Management Of Cyanide Poisoning Research Articles

Cyanide poisoning and antidotes

Emergency Medicine AustralasiaVolume 24, Issue 6 p. 680-680 Letter to the Editor Cyanide poisoning and antidotes Vikhyat S Bebarta, Vikhyat S Bebarta Medical Toxicology, Department of Emergency Medicine, San Antonio Military Medical Center, San Antonio, Texas, USASearch for more papers by this author Vikhyat S Bebarta, Vikhyat S Bebarta Medical Toxicology, Department of Emergency Medicine, San Antonio Military Medical Center, San Antonio, Texas, USASearch for more papers by this author First published: 06 December 2012 https://doi.org/10.1111/1742-6723.12004Citations: 1Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article. Volume24, Issue6December 2012Pages 680-680 RelatedInformation

An unusual cause of severe lactic acidosis: cyanide poisoning after bitter almond ingestion

Dear Editor, Although cyanide exists in various alimentary sources like manioc, corn, bitter almonds, peach or apricot kernels, food-related cyanide intoxications are rare [1]. A 58-year-old healthy woman was admitted for sudden headaches, dizziness, vomiting, and generalized seizures. Prehospital medical services found her comatose (Glasgow Coma Score: 5) with bradycardia (30/min) and nonmeasurable blood pressure. She was promptly intubated and received fluids. A brain CT scan was normal. On intensive care unit (ICU) admission, her blood pressure was 80/40 mmHg, heart rate 62/min, SpO2 100% (FiO2: 100%), and temperature 37.0 C. Physical examination, electrocardiogram, and echocardiography were unremarkable. Severe lactic acidosis (arterial pH: 6.59, base deficit: 36.0 mmol/l, anion gap: 33.0 mmol/l, and plasma lactate concentration: 26.0 mmol/l) was assessed without ketosis, osmolar gap, liver or renal dysfunction. Fluids (2,000 ml), norepinephrine (0.5 mg/h), insulin, and sodium bicarbonate were infused. Routine toxicological screening was negative. Blood cyanide concentration was 2.77 mg/l (spectrophotometric method; N \0.2 mg/l; limit of detection: 0.06 mg/l) 6 h after coma onset. Hydroxocobalamin (10 g, 140 mg/kg) was immediately infused, resulting in complete recovery: lactate normalization (within 12 h, Table 1), norepinephrine weaning (20 h), acid/base balance correction (36 h), extubation (day 2), and ICU discharge (day 3). Her husband finally remembered that she had ingested a large quantity of bitter almonds (around 50) from the garden, 2 h before symptom onset. Accidental food-related cyanide poisonings are unusual [1]. Signs are delayed after ingestion, in relation to enzymatic processes producing cyanide in the gut from the ingested cyanogenic glucosides. Cyanide poisoning is rapidly fatal if not promptly treated. Clinical features are not specific, misleading the diagnosis. However, when suspicion is based on compatible circumstances, plasma lactate concentrations C8 mmol/l are an excellent predictor of blood cyanide concentrations C1 mg/l [2]. In our case, despite no relevant anamnesis, cyanide poisoning was suspected because of severe lactic acidosis with coma, hypotension, and bradycardia in the absence of sepsis. Reported symptoms of cyanide poisoning following almond/seed ingestion included headaches, dizziness, sweating, pink cyanosis, coma, seizures, hyperthermia, hypotension, polypnea, bradypnea, hypoglycemia, and lactic acidosis [3, 4]. To our knowledge, hyperlactatemia (pH 7.17, lactate: 14.3 mmol/l) was reported in only one case after ingestion of bitter almonds with laetrile tablets (containing amygdaline) given for alternative cancer treatment [3]. The present case is unique for two reasons: the severity of almondinduced lactic acidosis and its dramatic improvement after hydroxocobalamin infusion. Management of cyanide poisoning is based on advanced life support and antidotes. Despite cyanide-induced deficient cell oxygen utilization, increased oxygen delivery (FiO2: 100%) is useful to reactivate mitochondrial enzymes and other oxidative systems. Hydroxocobalamin is an effective and safe antidote binding cyanide on an equimolar ratio to form stable cyanocobalamin, which is excreted in urine [5]. Although we should

Enhancing Public Health Preparedness for a Terrorist Attack Involving Cyanide

The US government considers cyanide to be among the most likely agents of chemical terrorism. Cyanide differs from many other biological or chemical agents for which little or no defense is available because its individual and public health effects are largely remediable through appropriate preparedness and response. Because the toxicity of the cyanide antidote currently available in the United States renders it ill-suited for use in terrorist incidents and other situations requiring rapid out-of-hospital treatment, hydroxocobalamin—an effective and safe cyanide antidote being used in other countries—has been introduced in the United States. Unlike the other available cyanide antidote, hydroxocobalamin can be administered at the scene of a cyanide disaster, and it need not be reserved for cases of confirmed cyanide poisoning but can be administered in cases of suspected poisoning. Both of these attributes facilitate the rapid intervention necessary for saving lives. To realize the potential benefits of hydroxocobalamin, progress also needs to be realized in other aspects of readiness, including but not limited to developing plans for ensuring local and regional availability of antidote, educating emergency responders and health care professionals in the recognition and management of cyanide poisoning, and raising public awareness of the potential for a chemical weapons attack and of how to respond.

From Smoke Inhalation to Chemical Attacks: Acute Cyanide Poisoning in the Prehospital Setting

The International Programme on Chemical Safety (IPCS)—a cooperative program of the World Health Organization (WHO), the International Labour Organization (ILO), and the United Nations Environment Programme (UNEP)—designates cyanide a priority chemical in relation to the potential impact on human health and the environment. Like other IPCS priority chemicals, cyanide is highly toxic, is a transboundary safety concern, is a target for risk management in multiple countries, is produced in large quantities, has dispersive use, and poses a risk for human exposure (Table 1). Acute exposure to cyanide has caused significant morbidity and mortality in household and industrial accidents, as well as in suicides and attempted genocides, wars, and acts of terrorism. The most common, but perhaps least recognized source of cyanide in cases of acute poisoning is from smoke caused by fires. This review is the product of a collaboration among experts in prehospital emergency medicine, public health and safety, and disaster preparedness. Current understanding of the causes, consequences, and management of cyanide poisoning are described as a potential advancement in antidotal therapy that could transform the provision of prehospital care to cyanide-poisoned victims.

Time to discontinue the use of solutions A and B as a cyanide 'antidote'.

Solutions A and B (15.8% ferrous sulfate in 0.3% citric acid and 6% sodium carbonate, respectively) have been available as a first-aid treatment for cyanide ingestion for many decades. Controversy surrounding the efficacy of solutions A and B has existed for much of that time, the main protagonists being in the UK. The current opinion in the UK is that solutions A and B should no longer be used as a first-aid measure in the management of cyanide poisoning. Similarly, oral sodium thiosulfate or activated charcoal should not be used. The recommended first-aid treatment of symptomatic cyanide poisoning is 100% oxygen and amyl nitrite, irrespective of the route of exposure.