Content uploaded by Wafa Masri
Author content
All content in this area was uploaded by Wafa Masri on Sep 14, 2015
Content may be subject to copyright.
134
Acute Cyanide Poisoning from Jewelry Cleaning Solutions
Ines Bel Waer1,2*, Wafa Masri1,2, Nedia Chaouali2, Fathia Khli1,2,
Ines Gana1,2, Anouar Nouioui1,2, Dorra Ben Salah1,2,
Dorra Amira1,2, Hayet Ghorbel1,2, Abderrazzek Hedhili1,2
1 Toxicology Department, Center of Medical Assistance and Emergency, Tunis, Tunisia
2 Research Unit, Toxicology and Environment Department LR12SP07,
10 rue Aboul KacemChabbi, 1008 Monteury, Tunis, Tunisia
Naif Arab University for Security Sciences
www.nauss.edu.sa
http://ajfsfm.nauss.edu.sa
Arab Journal of Forensic Sciences and Forensic Medicine
Open Access
:äGôgƒéŸG ∞«¶æJ π«dÉfi øY œÉædG ó«fÉ«°ùdÉH OÉ◊G ºª°ùàdG
ádÉM ôjô≤J
25
Introduction
Cyanide is one of the most deadly rapid-acting
poisons. Cyanide toxicity is generally considered to be a
rare form of poisoning [1]; however, cyanide has many
natural, industrial and even household sources. Exposure
occurs frequently in patients with smoke inhalation from
residential or industrial res. Cyanide poisoning may also
occur in industry, particularly in the metal trades, mining,
electroplating, jewelry manufacturing, and processes
involving silver recovery from radiographic lms and other
silver-containing medical waste. In addition, cyanide salts
such as mercury cyanide, copper cyanide, gold cyanide
and silver cyanide produce hydrogen cyanide gas when
Abstract
Cyanide is one of the most lethal and devastating
poisons. It causes acute toxicity through smoke
inhalation simultaneously with carbon monoxide,
or by ingestion of cyanide salts that are commonly
used in metallurgy and in jewelry or textile industries.
Cyanide intoxication is an extremely rare event; in the
present study, we report a case of cyanide poisoning
involving a 25-year-old jeweler, who ingested a
jewelry cleaning solution containing potassium
cyanide in a suicide attempt.
* Corresponding Author: Ines Belwaer
Email: ines.belwaer@yahoo.fr
1658-6794© 2015 Naif Arab University for Security
Sciences. All Rights Reserved. Peer review under the
responsibility of NAUSS / doi: 10.12816/0011258
Production and hosting by NAUSS
Key words: Cyanide, Poisoning, Jewelry Cleaning
Solution, Suicide.
Case Report
Arab Journal of Forensic Sciences and Forensic Medicine 2015; Volume 1 Issue (1), 134-137
135
Open Access
an intense cyanosis on the face and the conjunctival
hyperemia without any trauma or signs of violence. The
internal examination revealed a congestion of the viscera,
pulmonary edema and congestion of submucosal vessels of
the upper respiratory tract.
Methods
A toxicological screening was conducted in order to
nd out the possible cause of death; the rst phase began
with a liquid-liquid and solid-liquid extraction of various
uid samples. Acid and basic extracts were separated by
thin layer chromatography (TLC) and analyzed by gas
chromatography/mass spectrometry (GC/MS).
In addition, barbiturates, opiates, amphetamine,
cannabinoids, and cocaine were also evaluated semi-
quantitatively by uorescence polarization immunoassay
(FPIA). Cyanide in biological uids (urine and gastric
contents) as well as in the white and brown solutions found
at the crime scene was determined potentiometrically using
a cyanide ion-selective electrode. This method is based
upon the measurement of electrode potential as a function
of cyanide concentration in the sample.
Results
There were no detectable opiates, barbiturates,
salicylates, or any other drug in the samples analyzed. The
toxicological tests for ethanol and carboxyhemoglobin
were entirely negative. However, analysis of urine, gastric
contents and two unknown solutions (glass bottles) for
cyanide concentration turned out to be highly positive and
the results are shown in the table 1.
combined with acids, thus creating the opportunity for
industrial accidents or purposeful harmful exposures [2, 3].
Although not a common cause of poisoning, natural
sources can produce cyanide poisoning when taken in
large quantities or when they are packaged as alternative
medicines, such as Laetrile [4]. Cyanide occurs naturally
in the form of cyanogenic glycoside (amygdalin) in
apricot kernels, bitter almonds and apple and cherry seeds
[5]. Cyanogenic glycoside releases hydrogen cyanide
after enzymatic hydrolysis when seeds are crushed and
moistened.
Cyanide causes intracellular hypoxia by reversible
binding to mitochondrial cytochrome oxidase a3 [6]. Signs
and symptoms of cyanide poisoning usually occur less
than 1 minute after inhalation and within a few minutes
after ingestion [7]. Cyanide toxicity is largely attributed
to the cession of aerobic cell metabolism, resulting in
accumulation of lactate; lactic acidosis is a recognized
hallmark of acute cyanide poisoning in humans [8, 9].
Case report
A 25-year-old jeweler was found dead in his jewelry
store a few days after his disappearance. Two asks
containing white and brown uids were found near the
victim and then sent to the toxicology laboratory for
analysis.
The body was transported to the morgue for autopsy to
determine the cause and circumstances of death. Samples
of blood, urine and gastric contents were taken and sent to
the toxicology laboratory for further analysis.
The external examination of the body revealed
Table 1- Cyanide concentration in urine, gastric contents, and white and brown solutions.
Samples Cyanide concentration
Urine 15.5 mg/L
Gastric contents 146.2 mg/L
White solution 16.5 g/L
Brown solution 4.4 g/L
Acute Cyanide Poisoning from Jewelry Cleaning Solutions
136
Discussion
Cyanide ingestion is frequently lethal because of
the early onset of severe symptoms and the difculty in
making an immediate diagnosis. While cyanide poisoning
is rarely encountered by physicians, it continues to be used
in suicides and homicides [10]. As an intracellular poison,
cyanide is potentially lethal because it diffuses into tissues
and binds to target sites within seconds [3].
Symptoms depend on the dose taken and the time
since ingestion. Oral or transdermal ingestion may result
in gradual increases in cyanide concentration levels in
the bloodstream, which may cause a delay in signs and
symptoms [11]. The three most frequently reported signs
of cyanide intoxication are unconsciousness, dyspnea and
cyanosis [12]. These clinical manifestations are largely a
reection of intracellular hypoxia [13].
In our case, signicantly high cyanide concentrations
were found in urine (15.5 mg/L) and gastric contents
(146.2 mg/L). Serum concentration of cyanide greater
than 0.5 mg/L is typically associated with acute cyanide
poisoning [14].
In serious cases of poisoning, cytotoxic anoxia causes
an anion gap metabolic acidosis with elevated lactate [6].
The presence of a severe lactic acidosis with a high anion
gap may be the most valuable and reliable clue to acute
cyanide poisoning [15]. Unfortunately, the blood sample of
our victim was not suitable for blood gas analysis. However,
lactic acidosis is not specic to cyanide poisoning, and
future research is still needed to nd a rapid test to aid in
diagnosing it.
Concerning the white (16.5 g/L, Table 1) and brown
solutions (4.4 g/L) found at the crime scene, the contents
of both the bottles were probably metal-shining solutions
containing cyanide salts, which are routinely used by
jewelers to polish precocious metals such as silver and
gold.
The lethal oral dose of the absolute acid (Hydrogen
cyanide - HCN) has been reported as 50mg and that of its
potassium salt is 200-300mg [13].
These data should conrm the cyanide poisoning of the
jeweler by ingesting metal cleaning solution containing
cyanide salts in a suicide attempt.
Conclusion
Ingestion of cyanide salts is a common method of
suicide. Its lethality is related to the rapid onset of toxicity,
nonspecic nature of symptoms and the failure to consider
the diagnosis. Because of the rapidly lethal effects of this
toxin, any patient suspected of being poisoned by cyanide
should be removed from the source of the exposure,
treated with oxygen therapy and an antidote as soon as it
is available.
References
1. Yen D, Tsai J, Wang LM, Kao W, Hu S, Lee C et al.
The clinical experience of acute cyanide poisoning. Am
J Emerg Med 1995;13: 524-528.
2. Schnepp R. Cyanide: sources, perceptions and risks.
Nurs J 2006; 32: S3-S7.
3. Shephered GVL. Role of hydroxocobalamin in acute
cyanide poisoning. Ann Pharmacother 2008; 42: 661-
669.
4. Vettri JC, Litovitz TL. 1983 Annual Report of
the American Association of Poison Control Centers
national data collection system. Am J Emerg Med
1984; 3: 423-450.
5. Sanches-Perez R, Jorgenesn K, Olsen CE, Dicenta F,
Moller BL. Biterness in almonds. Plant Physiology
2008; 146: 1040-1052.
6. Vogel SN, Sultan TR,Ten Eyck RP. Cyanide poisoning.
Clin Toxicol 1981; 18: 367-83.
7. Harmel J. A review of acute cyanide poisoning with a
treatment update. Crit Care Nurse 2011; 31: 72-81.
8. Baud FJ, Barriot P, Toffis V. Elevated blood cyanide
concentrations in victims of smoke inhalation. N Eng J
Med 1991; 325: 1761-1766.
9. Baud FJ, Borron SW, Bavoux E. Relation between
plasma lactate and blood cyanide concentration in acute
cyanide poisoning. Br Med J 1996; 312: 26-7.
10. Kulig WK, Ballantyne B. Cyanide toxicity. Am Fam
Phys 1993; 18: 185-188.
11. Hall AH, Dart R, Bogdan G. Sodium thiosulfate or
hydroxocobalamin for the empiric treatment of cyanide
poisoning? Ann Emerg Med 2007; 49: 806-813.
12. Baskin SI, Horowitz AM, Nealley BA. The antidotal
action of sodium nitrite and sodium thiosulfate against
cyanide poisoning. J Clin Pharmacol 1992; 32: 368-
375.
13. Wood GC. Acute cyanide intoxication diagnosis and
I. Bel Waer, et al
137
management. Clinical toxicology Consultants 1982; 4: 140.
14. Borron SW. Recognition and treatment of acute cyanide
poisoning. J Emerg Nurs 2006; 32: S11-S18.
15. Gonzales J, Sabatini S. Cyanide poisoning :
pathophysiology and current approaches to therapy. Int
J Artif Organs 1989; 12: 347-355.
Acute Cyanide Poisoning from Jewelry Cleaning Solutions
