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Cyanide poisoning

INTRODUCTION

Cyanide is a mitochondrial toxin that is among the most rapidly lethal poisons known to man. Used in both ancient and modern times as a method of execution, cyanide causes death within minutes to hours of exposure. Though significant cyanide poisoning is uncommon, it must be recognized rapidly to ensure prompt administration of life-saving treatment. A summary table to facilitate emergent management is provided (table 1).

This topic review will discuss the toxicity and management of cyanide poisoning. A general approach to the poisoned patient is found elsewhere. (See "General approach to drug poisoning in adults".)

EPIDEMIOLOGY

According to the Toxic Exposure Surveillance System, there were 3165 human exposures to cyanide from 1993 to 2002. Of these, 2.5 percent were fatal [1]. Cyanide poisoning may result from a broad range of exposures (table 2).

  • Fire – In industrialized countries, the most common cause of cyanide poisoning is domestic fires [2]. Cyanide can be liberated during the combustion of products containing both carbon and nitrogen. These products include wool, silk, polyurethane (insulation/upholstery), polyacrylonitriles (plastics), melamine resins (household goods), and synthetic rubber [3-5]. Vehicular fires can also expose victims to cyanide. Toxicologic evaluation of passengers following the explosion in 1985 of a Boeing 737 during take-off in Manchester, England, revealed that 20 percent of the 137 victims who escaped had dangerously elevated levels of carbon monoxide, while 90 percent had dangerously elevated levels of cyanide [6]. Overall, it is reported that significant levels of cyanide are present in up to 35 percent of all fire victims [7].
  • Industrial – Worldwide industrial consumption of cyanide is estimated to be 1.5 million tons per year, and occupational exposures account for a significant number of cyanide poisonings [8]. Metal extraction in mining, electroplating in jewelry production, photography, plastics and rubber manufacturing, hair removal from hides, and rodent pesticide and fumigants have all been implicated in cyanide poisonings. Skin contact with cyanide salts can result in burns, which allow for enhanced absorption of cyanide through the skin. The combination of cyanide salts and acid, as utilized in electroplating, results in the release of cyanide gas, which can lead to lethal inhalational exposures. Splashes of cyanide solutions can result in skin as well as mucosal absorption [2,9].
  • Medical – Cyanide exposures can result from alternative and standard medical treatments. Amygdalin (trade name Laetrile), a substance derived from apricot and peach kernels, and introduced as an antineoplastic agent in the 1950s, can cause severe cyanide toxicity [10-12]. The drug is alleged to kill cancer cells selectively via its metabolite, hydrocyanic acid. Laetrile is available as a 500 mg oral tablet that contains 30 to 150 mg of amygdalin [13]. Intestinal beta-d-glucosidase digests the amygdalin, releasing hydrogen cyanide (HCN). This enzymatic reaction explains why only gastrointestinal exposure, in contrast to intravenous administration, results in toxicity [10].

    Sodium nitroprusside, a medication used in the treatment of hypertensive emergencies, contains five cyanide groups per molecule. Toxic levels of cyanide may be reached in patients who receive prolonged infusions of sodium nitroprusside, in patients with chronic renal failure, or in pediatric patients [14,15]. Treatment for 3 to 10 hours with 5 to 10 mcg/kg/min has resulted in fatalities [16]. Methods for preventing nitroprusside-induced cyanide poisoning include using silver foil on IV tubing (preventing light from decomposing the nitroprusside molecule), using maximal infusion rates of 2 mcg/kg/min, and adding sodium thiosulfate to the nitroprusside solution [17].
  • Diet – The family Rosaceae, which includes the bitter almond, cherry laurel, apricot, plum, peach, pear, and apple, is responsible for many reported cyanide poisonings. These foods all contain cyanogenic glycosides, such as amygdalin, in their pits and seeds. The common (ie, sweet) almond does not cause cyanide intoxication.
  • Other – Miscellaneous exposure to cyanide may occur during illicit synthesis of phencyclidine, terrorist attacks, ingestion of acetonitrile (artificial nail polish remover), product tampering, and cigarette smoking. Because of the natural cyanide found in tobacco, cigarette smokers have more than 2.5 times the mean whole blood cyanide level of nonsmokers (table 1) [18].

PATHOPHYSIOLOGY

In normal cellular metabolism, most adenosine triphosphate (ATP) is generated from oxidative phosphorylation. An important part of this process is the shuttling of electrons through the mitochondrial cytochrome complex (also known as the electron transport chain) (figure 1).

                                 

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Literature review current through: Mar 2014. | This topic last updated: Jul 15, 2013.
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References
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