Forensic Science, Medicine and Pathology (2023) 19:67–71

https://doi.org/10.1007/s12024-022-00552-8

CASE REPORT

Fatal hydrofluoric acid poisoning: histologic findings and review

of the literature
Harin Cheong1 · Junmo Kim2

Accepted: 23 October 2022 / Published online: 5 November 2022

© The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2022

Abstract
Hydrofluoric acid (HF), the inorganic acid of elemental fluorine, is a highly dangerous substance and death can result from
a very small exposure. In addition to local toxicity, HF can trigger fatal systemic reactions by its high affinity for calcium
and magnesium. The authors report the autopsy case of a male worker who was exposed to 50% HF while repairing the leak-
age from an HF tank valve in a semi-conductor washing factory. His colleagues found blisters on his neck after 6 h of work
and he was sent to the hospital. However, he expired from cardiac arrest despite an immediate calcium gluconate injection.
At autopsy, burns with eschar covering less than 5% of the total body surface were identified on the neck and around both
ears, and microscopic examination of the affected skin revealed extensive necrosis of the epidermis and dermis with pustule
formation. In chemical analysis, no fluoride ions were detected in blood, vitreous humor, urine, pleural fluid, bile, or skin
tissue from the neck. Considering the chemical burns on the neck and the circumstantial information, the cause of death
was determined to be HF poisoning. This article presents the clinical manifestations of local and systemic toxicity after the
accidental exposure to a high concentration of HF, with histologic demonstrations of chemical burns.

Keywords Hydrofluoric acid · Hypocalcemia · Burns, chemical · Histology · Autopsy

Introduction Numerous articles related to HF exposure have been pub-

Hydrofluoric acid (HF), the inorganic acid of elemental
fluorine, is used in a variety of industries and household
settings, although it is a highly dangerous substance and
death can result from a very small exposure. When a person
is exposed to HF, a superficial burn is induced by hydrogen
ions, and liquefactive necrosis of the soft tissue is caused
by fluoride penetration [1]. Free fluoride ions dissociated
from HF strongly bind to calcium and magnesium, causing
systemic hypocalcemia and hypomagnesemia, which cause
fatal impairments in cardiac function [2].
* Harin Cheong
hariny01@hanmail.net
Junmo Kim
brainy21@naver.com
1 a gas mask, with no cleanroom garment, during some parts
Department of Forensic Medicine, College of Medicine,
The Catholic University of Korea, 222, Banpo‑Daero,
Seocho‑Gu, Seoul 06591, Republic of Korea
2
Forensic Medicine Division, Daegu Institute, National
Forensic Service, Daegu, Republic of Korea
lished. However, only a few autopsy case reports appear in
the literature and articles focusing on the microscopic fea-
tures of HF burns are very rare. Here, the authors present
an autopsy case of a male worker who was exposed to 50%
HF while repairing the leakage from an HF tank valve in a
semi-conductor cleaning factory, with a demonstration of
the histologic findings of the chemical burns.
Case report
A 35-year-old male worker received an emergency call
warning him that a considerable amount of fluid was leaking
from an HF tank valve in a semi-conductor washing factory.
He and his colleagues began to repair the valve wearing
gas masks, cleanroom garments, face masks, gloves, and
boots according to the testimony of a colleague. However,
CCTV footage revealed that the deceased was wearing only
of the repair. After about 6 h of work, one of the work-
ers found blisters on his face and immediately was sent to
the hospital. He experienced sudden cardiac arrest in the
ambulance, but the cardiac rhythm was recovered after

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resuscitation. In the emergency room, he was treated with a

calcium gluconate injection and was transferred to a special
hospital with a burn unit. A second-degree localized burn
was detected on his neck, and calcium gluconate ointment
was applied to the skin lesion. According to the laboratory
data, his blood ionized calcium level (1.48 mmol/L) was
slightly higher than normal, and the blood ionized mag-
nesium level (0.57 mmol/L) was within the normal range.
The electrocardiogram (ECG) indicated tachycardia, an
incomplete right bundle branch block, occasional prema-
ture ventricular complexes, large T wave, and prolonged QT
interval. Despite the treatments, the patient was pronounced
dead about 11 h after HF exposure. A subsequent foren-
sic examination of the scene was performed, without a defect
inspection of the safety harnesses.
Fig. 2  a–d Microscopic examination of the neck lesion revealed
An autopsy was performed two days after death accord- abscess formation in the dermo-epidermal junction with extensive
ing to a court warrant requested by the public prosecu- infiltration of neutrophils in the dermis and adipose tissue (H&E, × 40
tor. In the external examination, burns covering less than magnification)
5% of the total body surface were found on the neck and
around both ears. The affected area showed numerous pus-
tules with eschar formation (Fig. 1). Focal abrasion was The heart weighed 352 g with moderate (40–50%) ath-
noted in the sternal area and both antecubital fossa and erosclerosis in the left anterior descending artery, and there
several subcutaneous hemorrhage foci were identified in were no gross abnormalities in the valves or myocardium.
the left posterior thigh. Microscopic examination of the Both lungs showed marked edema and congestion with focal
skin from the neck revealed extensive necrosis of the epi- pleural fibrosis. No gross or microscopic abnormalities were
dermis and dermis with abscess formation (Fig. 2). Internal found in the liver, kidney, pancreas, or spleen.
examination of the neck showed an erythematous mucosal Since there was no admission blood available, toxicologic
membrane in the trachea, with a grossly unremarkable oro- analysis was carried out using postmortem samples. In toxi-
pharynx. Microscopic examination of the tracheal mucosa cologic analysis, atropine, lidocaine, etomidate, midazolam,
showed suppurative inflammation extending into the lam- and amiodarone were detected at blood concentrations below
ina propria, and the epiglottis and oropharynx revealed the the therapeutic levels. No fluoride ions were detected in the
submucosal infiltration of mononuclear cells with a few blood, vitreous humor, urine, pleural fluid, bile, or skin tis-
neutrophils (Fig. 3). sue from the neck. Considering the chemical burns on the

Fig. 1  a–c HF burn on the neck

area shows numerous pustules
with eschar formation

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Forensic Science, Medicine and Pathology (2023) 19:67–71
Fig. 3  a The trachea displayed mucosal redness. b The tracheal
mucosa showed submucosal suppurative inflammation with hemor-
rhage (H&E, × 20 magnification). c, d The epiglottis and oropharynx
revealed the submucosal infiltration of mononuclear cells with a few
neutrophils (H&E, × 20 and × 40 magnification)
neck and the circumstantial information, the cause of death
was determined to be HF poisoning.
Discussion
Fluorine is a highly reactive electronegative non-metal
element, which naturally occurs as fluoride ions. Fluoride
ions are also recognized as an important trace element in
human dental health for their function in inhibiting dem-
ineralization, as well as increasing the rate of reminer-
alization [3]. HF is one of the strongest inorganic acids,
existing as a colorless gas or fuming liquid with a strong
irritating odor. It is used in a variety of industries and
household settings, for frosting, glass etching, mineral
processing, the removal of metal castings, cleaning stone
and marble, and the treatment of textiles, and also as a
constituent of rust removers, detergents, insecticides, and
heavy-duty cleaners [4, 5].
When HF is exposed to skin tissue, local toxicity from HF
is initiated by the immediate action of hydrogen ions, caus-
ing corrosive burns. Secondly, highly lipophilic fluoride ions
penetrate the tissue, leading to liquefactive necrosis. These
necrotic lesions are known to produce extreme pain because
of electrolyte shifting at the nerve ending, which is caused
by Na–K ATPase inhibition [1].
Acute systemic toxicity is induced when fluoride ions
access the circulation via inhalation and ingestion, as well
as skin contact. Systemic reactions occur by two different
mechanisms, direct toxicity and the high affinity of fluoride
ions for calcium and magnesium. Fluoride is directly toxic
69
to many important cellular enzymes and organs including
the central nervous system, heart, liver, kidney, and pulmo-
nary endothelium [6]. After disassociation from hydrogen
ions, free fluoride ions react strongly with calcium and
magnesium salts, causing hypocalcemia, hypomagnesemia,
and hyperkalemia [7]. The most lethal effect of fluoride is
cardiotoxicity. In addition to hypocalcemia, fluoride ions
directly activate myocardial adenylate cyclase, resulting in
profound myocardial irritability and life-threatening ven-
tricular arrhythmia [8].
The severity of HF poisoning depends upon the con-
centration, quantity, the total body surface area involved,
and duration of exposure. The National Institutes of
Health (NIH) classify HF burns based on the HF con-
centration of the offending agent [9]. Concentrations
greater than 50% always cause immediate pain and tissue
damage, concentrations of 20–50% result in a burn after
several hours, and less than 20% may take up to 24 h to
manifest as a burn. Hypocalcemia is likely to develop in
those with (i) > 1% burns with > 50% HF, (ii) > 5% burn
at any concentration, and (iii) those who inhale fumes
from 60% or stronger HF solutions [10]. Thus, minimal
dermal exposure to high concentrations of HF can become
fatal within a short time. Tepperman described the death
of a petroleum refinery worker whose face was exposed
to anhydrous HF involving 2.5% or less of the body sur-
face [11]. The concentration of the acid approached 100%
and he died from profound hypocalcemia and hypomagne-
semia. Buckingham reported the case of a petrochemi-
cal plant employee who recovered from an injury to 5%
of his body surface caused by anhydrous HF [12]. He
showed severe bradycardia with subsequent ventricular
fibrillation despite massive calcium administration. How-
ever, he was finally discharged after excision of the entire
burn and irrigation of the underlying fascia. In the pre-
sent case, less than 5% of the patient’s body surface was
exposed to 50% HF, but it was enough to induce systemic
hypocalcemia. The abundant vascularity of the face and
intense deep tissue damage of the exposed skin gives us
a clue to the reason why a minimal area of skin exposure
could trigger rapid systemic toxicity.
Currently, the mechanism of damage and manifestation
of symptoms after HF exposure are well known. However,
studies presenting the microscopic features of HF burns
are very rare. Ohtani reported an autopsy case of a man
exposed to 60% HF in a chemical plant [13]. In the micro-
scopic examination of the affected skin with greenish-gray
discoloration, severe degeneration of the entire skin layer
with accompanying vascular wall injury was seen. Accord-
ing to Takase, a male worker whose face was splashed with
an unknown concentration of HF showed a third-degree
burn to the face with a greenish-gray color and heavy
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70
and edematous lungs [14]. Both lungs displayed diffuse
intra-alveolar hemorrhage and edema, with no report on
the histologic findings of the skin lesion. In our case, a
thorough pathological examination of the victim’s body
surface and internal organs was performed. The histology
of the neck skin revealed abscess formation in the dermo-
epidermal junction with the extensive infiltration of neu-
trophils in the dermis and adipose tissue. The other areas
of the skin including the chest, back, arm, finger, thigh,
and knee showed no typical changes associated with HF
burns. Both lungs showed marked edema and congestion
with focal pleural fibrosis, and the tracheal mucosa showed
submucosal suppurative inflammation with hemorrhage.
Although a fluoride detection test was not performed in the
lung tissue, the alterations in the airway mucosa in our case
raise the possibility of concurrent fume inhalation.
The cause of death in the deceased was determined to be
fatal hypocalcemia due to HF exposure, and incorrectly or
not wearing safety harnesses was estimated to be the cause
of the exposure. According to the medical record, ionized
calcium levels were elevated after treatment with calcium
gluconate injection in the emergency room, although the
ionized magnesium level was within the normal range.
Several previous reports showed cases of hypocalcemia
accompanied by hypomagnesemia [6, 11]. However, a
case with normal magnesium levels on admission was also
found in the literature [10]. In regard to an influencing
factor in the death, the heart showed moderate (40–50%)
atherosclerosis with no gross abnormalities in the valves or
myocardium. Considering the extent of the cardiac lesions
and relatively rapid clinical course, underlying heart condi-
tions were concluded to have no contribution to the cause
of death.
In the autopsy of this patient, no traces of fluoride ions
were found in the blood, vitreous humor, urine, pleural fluid,
bile, or skin tissue from the neck. According to the medi-
cal record, the patient was sent to the hospital immediately
after he was found with suspicious signs of HF exposure
on his body. Fluoride ions are known to be highly reactive
in vivo, and he received adequate therapy in the emergency
room, including calcium gluconate injection and massive
fluid infusion. These can explain why no fluoride ions were
detected in the postmortem toxicologic study.
In this report, we presented an autopsy case of a worker
whose cause of death was considered mainly to be the result
of cardiac arrhythmia due to HF exposure. In cases of indus-
trial accidents relating to HF, forensic pathologists and cli-
nicians should be aware of the danger of HF and identify
any tiny areas of chemical burns at autopsy. The histologic
finding features can provide considerable information for
inferring the toxicity mechanism and cause of death, espe-
cially when fluoride ions are undetectable at postmortem
examination.
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Forensic Science, Medicine and Pathology (2023) 19:67–71
Key points
1. HF is a highly dangerous substance that can cause death
with minimal exposure.
2. The severity depends mostly upon the concentration
and body surface area involved.
3. Fluoride ions have a high affinity for calcium which
leads to fatal hypocalcemia.
4. HF burns show necrosis of the entire skin with abscess
formation microscopically.
Acknowledgements This article was based on a study first reported
in the Annual Report of The National Forensic Service, volume 46,
2014, as “Cheong H, Fatal Hydrofluoric Acid Poisoning: Histologic
Finding and Review of the Literature.”
Declarations
Ethics approval and consent to participate This article does not con-
tain any studies involving human participants or animals performed
by the author. Moreover, this case report was based on a medicole-
gal autopsy that underwent a court warrant requested by the public
prosecutor.
Conflict of interest The authors declare no competing interests.
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