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Battlefield Chemical Inhalation Injury
Published in Jacob Loke, Pathophysiology and Treatment of Inhalation Injuries, 2020
The observation that amyl nitrite reversed both respiratory and cardiac effects in dogs before significant methemoglobin was formed suggested at least that methemoglobin formation was not the most significant therapeutic effect of amyl nitrile and that perhaps the classic cytochrome oxidase-inhibition may not be the primary lethal effect (Vick and Froehlich, 1985). The observed vasodilating effect of amyl nitrite prompted further investigation of other vasoactive substances.
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.
Gases
Published in Frank A. Barile, Barile’s Clinical Toxicology, 2019
Disposable syringes, a stomach tube, a tourniquet, and instructions are also included in the kit. The primary mechanism of detoxification involves conversion of CN to the nontoxic thiocyanate ion in preparation for renal elimination. Initially, either intravenous (I.V.) sodium nitrite (300 mg over 3 to 5 min)* or amyl nitrite inhalant (1 or 2 crushed aspirols every 2 to 3 min if the I.V. route is not accessible) is administered. Nitrites convert reduced Hb-Fe2+ ([H]) to oxidized methHb ([O]), freeing the cytochrome oxidase enzyme to resume oxidative phosphorylation. The sequence is outlined in Equation 25.1:
Characteristics and circumstances of volatile solvent misuse-related death in Australia, 2000–2021
Published in Clinical Toxicology, 2023
Shane Darke, Emma Zahra, Johan Duflou, Amy Peacock, Michael Farrell, Julia Lappin
All closed cases (i.e., the coronial investigation had been completed) of volatile solvent misuse-related death aged ≥15 years at the time of death occurring between 1 July 2000 and 31 December 2021 were retrieved and inspected by the authors. Searches were conducted using the National Coronial Information System “Other non-pharmaceutical chemical substance” coding fields set contributory to death for “Fuel or solvent”, “Glue or adhesive”, “Paint, coating or stripping agents”, and “Cleaning agents”. In addition, the National Coronial Information System Drug coding fields set of “Pharmaceutical substance for human use” contributory to death were searched for “Nitrous oxide”. Text searches for amyl nitrite and alkyl nitrite were also conducted. Final searches were conducted in October 2022. Intentional self-harm was determined by the National Coronial Information System “Intentional self-harm” intent designation code. The identification of the incriminating volatile substances was determined by the coroner from toxicology and/or crime scene evidence.
The vitamin B12 analog cobinamide ameliorates azide toxicity in cells, Drosophila melanogaster, and mice
Published in Clinical Toxicology, 2023
John Tat, Stephen C. Chang, Cole D. Link, Suelen Razo-Lopez, Michael J. Ingerto, Behdod Katebian, Adriano Chan, Hema Kalyanaraman, Renate B. Pilz, Gerry R. Boss
No specific antidote is available for azide poisoning and treatment is solely supportive [14]. Due to mechanistic similarities between azide and cyanide, azide poisoning victims have been given cyanide antidotes such as sodium thiosulfate, amyl nitrite, sodium nitrite, or hydroxocobalamin [11,14,24–26]. Sodium thiosulfate detoxifies cyanide by converting it to thiocyanate, but no evidence exists that sodium thiosulfate reacts with azide. Amyl nitrite and sodium nitrite generate methemoglobin, which has a high affinity for cyanide, but binds azide only weakly [27,28]; nitrite might also exacerbate azide-induced hypotension by virtue of its reduction to nitric oxide. Hydroxocobalamin is a rational treatment for azide poisoning because it binds both azide and NO, and thereby could potentially neutralize both species [29–31]. However, hydroxocobalamin has low water solubility, necessitating administration in relatively large volumes via intravenous infusion. It, therefore, does not lend itself well to pre-hospital use.
A comprehensive review of treatments for hydrogen sulfide poisoning: past, present, and future
Published in Toxicology Mechanisms and Methods, 2023
Cristina Santana Maldonado, Abigail Weir, Wilson K. Rumbeiha
Hyperbaric oxygen has been used for years and remains a valuable tool for severe cases of H2S poisoning (Lindenmann et al. 2010; Price et al. 2021). However, the technique is only valuable for treating individual cases as this equipment is not widely available. It is not ideal for the treatment of mass casualties. Hyperbaric oxygen increases oxygen plasma diffusion which leads to improved oxygenation of tissue (Smilkstein et al. 1985; Whitcraft et al. 1985). Although there is no FDA-approved drug for H2S toxicity, certain antidotes have been used in cases of poisoning in a hospital setting. Much like inhaled cyanide, it is suggested to use inhaled nitrite therapy, specifically amyl nitrite, for 30 seconds every minute until the intravenous (IV) line is started. Once IV is introduced, sodium nitrite is given intravenously. Early citations of sodium nitrite therapy suggested clinical efficiency (Hall and Rumack 1997). Recently, however, nitrite therapy has become a controversial topic as the efficacy of nitrite therapy in H2S victims remains inconsistent (Baud et al. 2018). The H2S metabolite thiosulfate and antioxidants have also been used to treat H2S poisoning victims with little success.