A Review of Acute Cyanide Poisoning With a Treatment Update

Hamel, Jillian

doi:10.4037/ccn2011799

Cited by 180 publications

(127 citation statements)

References 18 publications

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“…These factors include: (i) the inability of hemoglobin to carry O 2 owing to the high affinity of cyanide to the ferric ion of heme, leading to tissue hypoxia (Hamel, 2011) and (ii) metabolic acidosis caused by high lactate concentrations that results in the inactivation of cytochrome oxidase a3 (Beasley;Glass, 1998). Inhibition of the respiratory chain (Sornyotha;Kyu;Ratanakhanokchai, 2010;Shama;Wasma, 2011) compromises ATP production and proper functioning of the calcium pump, leading to an imbalance in Ca ++ concentrations in the intra-and extracellular spaces.…”

Section: Groupmentioning

confidence: 99%

Pathological effects of acetone cyanohydrin in swiss rats

et al. 2016

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Cassava has been widely used for animal and human nutrition. It has also been demonstrated to have antineoplastic and anthelmintic properties. Toxicity due to cassava consumption has been reported in ruminants and laboratory animals; therefore, this study aimed to investigate the toxic effects of acetone cyanohydrin, a metabolite of linamarin that is present in cassava, in Wistar rats. Six groups of five animals each were used to evaluate the toxic effects of acetone cyanohydrin administered at 25 (G1), 50 (G2), 75 (G3), 100 (G4) and 125 (G5) µmol/kg as a single oral dose. The control group received acidified water (pH 3.5). The animals were monitored after administration of acetone cyanohydrin, and clinical symptoms were recorded. Serum enzyme levels were measured to assess the kidney and liver function. During necropsy, tissue samples were collected for histopathological examination. After administration, some animals in the G2, G4, and G5 groups presented neurological symptoms such as convulsions, involuntary muscle contraction, staggering gait, motor coordination disability, prostration, and mydriasis. All of the animals in the G5 and four animals in the G4 group died seven minutes after the administration of acetone cyanohydrin. Animals in the other groups, particularly in G2, recovered from the acute phase. Biochemical analysis revealed hepatic lesions and liver dysfunction. Histopathology revealed severe lesions in both the liver and brain. In conclusion, acetone cyanohydrin has toxic effects in the liver, lung, and central nervous system in rats; however, at concentrations up to 25 µmol/kg, the animals could survive the acute phase.Index terms: Neurotoxic; hepatotoxic; cyanide; acute intoxication. RESUMOA mandioca tem sido amplamente utilizada para alimentação animal e humana. Também tem sido demonstrado que possui propriedades anti-neoplásicas e anti-helmínticas. A toxicidade devido ao consumo da mandioca tem sido relatada em ruminantes e animais de laboratório. Assim, este estudo teve como objetivo investigar os efeitos tóxicos da acetona cianidrina, um metabólito da linamarina que está presente na mandioca, em ratos Wistar. Foram utilizados seis grupos de cinco animais cada para avaliar os efeitos tóxicos da acetona cianidrina administrada a 25 (G1), 50 (G2), 75 (G3), 100 (G4) e 125 (G5) umol / kg como uma dose oral única. O grupo controle recebeu água acidificada (pH 3,5). Os animais foram monitorados após a administração de acetona cianidrina e os sintomas clínicos foram registrados. Os níveis séricos das enzimas foram medidos para avaliar a função renal e hepática. Durante a necropsia, amostras teciduais foram coletadas para análise histopatológica. Após a administração, alguns animais dos grupos G2, G4 e G5 apresentaram sintomas neurológicos como convulsões, contração muscular involuntária, andar cambaleante, incordenação motora, prostração e midríase. Todos os animais do G5 e quatro animais do G4 morreram após sete minutos da administração de acetona cianidrina. Animais dos outros grupos,...

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Section: Groupmentioning

confidence: 99%

Pathological effects of acetone cyanohydrin in swiss rats

et al. 2016

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“…Hydroxocobalamin acts by binding with cyanide to form nontoxic cyanocobalamin that is excreted by kidneys [23,25,26]. Nitrites oxidize iron present in hemoglobin to the ferric state, leading to formation of methemoglobin which has a higher affinity for cyanide.…”

Section: Discussionmentioning

confidence: 99%

“…Progressively lower levels of consciousness, seizures and coma follow. CVS involvement is manifested as hemodynamic instability [23]. Early administration of one of the antidotes holds the key to treatment [24].…”

Section: Discussionmentioning

confidence: 99%

Awareness, among primary health care physicians, of acute cyanide poisoning being a possible consequence of fire accidents

Sood

Khandalkar

Sood³

2016

Int J of Biomed & Adv Res

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Objectives: To discern the degree of awareness amongst the primary health care physicians about the fact that cyanide poisoning is a possible consequence of fire accidents. Methods: Using an anonymous questionnaire, thirty allopath primary health care physicians were tested for awareness of acute cyanide poisoning being a possible consequence of fire accidents. Results: Only one (3%) of the physicians was aware of the possibility of acute cyanide poisoning due to fire accidents. Conclusions: We report dismal awareness among the primary health care physicians. Medical education curriculum must cater for emerging healthcare issues.

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“…Possible threat of cyanide being used by terrorists has generated renewed interest in its diagnosis and treatment (Baud, 2007). Life-threatening through cyanide poisoning is treatable when quickly recognized, and immediately and aggressively counteracted with an appropriate antidote (Hamel, 2011). Unlike poisons for which no specific antidote is available, cyanide has numerous antidotes with diverse mechanisms of action and safety profiles (Gracia & Shepherd, 2004;Mégarbane et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

Accelerated stability and bioassay of a new oralα-ketoglutarate formulation for treating cyanide poisoning

Bhattacharya

Gopalan

Singh

et al. 2013

Pharmaceutical Biology

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Context: Due to several limitations of existing cyanide antidotes, a-ketoglutarate (a-KG) has been proposed as a promising treatment for cyanide. Objective: This study reports the accelerated stability and bioassay of a new oral a-KG formulation. Materials and methods: Amber-colored PVDF bottles containing 100 ml of 10% a-KG in 70% sorbitol, preservative (sodium methyl paraben and sodium propyl paraben), sweetener (sodium saccharine), flavor (American ice-cream soda and peppermint) and color (tartrazine), at pH 7.0-8.0 were stored in stability chamber (40 AE 2 C and 75 AE 5% humidity) for 6 months in a GMP compliant facility. Various physical (pH, color, evaporation, extractable volume and clarity), chemical (identification and quantification of active ingredient) and microbiological (total aerobic count) analyses, together with protection studies were carried periodically in mice. Acute toxicity of the formulation and bioavailability of a-KG were assessed in rats at the beginning of the experiment. Results: No physical changes and microbiological growth were observed in the formulation. After 6 months, a-KG content in the formulation diminished by $24% but its protective efficacy against cyanide remained at 5.9-fold. Protection was further characterized spectrophotometrically by disappearance of a-KG spectrum in the presence of cyanide, confirming cyanohydrin formation. Oral LD 50 of a-KG formulation in rats was 47.0 g/kg body weight, and did not produce any acute toxicity of clinical significance. Also, an appreciable amount of a-KG was measured in blood. Conclusion: As per the guidelines of International Conference on Harmonization, the new a-KG formulation exhibited satisfactory stability, bioefficacy and safety as cyanide antidote.

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A Review of Acute Cyanide Poisoning With a Treatment Update

Cited by 180 publications

References 18 publications

Pathological effects of acetone cyanohydrin in swiss rats

Pathological effects of acetone cyanohydrin in swiss rats

Awareness, among primary health care physicians, of acute cyanide poisoning being a possible consequence of fire accidents

Accelerated stability and bioassay of a new oralα-ketoglutarate formulation for treating cyanide poisoning

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