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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.
Acute Cyanide Poisoning from Jewelry Cleaning Solutions
Ines Bel Waer1,2*, Wafa Masri1,2, Nedia Chaouali2, Fathia Khli1,2,
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 Monteury, Tunis, Tunisia
Naif Arab University for Security Sciences
Arab Journal of Forensic Sciences and Forensic Medicine
Open Access
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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
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
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
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.
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.
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
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
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
Cyanide ingestion is frequently lethal because of
the early onset of severe symptoms and the difculty 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
reection of intracellular hypoxia [13].
In our case, signicantly 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 specic 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
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 conrm the cyanide poisoning of the
jeweler by ingesting metal cleaning solution containing
cyanide salts in a suicide attempt.
Ingestion of cyanide salts is a common method of
suicide. Its lethality is related to the rapid onset of toxicity,
nonspecic 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.
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-
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-
13. Wood GC. Acute cyanide intoxication diagnosis and
I. Bel Waer, et al
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
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Full-text available
The nature of the toxic gases that cause death from smoke inhalation is not known. In addition to carbon monoxide, hydrogen cyanide may be responsible, but its role is uncertain, because blood cyanide concentrations are often measured only long after exposure. We measured cyanide concentrations in blood samples obtained at the scene of residential fires from 109 fire victims before they received any treatment. We compared the results with those in 114 persons with drug intoxication (40 subjects), carbon monoxide intoxication (29 subjects), or trauma (45 subjects). The metabolic effect of smoke inhalation was assessed by measuring plasma lactate at the time of admission to the hospital in 39 patients who did not have severe burns. The mean (+/-SD) blood cyanide concentrations in the 66 surviving fire victims (21.6 +/- 36.4 mumol per liter, P less than 0.001) and the 43 victims who died (116.4 +/- 89.6 mumol per liter, P less than 0.001) were significantly higher than those in the 114 control subjects (5.0 +/- 5.5 mumol per liter). Among the 43 victims who died, the blood cyanide concentrations were above 40 mumol per liter in 32 (74 percent), and above 100 mumol per liter in 20 of these (46 percent). There was a significant correlation between blood cyanide and carbon monoxide concentrations in the fire victims (P less than 0.001). Plasma lactate concentrations at the time of hospital admission correlated more closely with blood cyanide concentrations than with blood carbon monoxide concentrations. Plasma lactate concentrations above 10 mmol per liter were a sensitive indicator of cyanide intoxication, as defined by the presence of a blood cyanide concentration above 40 mumol per liter. Residential fires may cause cyanide poisoning. At the time of a patient's hospital admission, an elevated plasma lactate concentration is a useful indicator of cyanide toxicity in fire victims who do not have severe burns.
The combination of sodium thiosulfate and sodium nitrite has been used in the United States since the 1930s as the primary antidote for cyanide intoxication. Although this combination was shown to exhibit much greater efficacy than either ingredient alone, the two compounds could not be used prophylactically because each exhibits a number of side effects. This review discusses the pharmacodynamics, pharmacokinetics, and toxicology of the individual agents, and their combination.
The authors reviewed the clinical manifestations, complications, and the prognosis affected by Lilly Cyanide Antidote in 21 victims of acute cyanide poisoning over a 10-year period. The clinical signs and symptoms in cyanide poisoning are variable. Among 21 cases, loss of consciousness (15), metabolic acidosis (14), and cardiopulmonary failure (9) were the three leading manifestations of cyanide intoxication. Anoxic encephalopathy (6) was not uncommon in the severely intoxicated victims. Diabetes insipidus (1) or clinical signs and symptoms mimicking diabetes insipidus (3) may be an ominous sign to encephalopathy victims. The major cause of fatal cyanide poisoning is the intentional ingestion of cyanide compounds as part of a suicide attempt. Decrease of arteriovenous difference of O2 partial pressure may be a clue for the suspicion of cyanide intoxication. Although the authors cannot show a statistically significant difference (P = .47) for the Lilly cyanide antidote kit in terms of improving the survival rate for victims of cyanide poisoning, the antidote kit was always mandatory in our study in the cases of severely intoxicated victims who survived. Early diagnosis, prompt, intensive therapy with antidote, and supportive care are still the golden rules for the treatment of acute cyanide poisoning, whether in the ED or on the scene.
Cyanide poisoning must be seriously considered in victims of smoke inhalation from enclosed space fires; it is also a credible terrorism threat agent. The treatment of cyanide poisoning is empiric because laboratory confirmation can take hours or days. Empiric treatment requires a safe and effective antidote that can be rapidly administered by either out-of-hospital or emergency department personnel. Among several cyanide antidotes available, sodium thiosulfate and hydroxocobalamin have been proposed for use in these circumstances. The evidence available to assess either sodium thiosulfate or hydroxocobalamin is incomplete. According to recent safety and efficacy studies in animals and human safety and uncontrolled efficacy studies, hydroxocobalamin seems to be an appropriate antidote for empiric treatment of smoke inhalation and other suspected cyanide poisoning victims in the out-of-hospital setting. Sodium thiosulfate can also be administered in the out-of-hospital setting. The efficacy of sodium thiosulfate is based on individual case studies, and there are contradictory conclusions about efficacy in animal models. The onset of antidotal action of sodium thiosulfate may be too slow for it to be the only cyanide antidote for emergency use. Hydroxocobalamin is being developed for potential introduction in the United States and may represent a new option for emergency personnel in cases of suspected or confirmed cyanide poisoning in the out-of-hospital setting.