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Deaths Due to Asphyxiant Gases
Published in Sudhir K. Gupta, Forensic Pathology of Asphyxial Deaths, 2022
After considering all the facts about cyanide now the question come to summarize how to diagnose the case of cyanide poisoning. The most important clue to diagnosis is the circumstantial evidence, rather than the signs or symptoms. Detection of source of cyanide at the crime scene is an important clue. Apart from that, on autopsy bitter almond smell, bright red color lividity and gastric chemical injury add on to the diagnosis. However, the odor of bitter almond from the crime scene may not always be detected in a well-ventilated area. Moreover, the ability to sense the “cyanide smell” is genetically related. Last but not the least, laboratory confirmation of elevated cyanide in blood confirms the diagnosis to a great extent. 29
Asphyxia
Published in Kevin L. Erskine, Erica J. Armstrong, Water-Related Death Investigation, 2021
Cyanide is an asphyxiant that may be present in many different forms, but most commonly as hydrogen cyanide (HCN) or cyanide salts (potassium cyanide, sodium cyanide, and calcium cyanide). The reaction of the salt with a strong acid produces hydrogen cyanide gas.8 Sources of cyanide-containing compounds are found in a variety of chemicals, such as insecticides, or are used in the manufacturing of plastics and electroplating and metal polishing; thus, a relatively limited pool of people comprising industrial and laboratory workers have access to or are at risk of exposure.8,12 Cyanide may also be a by-product of structural fires liberated during the combustion of synthetic materials, and its toxicity is additive to that of CO.1 Other sources of small amounts of cyanide occur inside the body (in vivo) as a result of normal metabolism, metabolism of certain medications, and metabolism of chemicals such as acetonitrile contained in nail polish remover.8 Ingestion of only small amounts of cyanide by homicidal or suicidal means is the most common route for poisoning, resulting in collapse and death within minutes.12 The development of symptoms, such as shortness of breath, rapid breathing, change in mental status, metabolic acidosis, and coma may also precede death.8 In the hospital setting, a high index of suspicion will allow for prompt diagnosis and administration of a cyanide antidote.
Anti-Nutrients in Bamboo Shoots
Published in Nirmala Chongtham, Madho Singh Bisht, Bamboo Shoot, 2020
Nirmala Chongtham, Madho Singh Bisht
Cyanogenic glycosides are amino acid–derived constituents of plants produced as secondary metabolites that release hydrogen cyanide when chewed or digested. Plants synthesize cyanogenic glycosides as a defence mechanism against the attack of herbivores, insects and pathogens. They occur in at least 2,500 plant species, represented within most plant families of which a number of species are used as food. There are approximately 25 known cyanogenic glycosides and these are generally found in the edible parts of plants, such as apples, apricots, cherries, peaches, plums, almonds, cassava, bamboo shoots, linseed/flaxseed, lima beans, chickpeas, cashews, etc. The toxicity of cyanogenic glycosides and their derivatives is dependent on the release of hydrogen cyanide. The act of chewing or digestion leads to the hydrolysis of the substances, causing cyanide to be released. Symptoms of cyanide toxicity in humans have been reported to include rapid respiration, low blood pressure, headache, dizziness, vomiting, stomachache, diarrhea, convulsion and in severe cases death.
Life-Threatening Cyanide Intoxication after Ingestion of Amygdalin in Prehospital Care
Published in Prehospital Emergency Care, 2022
Patrik Cmorej, Petr Bruthans, Jaroslav Halamka, Irena Voriskova, David Peran
Amygdalin intoxication is manifested by clinical symptoms of cyanide intoxication. Early symptoms of acute cyanide poisoning include neurological manifestations such as giddiness, confusion, headache, dizziness, nausea and vomiting, palpitations and hyperventilation or shortness of breath. These symptoms reflect neurologic and respirators stimulation occurring as a reflexive attempt to compensate for tissue hypoxia. Later symptoms of acute cyanide poisoning reflect neurological, respiratory, and cardiovascular depression arising from inability to compensate for the tissue hypoxia. Seizures, coma, respiratory arrest, and cardiac arrest can occur within minutes after exposure to moderate to high concentrations of cyanide (7). The European Food Safety Authority reports a life-threatening dose of 0.5–3.5 mg of cyanide per kg of body weight (8). That means 35–245 mg of cyanide for a patient weighing 70 kg. Laboratory analysis of a sample of the food supplement Amygdalin 25 g Tachynon Technology Pharmacy, performed by the State Agricultural and Food Inspection Authority of the Czech Republic, revealed 1760 mg of amygdalin in one recommended dose. Hydrolysis of this amount of amygdalin can yield up to 104 mg of cyanide. The Amygdalin 25 g Tachynon Technology Pharmacy food supplement purchased by the patient contained chemically pure amygdalin, which was imported to the European market from China (9).
Development of sodium tetrathionate as a cyanide and methanethiol antidote
Published in Clinical Toxicology, 2022
Adriano Chan, Jangwoen Lee, Subrata Bhadra, Nesta Bortey-Sam, Tara B. Hendry-Hofer, Vikhyat S. Bebarta, Sari B. Mahon, Matthew Brenner, Brian Logue, Renate B. Pilz, Gerry R. Boss
Cyanide is a well-known toxic chemical. It is generated as hydrogen cyanide gas in structural fires and is a major contributor to death by smoke inhalation [1]. It is used in a variety of industries, with over three billion pounds of cyanide salts produced annually worldwide [2]. It has the potential to be released by terrorists and is considered a high-priority chemical threat by the Center for Disease Control. Currently approved treatments for cyanide poisoning in the United States are hydroxocobalamin and the combination of sodium nitrite and sodium thiosulfate. Both treatments must be given intravenously over 10–15 min, which would not be practical in the setting of a major fire, industrial accident, or terrorist attack. A treatment is needed that can be given quickly, for example by intramuscular injection using an autoinjector. This requires that the drug is sufficiently potent and soluble that it can be administered in a small volume.
Sodium azide poisoning: a narrative review
Published in Clinical Toxicology, 2021
John Tat, Karen Heskett, Shiho Satomi, Renate B. Pilz, Beatrice A. Golomb, Gerry R. Boss
Azide has several mechanisms of toxicity. At the cellular level, it inhibits mitochondrial cytochrome C oxidase and catalase [16,17]. The former enzyme is part of complex IV in the mitochondrial electron transport chain and the latter enzyme detoxifies hydrogen peroxide to water and oxygen. Thus, azide can reduce ATP synthesis and cause oxidative stress, the latter due both to mitochondrial electron leakage and reduced catabolism of reactive oxygen species. Cyanide also inhibits cytochrome C oxidase, and azide and cyanide are especially toxic to cells with high respiratory rates, such as neurons and cardiomyocytes. At the organismal level, azide is a potent vasodilator and inhibits platelet aggregation, likely via conversion to nitric oxide. Azide generates nitric oxide in vitro in erythrocytes, platelets, and isolated blood vessels, and recently, nitrosyl-hemoglobin was found in the blood of mice that had received azide [18]. Cytochrome C oxidase inhibition and nitric oxide generation likely underlie the hypotension, myocardial and respiratory failure, and metabolic acidosis that occur in azide poisoning.