Clinical Overview

Cyanide has been recognized since antiquity as a poison that is present in bitter almonds, cassava and other foods. The purified gaseous form, hydrogen cyanide [HCN], was discovered in the 18th century. Currently several forms are used extensively in industry for tasks such as fumigation, electroplating and mining activities.

Cyanide gas exists as the vapor of preparations that are liquid at room temperature: examples are HCN and cyanogen chloride [CNCl, also known as CK]. Solid preparations are the cyanide salts formed with sodium, potassium or calcium.

Cyanide has been utilized in various forms to inflict intentional harm, and is considered a chemical weapon of concern for use by terrorists. Cyanide is relatively easy and cheap to generate. A terrorist event could occur using any form of cyanide, but solid preparations may be preferentially utilized. A large-scale terrorist event – such as contamination of municipal water supplies – is unlikely, due to the enormous amount of cyanide that would be required to achieve meaningful levels in a large body of water. Single or multiple local events are more likely. The current threat of cyanide use is both domestic and international, with caches being uncovered in raids in the United States and abroad.

Clinical Presentation

Note that this discussion focuses on acute cyanide toxicity. Exposure, diagnosis, treatment, and outcomes of chronic cyanide poisoning may be significantly different and will not be addressed here.

Cyanide inhibits mitochondrial cytochrome oxidase, which is necessary for oxidative respiration. Cells are unable to utilize oxygen; for this reason, cyanide has been described as an asphyxiating agent. The primary target organ in cyanide poisoning is the brain, but multiple systems are involved and there may be additional toxicity mechanisms that cause direct cardiovascular damage.

Cyanide toxicity depends on dose and route of exposure. Direct comparisons between lethality of inhaled, ingested and absorbed forms of cyanide are difficult, but any preparation of cyanide can be fatal. As discussed above, the route of exposure will depend upon the particular cyanide formulation. Clinical presentation will depend on route of exposure, but the hallmark of cyanide poisoning is shock and acidosis.

Inhalation (gas) Ingestion (solid, liquid, or aerosol liquid)

Skin: Gas, liquid, or solid

Eyes: Gas only

 Onset Rapid (seconds to minutes) Delayed (15-30 minutes) Delayed (15-30 minutes)
 Symptoms Headache; confusion; weakness; dyspnea; “metallic” taste Sore throat; burning sensation; nausea; vomiting; diarrhea; and symptoms of inhalation Redness; pain; and symptoms of inhalation
Signs Convulsions; coma; respiratory arrest; cardiac arrest Convulsions; coma; respiratory arrest; cardiac arrest Convulsions; coma; respiratory arrest; cardiac arrest

The common final pathway for cyanide intoxication is cellular hypoxia with acidosis, leading to nonspecific symptoms such as headache and delirium. Other signs can be described by system:

  • CNS: Dizziness, nausea, vomiting, drowsiness, tetany, trismus, hallucations
  • Cardiovascular: Arrhythmia, hypotension. Tachycardia and hypertension may occur transiently in early stages
  • Respiratory: Dyspnea, with initial hyperventilation followed by hypoventilation and pulmonary edema. Cyanosis is usually not apparent, since blood is adequately oxygenated – hypoxia occurs because cells are unable to utilize available oxygen.


Because cyanide toxicity following ingestion or absorption may be delayed and presents with nonspecific clinical signs, a physician must have a reasonable index of suspicion. Cyanide is renowned for its odor of almonds, apparent at the time of exposure and on the breath of intoxicated patients, but this has been found to be undetectable by up to 5% of women and nearly 20% of men in the general population. Nonetheless there may be significant clues in the case history, including apparent release of a gas, exposure to a powder or onset of illness immediately after a particular ingestion.

Laboratory diagnosis can confirm cyanide exposure. RBC cyanide levels of 0.5-1.0 mcg/mL indicate mild exposure; higher levels indicate more severe intoxication. Urine analysis for cyanide is also available. Note that there is frequently a baseline low level of cyanide due to normal environmental exposure.

Other laboratory test results, such as high anion gap metabolic acidosis, can support the diagnosis of cyanide toxicity but do not provide specific evidence. There may also be evidence of elevated arterial and venous pO2. In general, cyanide poisoning should be suspected in any patient with evidence of hypoxia without cyanosis. Cyanide poisoning should also be considered in any of the following conditions:

  • Sudden collapse of victim(s).
  • The presence of a resistant metabolic acidosis and or severe hypotension unresponsive to usual therapy in an individual with normal color or normal arterial pO2 should suggest the diagnosis.
  • Venous pO2>50 mm Hg.
  • Differential diagnosis must include carbon monoxide exposure since the treatment for cyanide may increase the severity of illness in cases of carbon monoxide intoxication.
  • Reports of dead insects, animals and unusual smells in an unusual location

The differential Diagnosis list for Cyanide might include any of the following:

Encephalitis, meningitis, headaches, GI symptoms, sedation, smoke inhalation, methemoglobinemia, hemlock poisoning, carbon monoxide toxicity, hydrogen sulfide toxicity, strychnine poisoning, ethanol toxicity and azide toxicity


Due to the rapid action of cyanide and relatively long time frame needed to analyze blood samples (several hours), empiric treatment is often necessary prior to laboratory diagnosis. Because the drugs used in cyanide treatment have potential adverse effects, clinical decision-making in the absence of lab data may be important. If possible, supportive treatment should be administered prior to diagnosis; the focus is maintaining cardiac output and the airway, including endotracheal intubation if necessary. Upon identifying cyanide toxicity, specific treatment should be immediately instituted.

  1. Activated charcoal: for alert, asymptomatic patients following ingestion
  2. Supplemental oxygen at 100%
  3. ACLS and shock protocols may be required for symptomatic patients
  4. Sodium nitrite: a methemoglobin forming agent. Methemoglobin competes with cytochrome oxidase for free cyanide and combines with cyanide to form cyanmethemoglobin
    1. Adults: 300mg IV over 5 minutes; slower if hypotension develops
    2. Children: 0.12 to 0.33 mg/kg IV infused as above in a child. The dose is dependent upon both weight and hemoglobin concentration ranging from 5.8 mg/kg (019 ml/kg) in a child with a hemoglobin of 7 to 11.6 mg/kg (0.39 ml/kg) in a child with a hemoglobin of 14.
    3. Adverse reactions: Hypotension associated with rapid infusion, tachycardia, syncope, cyanosis due to methemoglobin formation, headache, dizziness, nausea, vomiting. Frequency of events is not clearly defined.
  5. Amyl nitrite: a second line methemoglobin forming agent which is inhaled. Utilized only when other methemoglobin forming agents are not immediately available; only effective in a closed respiratory system and there is little systemic absorption
    1. Adults: 0.3mL ampule crushed every minute and inhaled for 15-30 seconds until sodium nitrite infusion is available
    2. Children: Inhale as in adults. Only used until adequate IV access can be achieved.
    3. Adverse reactions: Postural hypotension, tachycardia, palpitations, vasodilation, syncope, headache, dizziness, nausea, vomiting, hemolytic anemia, increased intraocular pressure, contact dermatitis. Frequency of events is not clearly defined.
  6. Sodium thiosulfate promotes rhodanase activity, which assists in conversion of cyanide into a less toxic form, thiocyanate. Used in combination with methemoglobin forming agents, sodium thiosulfate allows detoxification of cyanide as it is released from cyanmethemoglobin and also assists in direct detoxification of cyanide, although this occurs too slowly to be useful as a first-line application.
    1. Adults: 12.5g IV over 10-20 minutes following administration of sodium nitrite
    2. Children: 1.65 ml/kg IV in a child over 10-20 minutes
    3. Can repeat one-half of the original dose after 30 minutes if clinical response is inadequate
    4. Adverse reactions: Hypotension, CNS depression and coma due to thiocyanate intoxication, psychosis, confusion, weakness, tinnitus, contact dermatitis. Frequency of events is not clearly defined.
  7. Hydroxocobalamin: The FDA has not approved the use of Hydroxocobalamin in the United States.

Speed is critical: for survival, symptomatic patients must receive supportive care and specific antidotes immediately due to the rapid action of cyanide. Note that accurate laboratory diagnosis of cyanide exposure is not possible after administration of antidotes.

Exposed patients who have not exhibited symptoms within 4 to 6 hours can be safely discharged. Note that patients known to be exposed to cyanide gas are likely to remain asymptomatic if they have not exhibited symptoms within five minutes after removal from exposure, and they will not require treatment.


Gas exposure does not require decontamination or contact precaution. For patients with clothing or skin contaminated with liquid or solid cyanide, the treatment team is at risk for contact exposure or inhalation of gas produced by remaining cyanide compounds. Due to the rapid evaporation and dispersal of cyanide, however, substantial quantities must be present in order to pose a real risk.

Skin decontamination can be achieved using a rinse with dilute detergent. Contaminated clothing should be removed, preferentially by the patient if alert and asymptomatic, and placed in sealed bags.

Special thanks to Daniel Shodell, MD, MPH, Johns Hopkins General Preventive Medicine Resident, for his work on this information

Patient Handouts

What is cyanide?
Cyanide is a naturally occurring poison that can be concentrated in the form of a colorless gas, blue or clear liquid, or powdery white solid. Depending on the form of cyanide, the poison has many different names such as hydrogen cyanide (gas), hydrocyanic acid (liquid) or cyanide salts (solids). Any form of cyanide may have an odor of bitter almonds.

Where does cyanide come from?
Small amounts of cyanide occur naturally in some foods such as cherry laurel and cassava root. Larger concentrations of cyanide are generated for uses in industry such as gold mining, fumigation and electroplating.

How long does cyanide stay in the environment?
Cyanide gas disperses quickly (within minutes in open air). Liquid forms are more stable but may still evaporate quickly once exposed to the atmosphere. Solid forms are stable and will remain dangerous.

How might I be exposed to cyanide?
Cyanide can be inhaled, ingested or absorbed through the skin to cause cyanide poisoning. Accidental cyanide poisoning can occur in industrial accidents or by eating foods that naturally contain cyanide. Intentional use of cyanide for terrorism activities is another possible way you can be exposed to cyanide in any of its gas, liquid or solid forms.

What immediate health symptoms can be caused by cyanide?
Exposure to a significant dose of cyanide can cause headache, confusion, nausea, weakness and shortness of breath. Cyanide exposure may lead to convulsions, coma, and death. Additional symptoms depend on how you are exposed to cyanide, for instance a sore throat and a burning sensation can occur with ingestion of cyanide.

How soon do symptoms appear?
This depends on how you are exposed to cyanide. After inhaling cyanide gas or liquid vapor, symptoms start almost immediately, within seconds or minutes. Ingesting liquid or solid cyanide or absorbing cyanide through the skin will cause symptoms within 15 to 30 minutes

How do I know if I have been exposed to cyanide?
Diagnosis is usually based on signs and symptoms after cyanide exposure. There is also a blood test for cyanide. In addition, you may be aware of an industrial accident or intentional terrorist release.

Can cyanide poisoning be treated?
Yes. Rapid treatment with specific antidotes and general medical care can effectively counteract cyanide poisoning. It is critical to seek emergency room treatment immediately.

What are the long-term effects of cyanide poisoning?
Acute poisoning generally has no long-term effects. In severe cases, however, there may be residual damage to the heart or nervous system. Chronic poisoning – when a person has been exposed to low levels of cyanide over long periods of time, as occurs with certain industrial workers – may have additional effects.

Can cyanide poisoning be prevented?
Like any terrorist activity, the best prevention is to stop cyanide from being released. There is no pre-treatment that can protect against the effects of cyanide.

Where can I find more information?
Additional information may be obtained at Centers for Disease Control and Prevention

Trainings/Powerpoint Presentations

The Cyanide Presentation is available as a PowerPoint and a PDF.

Additional Resources

Essential Reading

Cummings, TF. The treatment of cyanide poisoning. Occupational Medicine. 2004; 54:82-85

Additional Readings

Centers for Disease Control and Prevention.  Recognition of illnesses associated with exposure to chemical agents – United States 2003. Morbidity and Mortality Weekly Report. 2003: 52(39);938-940

Centers for Disease Control and Prevention.  Biological and chemical terrorism: Strategic plan for preparedness and response. Morbidity and Mortality Weekly Report. 2000; 49(RR-4):1-14

Mokhlesi B, Leiken JB, Murray P, Corbridge TC.  Adult toxicology in critical care: Part II: Specific poisonings. Chest. 2003 Mar;123(3):897-922

Internet Resources

The National Institute for Occupational Safety and Health, Online NIOSH Pocket Guide to Chemical Hazards

Agency for Toxic Substances and Disease Registry Public Health Statement for Cyanide

Agency for Toxic Substances and Disease Registry Medical Management Guidelines for Hydrogen Cyanide

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