From the Department of Emergency Medicine (Ko SY, Wang TL), Shin-Kong Wu Ho-Su Memorial Hospital, Taiwan

Correspondence to Dr. Tzong-Luen Wang, Department of Emergency Medicine, 95 Wen Chang Road, Shin-Kong Wu Ho-Su Memorial Hospital, Taipei, Taiwan . E-mail M002183@ms.skh.org.tw

 

Cyanide is found in a variety of substances: plastics, glue removers, wool, silks, nylons, and plants.¹ Numerous forms of cyanide exist, including hydrogen cyanide ( HCN ) and cyanogen chloride ( CNCl ), water-soluble potassium and sodium cyanide salts, and poorly water-soluble mercury, copper, gold, and silver cyanide salts.² Poisoning may occur iatrogenicaly such as nitroprusside infusion, inhalation of hydrogen cyanide gas, or during a combustion byproduct of cyanide-containing products.
Cyanide is one of the lethal chemical agent that can be spread as accidental exposure, chemical warfare and act as a terrorism. After the terroric attack in New York on Sep 11, 2001, the knowledge of lethal chemical agents became more and more important for an emergency physician. In our country, the Republic of China, lethal chemical agents are act as threatening tools to make an illegal profit by evildoers, so all the emergency personnel have to prepare for the scenario: the next patient who appears in front of you might be the victim of chemical agents poisoning such as cyanide.

 

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The common sources of cyanide poisoning including: 1) Smoke inhalation of household fires during the burning of common substances such as rubber, plastic, and silk can create cyanide fumes. 2) Photography, chemical research, synthetic plastics, metal processing, and electroplating industries use cyanide. 3) Certain rare plants containing cyanide include apricot pits and a type of potato called cassava. Fortunately, only chronic or massive ingestion of any of these plants can lead to serious poisoning. 4) Certain chemicals, after ingestion, can be converted by the body into cyanide. Most of these chemicals have been removed from the market, but some old artificial nail polish remover, solvents, and plastics manufacturing solutions can contain these substances.³
Cyanide is a rapidly acting poison, particularly when it is inhaled. Hydrogen cyanide has a bitter almond odor⁴ (The odor of hydrogen cyanide is detectable at 2-10 ppm ) ,⁵ but some individuals cannot detect it and consequently it may not provide adequate warning of hazardous concentrations. The lethal dose for adults is 200–300?mg of potassium or sodium cyanide, or 50 mg of hydrogen cyanide. ^5-6
The mechanism of toxicity involves the binding of the ferric ion in mitochondrial cytochrome oxidase, preventing electron transport in the cytochrome system and bringing oxidative phosphorylation and ATP production to a halt. The inhibition of oxidative metabolism increases demands on anaerobic glycolysis, which results in lactic acid production and may produce severe acid-base imbalance.
Once ingested, cyanide is detoxified by enzymatic conversion to the less toxic, renally excreted metabolite, thiocyanate. A small amount of cyanide is also detoxified by the vitamin B12 precursor, hydroxycobalamin. This chelating agent binds cyanide to form nontoxic cyanocobalamin.^8,9

Cyanide May be absorbed through skin and eyes. If the compound was inhaled, people might have sorethroat and persistent running nose. Then the systemic symptoms appear. Early manifestations of poisoning include anxiety, dyspnea, headache, confusion, tachycardia, and hypertension. All above symptoms and signs will be followed by stupor or coma, seizures, fixed and dilated pupils, hypoventilation, hypotension, bradycardia, heart block, ventricular arrhythmias, and complete cardiopulmonary collapse.^{1,2,3,8,10,11}

The general principles of handling an acute chemical emergency begin with stopping the exposure, which can be accomplished by evacuating or extricating the affected persons, and then by thorough decontamination. Ideally, the persons who might be exposed to chemicals should move upwind of the contaminant and move to an adequate shelter. Then they should remove and bag their clothing and shower thoroughly with soap and water as soon as possible.
Early decontamination of persons with hazardous exposure should be performed by trained first responders. In Taiwan, the first responder may be the EMT personnel or the triage personnel of an emergent department of hospital. And the decontamination spot should be far from the ordinary pathway. Removing contaminated clothing can eliminate 85 to 90 percent of trapped chemical substances.^14,15,16
The initial supportive therapies of chemical exposure after decontamination focus on airway patency, ventilation, and circulation. Besides, patients might suffer from an explosion, we have to keep in mind that they might have concurrent injuries of burn, or trauma.^1,2
In cases of ingestion, do not induce emesis. If activated charcoal has not been administered previously, and the victim is alert, asymptomatic, and has a gag reflex, administer activated charcoal (administer at 1 gm/kg, usual adult dose 60-90 g, child dose 25-50 g). ^11,12,16. A soda can and a straw may be of assistance when offering charcoal to a child. If the patient is symptomatic, immediately institute emergency life support measures, including the use of a cyanide antidote kit ^1,3,5

Treatment of cyanide poisoning tends to be effective if started early. Oxygen, decontamination, nitrites, and sodium thiosulfate are the main therapeutic modalities.¹¹ Oxygen therapy at 100% fraction of inspired oxygen either by face-mask or endotracheal tube should be instituted immediately. Hyperbaric oxygen is as of yet unproved in cyanide poisoning.¹⁷
Antidote: Cyanide antidotes-amyl nitrite perles and intravenous infusions of sodium nitrite and sodium thiosulfate-are packaged in the cyanide antidote kit. Amyl and sodium nitrites induce formation of methemoglobin. Cyanide has a high affinity for the ferric iron contained in methemoglobin, thereby rendering methemoglobin an effective scavenger of unbound cyanide. Amyl nitrite is administered by inhalation of crushable pearls, which are inhaled for 15 to 30 s with 30 s of rest between inhalations. One pearl lasts approximately 2 to 3 min. This therapy induces a 5% methemoglobenemia and can be used in spontaneously breathing patients or in patients receiving ventilatory support until administration of sodium nitrite.^10,12
Sodium nitrite is administered IV at a dose of 300 mg ( 10 ml of 3 % solution) over 3 min to convert more hemoglobin to methemoglobin. ^12,15. The average pediatric dose is 0.12 to 0.33 mL/kg body weight up to 10 mL infused as above. Monitor blood pressure during sodium nitrit e administration, and slow the rate of infusion if hypotension develops. ^1,2,10,12. Half this dose may be repeated after 2 h if there is persistent toxicity, and a tolerable degree of methemoglobinemia. Usually, methemoglobin levels remain <20% and the reduction of total oxygen-carrying capacity by the combination of carboxyhemoglobin and methemoglobin is 21%.¹⁸

In all serious cases of exposure to cyanide, a successful outcome hinges on the immediate provision of basic life support and decontamination, and follow-up with excellent supportive care. Community preparedness for possible toxic chemical releases requires well-organized emergency-medical-response systems, as well as clinicians and hospitals trained for readiness. Emergency planning should be applicable to both accidental and deliberate chemical releases. Besides, the country should intervene and stockpile antidote kit. If whole the hinges are set down, the tragedy will be prevented.

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