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Cyanide Toxicity

  • Author: Inna Leybell, MD; Chief Editor: Asim Tarabar, MD  more...
 
Updated: Dec 07, 2015
 

Background

Cyanide toxicity is generally considered to be a rare form of poisoning. However, cyanide exposure occurs relatively frequently in patients with smoke inhalation from residential or industrial fires. In addition, intensive treatment with sodium nitroprusside or long-term consumption of cyanide-containing foods is a possible source of cyanide poisoning. Historically, cyanide has been used as a chemical warfare agent, and it could potentially be an agent for a terrorist attack.[1, 2]

Cyanide exists in gaseous, liquid, and solid forms. Hydrogen cyanide (HCN, also known as prussic acid) is a volatile liquid that boils at 25.6° C (78.1° F). Potassium and sodium cyanide salts are water soluble, whereas mercury, copper, gold, and silver cyanide salts are poorly water soluble.

In addition, a number of cyanide-containing compounds, known as cyanogens, may release cyanide during metabolism. These include, but are not limited to, cyanogen chloride and cyanogen bromide (gases with potent pulmonary irritant effects), nitriles (R-CN), and the vasodilator nitroprusside sodium, which may produce iatrogenic cyanide poisoning during prolonged or high-dose intravenous (IV) therapy (>10 mcg/kg/min). (See Etiology.)

Industry widely uses nitriles as solvents and in the manufacturing of plastics. Nitriles may release HCN during burning or when metabolized after absorption by the skin or gastrointestinal tract. A number of synthesized and natural compounds produce HCN when burned. These combustion gases likely contribute to the morbidity and mortality from smoke inhalation. Finally, long-term consumption of cyanide-containing foods, such as cassava root or apricot seeds,[3] may lead to cyanide poisoning.

Depending on its form, cyanide may cause toxicity through inhalation, ingestion, dermal absorption, or parenteral administration. Clinical manifestations vary widely, depending on the dose and route of exposure, and may range from minor upper airway irritation to cardiovascular collapse and death within minutes. (See Clinical Presentation.) In severe cases, rapid, aggressive therapy consisting of supportive care and antidote administration can be lifesaving. (See Treatment and Medication.)

Cyanide as a chemical weapon

HCN (North Atlantic Treaty Organization [NATO] designation AC) is one of two cyanide chemical warfare agents[4, 5, 6] ; the other is cyanogen chloride (NATO designation CK). Cyanide is a rapidly lethal agent when used in enclosed spaces where high concentrations can be achieved easily.[7, 8, 9, 10] In addition, because of the extensive use of cyanide in industry in the United States, this agent presents a credible threat for terrorist use.[5]

Cyanide was first used as a chemical weapon in the form of gaseous HCN in World War I. Starting in 1915, the French military used approximately 4000 tons of cyanide, without notable success. The failure of this measure was probably attributable to the high volatility of cyanide and the inability of the 1- to 2-lb munitions used to deliver the amounts of chemical required for biologic effects.[5, 6]

The introduction of cyanogen chloride by the French in 1916 made available a compound that, being both more toxic and less volatile, was a more effective chemical agent. Other alleged military uses of cyanide include Japanese attacks on China before and during World War II and Iraqi attacks on Kurds in the 1980s.

For related information, see the Disaster Preparedness and Aftermath Resource Center.[11, 12]

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Pathophysiology

Cyanide exposure most often occurs via inhalation or ingestion, but liquid cyanide can be absorbed through the skin or eyes. Once absorbed, cyanide enters the blood stream and is distributed rapidly to all organs and tissues in the body.[13]

Inside cells, cyanide attaches itself to ubiquitous metalloenzymes, rendering them inactive. Its principal toxicity results from inactivation of cytochrome oxidase (at cytochrome a3), thus uncoupling mitochondrial oxidative phosphorylation and inhibiting cellular respiration, even in the presence of adequate oxygen stores. Cellular metabolism shifts from aerobic to anaerobic, with the consequent production of lactic acid. Consequently, the tissues with the highest oxygen requirements (brain and heart) are the most profoundly affected by acute cyanide poisoning.

The LCt50 (the concentration-time product capable of killing 50% of the exposed group) for hydrogen cyanide is 2500-5000 mg/min/m3. Vapor exposures in high concentrations (at or above the LCt50) typically can cause death in 6-8 minutes.[1] The lethal oral doses of HCN and cyanide salts are estimated to be 50 mg and 100-200 mg, respectively. For skin exposures, the LD50 (the dose capable of killing 50% of the exposed group) is estimated to be 100 mg/kg.

Cyanogen chloride is used in mining and metalworking, and thus may be involved in an industrial accident. By nature of its chlorine moiety, cyanogen chloride causes irritation of the eyes and respiratory tract and potential delayed pulmonary toxicity similar to chlorine or phosgene gases. In high concentrations (eg, in enclosed spaces), this agent is rapidly acting and lethal, causing death within 6-8 minutes if inhaled at doses at or above its LCt50 of 11,000 mg/min/m3.

Defective cyanide metabolism due to rhodanese deficiency may explain development of Leber optic atrophy, leading to subacute blindness. Cyanide also may cause some of the adverse effects associated with chronic smoking, such as tobacco amblyopia.

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Etiology

Smoke inhalation, suicidal ingestion, and industrial exposures are the most frequent sources of cyanide poisoning. Treatment with sodium nitroprusside or long-term consumption of cyanide-containing foods is a possible source. Historically, cyanide has been used as a chemical warfare agent, and it could potentially be an agent for a terrorist attack.[1, 2]

Smoke inhalation

Smoke inhalation during house or industrial fires is the major source of cyanide poisoning in the United States. Individuals with smoke inhalation from enclosed space fires who have soot in the mouth or nose, altered mental status, or hypotension may have significant cyanide poisoning (blood cyanide concentrations >40 mmol/L or approximately 1 mg/L).

Many compounds containing nitrogen and carbon may produce hydrogen cyanide (HCN) gas when burned. Some natural compounds (eg, wool, silk) produce HCN as a combustion product.[4, 14] Household plastics (eg, melamine in dishware, acrylonitrile in plastic cups), polyurethane foam in furniture cushions, and many other synthetic compounds may produce lethal concentrations of cyanide when burned under appropriate conditions of oxygen concentration and temperature.

Intentional poisoning

Cyanide ingestion is an uncommon, but effective, means of suicide.[15] These cases typically involve health-care and laboratory workers who have access to the cyanide salts found in hospital and research laboratories.

Industrial exposure

Countless industrial sources of cyanides exist. Cyanides are used particularly in the metal trades, mining, jewelry manufacturing, dyeing, photography, and agriculture. Specific industrial processes involving cyanide include metal cleaning, reclaiming, or hardening; fumigation; electroplating; and photo processing.[2] In addition, industry uses cyanides in the manufacture of plastics, as reactive intermediates in chemical synthesis, and as solvents (in the form of nitriles).

Exposure to salts and cyanogens occasionally causes poisonings; however, a significant risk for multiple casualties occurs when these products come into contact with mineral acids because HCN gas is produced. A mass casualty incident may develop in an industrial accident in which cyanogen chloride comes in contact with water (eg, during fire-fighting). Containers of cyanogen chloride may rupture or explode if exposed to high heat or following prolonged storage.

Iatrogenic exposure

The vasodilator nitroprusside sodium, when used in high doses or over a period of days, can produce toxic blood concentrations of cyanide. Patients with low thiosulfate reserves (eg, malnourished, postoperative) are at increased risk for developing symptoms, even with therapeutic dosing. Resultant confusion and combativeness initially may be mistaken as intensive care unit (ICU) syndrome (ie, sundowning). Problems may be avoided by coadministration of hydroxocobalamin or sodium thiosulfate.

Ingestion of cyanide-containing supplements or plants

Ingestion of cyanide-containing supplements is rare. Amygdalin (synthetic laetrile, also marketed as vitamin B-17), which contains cyanide, was postulated to have anticancer properties due to the action of cyanide on cancer cells. However, laetrile showed no anticancer activity in human clinical trials in the 1980s and is not available in the United States,[16] although it can be purchased on the Internet.

Amygdalin can be found in the pits of many fruits, such as apricots and papayas; in raw nuts; and in plants such as lima beans, clover, and sorghum. Amygdalin can be hydrolyzed to hydrogen cyanide, and ingestion of large quantities of such foods may result in toxicity.[2]

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Epidemiology

United States statistics

Cyanide may be a major contributor to the morbidity and mortality observed in the approximately 5000-10,000 deaths from smoke inhalation occurring each year in the United States. Suicidal exposures are rarely reported to poison centers: intentional exposures accounted for 19 of the 187 cyanide poisoning cases reported to the American Association of Poison Control Centers in 2014.[17] However, a rapidly fatal suicide from cyanide salts in an adult patient might easily be mistaken for sudden death from myocardial infarction, pulmonary embolus, or ventricular dysrhythmia.

Suicide by cyanide poisoning occurs predominantly in males, as does industrial exposure. Leber optic atrophy has shown a very strong male predominance in European studies.

Deliberate ingestion of cyanide occurs mostly in adults. Smoke inhalation and chronic cyanide poisoning affect all ages.

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Prognosis

The prognosis in cyanide toxicity is good for patients who have only minor symptoms that do not necessitate the administration of antidotes. The prognosis is reasonably good for patients with moderate symptoms if rapid supportive intervention and effective antidotal therapy are provided. Suicidal poisonings tend to have severe outcomes because large doses are often involved.

The prognosis in patients with cyanogen poisoning is better in those with low-level exposures with minor symptoms that resolve after they are removed from exposure. The prognosis is fair for patients with seizures or recent-onset apnea if antidotes can be administered rapidly. The prognosis is generally poor in patients who suffer cardiac arrest secondary to cyanide toxicity, even if antidotes are administered promptly.

Mortality/morbidity

According to the American Association of Poison Control Centers Toxic Exposure Surveillance System, 7 of the 202 cyanide exposure cases in 2012 were fatal.[17] Cyanide induces fatality in seconds to minutes following inhalation or intravenous injection, in minutes following ingestion of soluble salts, or minutes (hydrogen cyanide) to several hours (cyanogens) after skin absorption.

Individuals who survive cyanide poisoning are at risk for central nervous system dysfunction, such as anoxic encephalopathy. Acute and delayed neurologic manifestations (Parkinson-like syndrome, other movement disorders, neuropsychiatric sequelae) have been reported.

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Patient Education

Educate patients using cyanide in their jobs about safe work practices, including the use of personal protective equipment. Certain cyanide compounds are well absorbed dermally; thus, gloves and other forms of skin protection should be worn. Moreover, cyanide compounds should be scrupulously isolated from exposure to acids.

Educate patients with cancer or human immunodeficiency virus (HIV) who might purchase anticancer supplements over the Internet about the possible risks from such medicines. Encourage them to discuss supplement use with their oncologist.

Patients who have been exposed to cyanide should be educated about potential neurologic sequelae and the importance of follow-up evaluation. Patients treated with hydroxocobalamin who develop skin erythema should be cautioned to avoid exposure to sunlight while the discoloration persists, due to possible photosensitivity. These patients may also develop red discoloration of their urine as an expected side effect that resolves without treatment.

For patient education information, see Personal Protective Equipment , theFirst Aid and Emergency Center and the Lung Disease and Respiratory Health Center, as well as Cyanide Poisoning and Smoke Inhalation.

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Contributor Information and Disclosures
Author

Inna Leybell, MD Clinical Assistant Professor, Department of Emergency Medicine, NYU Langone Medical Center

Inna Leybell, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Student Association/Foundation, Phi Beta Kappa

Disclosure: Nothing to disclose.

Coauthor(s)

Stephen W Borron, MD, MS, FAAEM, FACEP, FAACT, FACMT Professor of Emergency Medicine and Medical Toxicology, Division of Medical Toxicology, Department of Emergency Medicine, Paul L Foster School of Medicine, Texas Tech University Health Sciences Center; Associate Medical Director, West Texas Regional Poison Center

Stephen W Borron, MD, MS, FAAEM, FACEP, FAACT, FACMT is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Emergency Physicians, American Industrial Hygiene Association, American College of Occupational and Environmental Medicine, European Association of Poisons Centres and Clinical Toxicologists, American College of Medical Toxicology

Disclosure: Received consulting fee from Meridian Pharmaceuticals for consulting.

Carlos J Roldan, MD, FAAEM, FACEP Associate Professor, Department of Emergency Medicine, University of Texas Health Science Center at Houston Medical School; Consulting Staff, Department of Emergency Medicine, Memorial Hermann Hospital Lyndon Baines General Hospital and MD Anderson Cancer Center

Carlos J Roldan, MD, FAAEM, FACEP is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Pain Society, American Society of Regional Anesthesia and Pain Medicine, International Association for the Study of Pain, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Colleen M Rivers, MD Senior Fellow in Medical Toxicology, New York City Poison Control Center, Bellevue Hospital Center

Colleen M Rivers, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Emergency Physicians, American College of Medical Toxicology, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

Asim Tarabar, MD Assistant Professor, Director, Medical Toxicology, Department of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital

Disclosure: Nothing to disclose.

Acknowledgements

Frederic J Baud, MD Director, Professor, Toxicological and Medical Intensive Care Unit, Hôpital Lariboisiere of Paris, France

Disclosure: Nothing to disclose.

John G Benitez, MD, MPH, FACMT, FAACT, FACPM, FAAEM, Associate Professor, Department of Medicine, Medical Toxicology, Vanderbilt University Medical Center; Managing Director, Tennessee Poison Center

John G Benitez, MD, MPH, FACMT, FAACT, FACPM, FAAEM, is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American College of Medical Toxicology, American College of Preventive Medicine, Society for Academic Emergency Medicine, Undersea and Hyperbaric Medical Society, and Wilderness Medical Society

Disclosure: Nothing to disclose.

Robert S Hoffman, MD, FAACT, FACMT Associate Professor, Departments of Emergency Medicine and Medicine, Clinical Pharmacology, New York University School of Medicine, Consulting Staff, Department of Emergency Services, Bellevue and New York University Hospital

Robert S Hoffman, MD, FAACT, FACMT is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Emergency Physicians, American College of Medical Toxicology, American College of Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

David C Lee, MD Research Director, Department of Emergency Medicine, Associate Professor, North Shore University Hospital and New York University Medical School

David C Lee, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Medical Toxicology, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Jorge A Martinez, MD, JD Clinical Professor, Department of Internal Medicine, Louisiana State University School of Medicine in New Orleans; Clinical Instructor, Department of Surgery, Tulane School of Medicine

Jorge A Martinez, MD, JD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Cardiology, American College of Emergency Physicians, American College of Physicians, and Louisiana State Medical Society

Disclosure: Nothing to disclose.

Heather Murphy-Lavoie, MD, FAAEM Assistant Professor, Assistant Residency Director, Emergency Medicine Residency, Associate Program Director, Hyperbaric Medicine Fellowship, Section of Emergency Medicine and Hyperbaric Medicine, Louisiana State University School of Medicine in New Orleans; Clinical Instructor, Department of Surgery, Tulane University School of Medicine

Heather Murphy-Lavoie, MD, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, Society for Academic Emergency Medicine, and Undersea and Hyperbaric Medical Society

Disclosure: Nothing to disclose.

Lewis S Nelson, MD, FACEP, FAACT, FACMT Professor, Department of Emergency Medicine, New York University School of Medicine; Attending Physician, Department of Emergency Medicine, Bellevue Hospital Center, New York University Medical Center

Lewis S Nelson, MD, FACEP, FAACT, FACMT is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Emergency Physicians, American College of Medical Toxicology, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Andre Pennardt, MD, FACEP, FAAEM, FAWM Clinical Associate Professor of Emergency Medicine, Georgia Health Sciences University; Assistant Professor of Military and Emergency Medicine, Uniformed Services University of the Health Sciences; Consulting Staff, Department of Emergency Medicine, Eisenhower Army Medical Center

Andre Pennardt, MD, FACEP, FAAEM, FAWM is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, Association of Military Surgeons of the US, International Society for Mountain Medicine, National Association of EMS Physicians, Special Operations Medical Association, and Wilderness Medical Society

Disclosure: Nothing to disclose.

Erik D Schraga, MD Staff Physician, Department of Emergency Medicine, Mills-Peninsula Emergency Medical Associates

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

John T VanDeVoort, PharmD Regional Director of Pharmacy, Sacred Heart & St. Joseph's Hospitals

John T VanDeVoort, PharmD is a member of the following medical societies: American Society of Health-System Pharmacists

Disclosure: Nothing to disclose.

Suzanne White, MD Medical Director, Regional Poison Control Center at Children's Hospital, Program Director of Medical Toxicology, Associate Professor, Departments of Emergency Medicine and Pediatrics, Wayne State University School of Medicine

Suzanne White, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Clinical Toxicology, American College of Epidemiology, American College of Medical Toxicology, American Medical Association, and Michigan State Medical Society

Disclosure: Nothing to disclose.

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