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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
Homicide
Published in Burkhard Madea, Asphyxiation, Suffocation,and Neck Pressure Deaths, 2020
Burkhard Madea, Musshoff Frank, Schmidt Peter
The treatment of cyanide poisoning begins with removing the patient from exposure, administering 100 per cent oxygen, and giving aggressive cardiorespiratory support and an antidote. Inhalation of amyl nitrite has been recommended as a first-aid measure, followed by the intravenous administration of sodium nitrite and/or sodium thiosulfate. Nitrites induce methaemoglobinaemia, which detoxifies cyanide by forming cyanomethaemoglobin. Thiosulfate serves as a sulfur donor in the rhodanese-catalyzed conversion of cyanide to less toxic thiocyanate. Methaemoglobin levels should be monitored serially during treatment. Blood cyanide levels are useful in confirming the diagnosis of intoxication, but therapeutic interventions must usually be initiated before the results of analysis are available.
Chemical and Biological Threats to Public Safety
Published in Frank A. Barile, Barile’s Clinical Toxicology, 2019
As a terrorist threat, AN gas is most toxic. The colorless gas has a faint bitter almond odor. The Environmental Protection Agency (EPA) allows a maximum contaminant level of 0.2 mg/l of cyanide in drinking water. It requires the reporting of spills or accidental releases into the environment of 1 lb or more of cyanide compounds. The clinical toxicity and treatment of cyanide poisoning are discussed in Chapter 23.
Intramuscular dimethyl trisulfide: efficacy in a large swine model of acute severe cyanide toxicity
Published in Clinical Toxicology, 2019
Tara B. Hendry-Hofer, Alyssa E. Witeof, Dennean S. Lippner, Patrick C. Ng, Sari B. Mahon, Matthew Brenner, Gary A. Rockwood, Vikhyat S. Bebarta
Cyanide poisoning remains a major threat to civilians and military personnel worldwide from accidental, as well as intentional exposures [1]. The mechanism of cyanide toxicity is primarily by binding cytochrome c oxidase and inhibiting cellular respiration, causing lactic acidosis, altered mentation, apnea, hypotension, and finally cardiac arrest [2,3]. The threat of cyanide use by terrorists is a major concern of the US chemical defense program, which makes finding a non-intravenous, safe antidote for acute cyanide toxicity a high priority [1]. While effective antidotes are available for treating individual victims, current antidotes must be given intravenously and often in large volumes [2]. Currently, an antidote that could be administered in a mass casualty cyanide poisoning event does not exist, representing a major gap in treating patients in this type of scenario.
Development of a hydrogen cyanide inhalation exposure system and determination of the inhaled median lethal dose in the swine model
Published in Inhalation Toxicology, 2018
Jillian M. Staugler, Michael C. Babin, M. Claire Matthews, Matthew K. Brittain, Mark R. Perry
Current recommendations for the treatment of cyanide poisoning include supportive treatment and the administration of specific antidotal therapeutics (Baskin & Brewer, 1997; Jackson & Logue, 2017; Simeonova et al., 2004). Existing antidotal therapies for cyanide must be administered quickly, ideally at the scene, for optimal outcomes (Hamel, 2011). Treatment recommendations vary in different countries based on where the drugs were originally developed and used. Current treatment options are limited in the event of mass exposure as they require rapid identification of cyanide poisoning for administration and have potentially harmful side effects (Baskin & Brewer, 1997). Further testing is needed to evaluate current therapies and develop optimal treatment plans for potential large scale HCN toxicity.
Cyanide poisoning in Thailand before and after establishment of the National Antidote Project*
Published in Clinical Toxicology, 2018
Sahaphume Srisuma, Aimon Pradoo, Panee Rittilert, Sunun Wongvisavakorn, Achara Tongpoo, Charuwan Sriapha, Wannapa Krairojananan, Netnapis Suchonwanich, Sumana Khomvilai, Winai Wananukul
The population in this study originated from a single poison center database, which combines both voluntarily reported data and NAP notifications. Cases undetected by these two methods are not reported to the poison center database, so the overall number of exposures might be underreported. The diagnoses of cyanide poisoning from the two reporting sources were based largely on reported histories rather than laboratory-confirmed exposures. However, cases with poison center consultation and/or with requests for antidotes might represent more clinically severe poisonings, while rates of clinical effects and fatality may not be generalizable to studies with other designs or populations.