dysfunction. Despite research and continued
progress, patients with systemic inflammatory response syn-
drome have a grave prognosis.13 Case 5 in the present series
represents an example of a death related to extensive exposure
of the skin to multiple chemical agents. Because the cleaning
solution mixture was not sufficiently flushed from the skin sur-
face and then petroleum jelly was applied (thus essentially
sealing the chemicals in the skin), the chemicals remained in
contact with the skin surface for many hours, continuing to cause
tissue injury. It also serves as an example of how the general
public is often unaware of the effects that household bleach and
other solutions of sodium hypochlorite, such as pool chemicals,
have on the skin. The effects can range from minor skin irrita-
tion to complete denuding of soft tissue.14
The second major route of contact with chemicals is in-
gestion. Ingestion occurring in 2 different age groups has dif-
ferent implications. In infants and toddlers, ingestion of caustic
substances is usually accidental, whereas in adolescents and
adults, ingestion of caustic substances is usually an attempt at
suicide. More than 5000 caustic ingestions are estimated to occur
each year.15 Acids are present in approximately 15% of caustic
ingestions, and the coagulum formed helps to inhibit penetration
into deeper muscle layers. The esophagus is slightly alkaline,
and the epithelium is resistant to acid, so esophageal burns occur
in only 6% to 20% of acid ingestions. The antrum of the stom-
ach is the most sensitive to acids.15 Ingestion of acid is also
painful and generally evokes expulsion of the chemical, which
tends to limit the extent of injury.16 This protective response,
unfortunately, can be countermanded. This is evidenced by a
suicide case where an overdose of sleeping medication allowed
retention of a corrosive drain cleaner containing sulfuric acid.
This prolonged contact produced extensive coagulative necro-
sis, where the main findings at autopsy included corrosive burns
of the oral cavity, with erosive digestion of the esophagus,
complete digestion of the cardia and fundus of the stomach, and
perforation of the pylorus. Denaturation of the surfaces of the
kidney, liver, spleen, and fallopian tubes was also present.17
As previously discussed, alkalis penetrate deeply into the
tissues by causing liquefactive necrosis. Typically, the esopha-
gus is the prime target of alkali injury. Sometimes, the damage
is so severe that surrounding mediastinal structures are also
affected. If sufficient quantities are ingested, the duodenum
may be involved (the stomach is spared in 80% of cases).15 At
approximately 3 weeks after ingestion, fibroblast proliferation
causes contraction of the granulation tissue that can produce
severe strictures. In the long term, these patients are also at a
1000- to 3000-fold increase in risk over the healthy population
for the development of squamous cell carcinoma of the esoph-
agus.15 With ingestion of a caustic substance, the pharynx and
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Deaths Related to Chemical Burns
larynx can also be affected. In the case of our series, the infant
developed strictures of the trachea 4 months after ingestion of
lye. Because the strictures did not involve the esophagus and did
not present at the usual time, it was believed to be more likely that
the strictures in that case were a complication of the tracheostomy
rather than a result of the lye ingestion.
Because chemical ingestions in infants, toddlers, and young
children are most likely accidental, whereas chemical ingestions
in adults are most likely suicidal, the amount ingested by adults
and the damage caused are typically greater than those in chil-
dren.16 In 1 study looking at caustic ingestion in adults, more
than half of the patients who attempted suicide through inges-
tion of a caustic substance had a history of a psychiatric illness,
61% were women, 33% were under the influence of alcohol,
and the median age was 40 years.18 Accidental ingestion does
occur with some frequency among adults as well. In the same
study of caustic ingestions in adults, 38% of the total number of
patients had accidental ingestions, and in 1 patient, the ingestion
was the result of a homicidal attempt with an aqueous ammonia
solution.18 In the group of patients with unintentional (acci-
dental) ingestions, the mean age was 20 to 25 years as opposed to
40 years in the group attempting suicide. The accidental inges-
tions resulted from situations in which the container storing the
caustic substance was stored with regular food or in which the
caustic substance was decanted into containers normally used
for food and drink with subsequent accidental consumption.18
The demographics and statistics of our series of deaths by
chemical burns match those of the published literature.4 Two of
the deaths were infants who accidentally ingested caustic sub-
stances. Of the 2 adults who ingested caustic substances, the
manner in one was ruled as a suicide whereas that in the other
was undetermined. Of the 2 noningestion cases, one was an ac-
cident and the other was an unusual suicide. As is apparent from
the autopsy findings, chemical burns produced both by skin con-
tact and ingestion/insufflation result in extensive damage of the
epidermis of the skin or mucosa of the respiratory or gastroin-
testinal tract. The damage can cause the death of the patient
acutely, or it can result in changes that result in death at a later
date. Extensive loss of the epidermis can result in death through
fluid loss, electrolyte disturbances, or infection or by invoking
the systemic inflammatory response syndrome. In cases of in-
gestion and insufflation, the cause of death may be esophageal
or gastric rupture, extensive gastrointestinal bleeding from ul-
ceration of the mucosa, effects of the systemic inflammatory re-
sponse syndrome, or, in the long term, production of strictures or
carcinoma.
The unusual toxicologic findings of increased sulfhemo-
globin and methemoglobin levels in cases 7 to 10 can readily be
explained by exposure to the chemicals and their subsequent
combustion products that were known to be used by the dece-
dents: sulfate and the oxidants potassium nitrate and potassium
perchlorate, respectively. Likewise, the increased levels of car-
boxyhemoglobin from carbon monoxide generated in building
fires are not an unusual finding.19 However, the high levels of
cadmium are not consistent with the chemicals used for manu-
facturing fire suppressants and support allegations of the illegal
production of fireworks. The marked pink discoloration of tis-
sues seen on internal examination could have its origins in car-
bon monoxide and/or cyanide exposure because these chemicals
are often produced during combustion. The green and gray
discoloration of the gray matter in one of the victims speaks to
hydrogen sulfide exposure, a distinct possibility considering the
presence of sulfur stored on-site. However, that this discoloration
was selective for the brain with no similar discoloration of the
viscera is puzzling. Although these 4 cases do not represent
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Pavelites et al
classic ‘‘chemical burn’’ cases, they are included in this review
to highlight that certain chemical-related burns and deaths are
due to thermal injuries and toxic gas inhalation that result from
fires produced by chemical explosions.
Cases 11 to 13 involve petroleum-based fuels as the source
of the chemical burns and are consistent with those found in
gasoline burns.20,21 Although well known, gasoline immersion
burns are not commonly encountered in emergency depart-
ments.22 These and other related hydrocarbon solvents are
irritating to the skin, and their lipid solubility allows them to
dissolve fatty tissue and penetrate cell membranes. It is not
common to develop systemic toxicity from cutaneous absorp-
tion, and most hepatic and renal injuries are from prolonged
inhalation of fumes, oral ingestion, or secondary to skin ex-
posure. In the plane crash deaths, the absence of rapidly lethal
blunt force trauma led to the conclusion that drowning was
likely the major factor in death. It is possible that the airplane
fuel skin burns were incidental or even totally postmortem in
nature; however, it can be argued that the presence of the fuel in
the water within the enclosed and damaged cockpit may have
contributed to the relatively rapid deterioration and death of the
pilots. The case serves to remind forensic pathologists that dif-
ferentiating antemortem and postmortem chemical skin burns
can be extremely difficult, if not impossible. The garden tractorY
versusYsemitractor trailer case represents the type of chemical
burn case that is probably most commonly encountered within
medicolegal death investigations, wherein postmortem chemical
skin burns are present because of the body being exposed to
gasoline at the site of a motor vehicle collision.
For persons investigating deaths caused by chemical burns,
several important points must be emphasized. Following proper
scene/death investigation protocols is often critical in these cases.
Care must always be taken to ensure the safety of all persons
involved in the investigation. Although many of the chemicals
involved in the cases presented here might be considered rela-
tively safe if accidental skin contact occurred during death inves-
tigation or autopsy, this is not always the case. Some chemicals
present a severe health hazard, either by skin contact or by inha-
lation. Consultation with the fire department or other hazardous
materialYtrained agencies may be necessary to protect others from
hazardous chemical exposure.
Collection of chemical containers, samples of chemical
spills, or even vomitus may be necessary to identify the chemical
involved. At autopsy, collection of samples from the skin sur-
face or the gastrointestinal tract may provide samples for iden-
tification. Consultation with a toxicologist may be necessary to
properly collect and identify the chemical involved. Collection
of various bodily fluids for toxicology must also be considered
if concomitant chemical toxicity is felt to contribute to the
chemical burn in causing death. Careful dissection of the gas-
trointestinal tract is essential in chemical ingestion cases to
properly document all injuries. Finally, photographic documen-
tation of chemical burns should be considered a requirement
whenever such a case is encountered.
CONCLUSIONS
Chemical burns due to caustic substances are an uncom-
mon cause of death. In most instances, the method of exposure
is ingestion. However, extensive skin contact and other rare
routes of exposure may occur. Death may occur acutely, or it
may follow a prolonged course, occurring days to years after the
chemical exposure. Caustic substances may cause skin, mucosal,
and other tissue damage by a variety of mechanisms, and in some
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Am J Forensic Med Pathol & Volume 32, Number 4, December 2011
cases, the chemical’s pharmacologic toxicity may play a con-
tributory role in death. Ingestion in infants and toddlers is usually
accidental, whereas in adults, ingestion is often suicidal. Cases
with skin exposure are typically accidental. Special care must be
taken by pathologists and death investigators when dealing with
such deaths, particularly with regard to safety issues if the caustic
chemical is still present on or in the body or at the death scene.
Consultation with the fire department or other agencies with
hazardous material training is encouraged if any safety concerns
exist.
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