• Ascending dose
• Cyanide poisoning
• Healthy participants
• Intranasal
• Nasal spray
• Stabilized isoamyl nitrate

• exposures
• countermeasure
• cyanide
• pharmacokinetics
• chemical threat
• safety and efficacy

• P30 CA023168 NCI NIH HHS
• U54 NS112107 NINDS NIH HHS
• National Institutes of Health
• Department of Education Graduate Assistance in Areas of National Need
• Purdue Center for Cancer Research

Autopsies of accidental deaths in industrial scenarios have always been a challenging job for a forensic pathologist. Industries that employ chemical agents pose a unique risk, especially when safety protocols are ignored. Exposure to cyanide salts creates an additional risk since death may occur quickly. We present one such incident of the accidental deaths of three industrial workers, which could have been prevented if proper safety measures had been followed. Four workers fell unconscious while cleaning the electroplating chamber of the handicraft industry. Three were declared dead on arrival at the emergency department, while one survived. Autopsy of all three victims showed similar findings of pink-colored post-mortem staining and multiple petechial hemorrhages over the heart and lungs. After histopathological and chemical analysis, the cause of death was opined to be due to complications of cyanide poisoning. In accidental industrial deaths, the forensic pathologist should consider the possibility of death due to toxic chemicals, such as cyanide, used in the manufacturing process. The industrial personnel should be educated about the risks involved, and proper use of safety equipment should be encouraged to avoid such hazardous outcomes. Additionally, the people employed in the autopsy of the deaths related to chemical disasters should ensure their personal safety and preventive measures.

Suicide with cyanides is relatively rare but highly lethal. The lethal oral dose of cyanide salts is 200 mg, and concentrations >3 mg/L may be potentially lethal. The symptoms of poisoning are predominating in the central nervous system and cardiovascular system. We report the case of a 43-year-old goldsmith man who presented with self-poisoning by cyanide salt ingestion. Patient's symptoms included confusion, cardiac arrhythmias, hyperkalemia, leukocytosis, metabolic acidosis with high anion gap, hypotension, and then hypertension. The cause of the patients poisoning was not initially diagnosed. Intensive supportive treatment was performed. The patient died on the 3^rd day of admission following cardiac arrest. At autopsy, hemorrhagic gastritis and cherry-red discoloration of the chest muscles were observed. Forensic toxicology showed cyanide in the blood and tissues. Cyanide poisoning could appear in different forms, and like our case, the symptoms can last for several days with nonspecific symptoms.

• Cyanides
• poisoning
• suicide
• symptom

• antidotes
• carbon monoxide
• cyanides
• hydroxocobalamin
• pre-hospital
• smoke
• thiosulfates

• CT
• MRI
• Metal Ions
• Neuroimaging

This paper reviews milestones in antidotal therapies for cyanide (CN) spanning early remedies, current antidotal systems and research towards next generation therapies. CN has been a part of plant defense mechanisms for millions of years. It became industrially important in the nineteenth century with the advent of CN assisted gold mining and the use of CN as a pest control agent. The biochemical basis of CN poisoning was actively studied and key mechanisms were understood as early as 1929. These fundamental studies led to a variety of antidotes, including indirect CN binders that generate methemoglobin, direct CN binders such as hydroxocobalamin, and sulfur donors that convert CN to the less toxic thiocyanate. Research on blood gases at the end of the twentieth century shed new light on the role of nitric oxide (NO) in the body. The discovery of NO’s ability to compete with CN for enzymatic binding sites provided a previously missed explanation for the rapid efficacy of NO generating antidotes such as the nitrites. Presently used CN therapies include: methemoglobin/NO generators (e.g., sodium nitrite, amyl nitrite, and dimethyl aminophenol), sulfur donors (e.g., sodium thiosulfate and glutathione), and direct binding agents [(e.g., hydroxocobalamin and dicobalt salt of ethylenediaminetetraacetic acid (dicobalt edetate)]. A strong effort is being made to explore novel antidotal systems and to formulate them for rapid administration at the point of intoxication in mass casualty scenarios. New antidotes, formulations, and delivery systems are enhancing bioavailability and efficacy and hold promise for a new generation of improved CN countermeasures.

• Cyanide
• Hydrocyanic acid
• Antagonist
• Antidote
• Cobinamide
• Sulfanegen
• Sulfane sulfur donor

• Cassava
• Cyanate
• Cyanide
• Konzo
• Neurotoxicity
• Rhodanese