Cyanide exists in gas, liquid, and solid forms. Hydrogen cyanide (HCN) is a highly volatile liquid, while cyanide salts vary in water solubility depending on the metal involved. Some compounds, known as cyanogens—including cyanogen chloride, bromide, nitriles, and sodium nitroprusside—can release cyanide during metabolism, posing health risks, especially in high doses or prolonged exposure. 

Industrially, nitriles are widely used and can release toxic HCN during combustion or absorption. Burning various substances, including certain foods like cassava and apricot seeds, can also result in cyanide exposure, potentially causing poisoning. 

In warfare, cyanide compounds like HCN (NATO: AC) and cyanogen chloride (NATO: CK) have been used as chemical weapons due to their high toxicity in enclosed spaces. Though initially ineffective in World War I, cyanogen chloride later became a more potent agent. Historical uses include attacks by Japan and Iraq in the 20th century. 

Cyanide is believed to significantly contribute to the 5,000–10,000 annual deaths from smoke inhalation in the U.S. Suicidal cyanide poisoning is uncommon and often underreported; in 2021, only 15 of 163 cyanide poisoning cases reported to U.S. poison centers were due to intentional ingestion. Fatal cyanide overdose can be mistaken for sudden cardiac events like heart attacks or arrhythmias. 

In the UK, from 2008 to 2019, there were 1,253 suspected cyanide poisoning cases reported, with 239 involving children under 10. The leading causes were plant ingestion (35%) and smoke inhalation (32%), with the most severe or fatal outcomes primarily linked to smoke inhalation (71%). 

Cyanide-related suicides and occupational exposures are more common in males. Similarly, Leber optic atrophy, associated with cyanide, shows a male predominance in European research. While intentional cyanide ingestion mainly occurs in adults, smoke-related and chronic cyanide exposures can affect individuals of all ages. 

Cyanide can enter the body through inhalation, ingestion, or absorption via the skin or eyes. Once absorbed, it spreads quickly and disrupts cellular respiration by inhibiting cytochrome oxidase, leading to a shift to anaerobic metabolism and lactic acid buildup. The brain and heart are most affected due to their high oxygen needs. 

Hydrogen cyanide (HCN) can be fatal within minutes at high concentrations, with a lethal dose as low as 50 mg orally. Cyanide salts and skin exposure also pose serious risks. Cyanogen chloride, used in industry, can cause severe eye and lung irritation and is rapidly lethal in enclosed spaces. 

A deficiency in the enzyme rhodanese, which helps detoxify cyanide, is linked to vision loss in Leber optic atrophy. Cyanide exposure is also associated with vision problems from long-term smoking. 

Cyanide poisoning commonly arises from smoke inhalation, intentional ingestion, and industrial exposure, with rare cases from medical treatments or consumption of cyanide-containing foods. 

Smoke Inhalation: The most frequent cause in the U.S. is inhalation during house or industrial fires, especially in enclosed spaces. Signs like soot in the mouth/nose, low blood pressure, and altered mental state may suggest toxic cyanide levels (>40 µmol/L). Materials such as wool, silk, plastic, polyurethane foam, and other synthetic products release hydrogen cyanide (HCN) when burned. 

Intentional Poisoning: Suicidal cyanide ingestion, although uncommon, usually occurs among healthcare or lab personnel with access to cyanide salts. Large-scale food contamination is a possible method for terrorist attacks, often resulting in unresponsive patients by the time of hospital presentation. 

Industrial Exposure: Cyanide is extensively used in mining, metalworking, electroplating, photography, agriculture, and plastics manufacturing. Accidental release of cyanogen chloride or exposure to cyanide salts mixed with acids can lead to mass casualties due to the release of HCN gas. 

Medical (Iatrogenic) Exposure: Sodium nitroprusside, used to manage blood pressure, can produce cyanide as a byproduct. Toxicity may occur with prolonged or high-dose use, particularly in patients with low thiosulfate reserves. Symptoms can resemble ICU-related delirium but may be mitigated by using hydroxocobalamin or sodium thiosulfate alongside treatment. 

Ingestion of Cyanogenic Compounds: Rare cases arise from ingesting cyanide-rich supplements like amygdalin (laetrile), falsely marketed as “vitamin B17.” Found in fruit pits (apricots, papayas), raw nuts, and certain plants (lima beans, sorghum), amygdalin can release HCN and cause poisoning when consumed in large amounts. 

The prognosis of cyanide poisoning depends on exposure level and treatment speed. Mild cases usually recover without antidotes, while moderate cases can recover well with rapid medical intervention. Suicidal cases often involve higher doses and have poorer outcomes. 

Low-level cyanogen exposures typically resolve once the individual is removed from the source. However, if symptoms like seizures or apnea occur, quick treatment is crucial. Cardiac arrest due to cyanide toxicity generally results in poor prognosis, even with fast intervention. 

In 2021, 4 of 163 cyanide exposure cases reported to poison control were fatal. Cyanide can kill rapidly, especially via inhalation or injection. Survivors may experience lasting neurological damage, including cognitive or movement disorders. 

Fire-related deaths often involve simultaneous carbon monoxide and cyanide inhalation, which together impair oxygen use in the body. No antidote currently exists for this dual exposure. 

Age Group:   

All age groups can be affected, but: 

Adults: More commonly affected due to occupational, intentional (suicidal), or iatrogenic exposure. 

Children: May be involved in accidental household exposures or smoke inhalation during fires. 

Physical signs of cyanide poisoning are often nonspecific but can present suddenly and severely. Vital signs may fluctuate—initially showing bradycardia and hypertension, followed by hypotension with reflex tachycardia, and eventually bradycardia with hypotension again. Cardiac arrhythmias and arrest may occur. Respiratory changes can progress from early tachypnea to bradypnea and apnea. Despite impaired oxygen use at the cellular level, pulse oximetry may falsely appear normal, and the skin may appear cherry red due to high venous oxygen levels. Other signs include soot in the mouth or nose (after smoke inhalation), a bitter almond odor on the breath (detectable by only 40% of people), normal or dilated pupils, and sweating. 

Neurologically, patients may display confusion, ataxia, dilated pupils, seizures, or coma. 

Cyanide poisoning can present with varying acuity depending on the type and route of exposure. Inhalation of hydrogen cyanide gas or cyanogen chloride leads to a highly acute presentation, with symptoms developing within seconds to minutes. Individuals may initially experience transient hyperpnea and hypertension within 15 seconds, followed by convulsions within 30–45 seconds, loss of consciousness around 30 seconds, respiratory arrest within 3–5 minutes, and cardiac arrest by 5–8 minutes post-exposure. In cases of cyanide salt ingestion or liquid exposure, the onset is moderately acute, typically occurring within minutes. Affected individuals may present with symptoms such as anxiety, vertigo, dyspnea, nausea, headache, and muscle trembling.  

Suicidal Intent: Common in adults with a history of depression or mental health disorders. 

Intensive Care Patients: At risk of iatrogenic toxicity from sodium nitroprusside, especially those with low thiosulfate reserves (e.g., malnourished or postoperative patients). 

Fire Victims: Often exposed during house or industrial fires due to combustion of synthetic materials. 

Industrial Workers: Exposure in industries like metal refining, electroplating, dyeing, or chemical manufacturing. 

Chemical Accidents or Terrorism: Cyanide or cyanogen chloride may be used as chemical warfare agents. 

Emergency Medicine

Non-pharmacological approaches for treating cyanide toxicity focus on supportive care and safety measures. Immediate actions include optimizing oxygenation with high-flow oxygen and airway management to ensure effective oxygen delivery, particularly in cases of respiratory distress or failure. Continuous cardiac monitoring is essential to track any dysrhythmias, and vital signs should be closely monitored. In the event of acute symptoms, endotracheal intubation may be required for severe cases. Early decontamination is critical for patients with oral or dermal exposure, including removing contaminated clothing and flushing the skin with soap and water. If cyanide poisoning is suspected from smoke inhalation, emergency personnel should use appropriate personal protective equipment to avoid exposure. 

Supportive care also includes fluid resuscitation and maintaining hemodynamic stability through the use of crystalloids and vasopressors as necessary. It’s crucial to provide observation and follow-up care, especially for patients exposed to cyanide compounds with delayed symptom onset, such as nitriles. For pregnant women, immediate maternal stabilization is paramount, and fetal evaluation may be necessary following treatment. 

Overall, although antidotes like hydroxocobalamin and sodium thiosulfate are commonly used in treatment, these non-pharmacological interventions play a critical role in the management of cyanide toxicity, ensuring patient stability and preventing further complications. 

Emergency Medicine

Hydroxocobalamin (Cyanokit): Hydroxocobalamin binds to cyanide more effectively than cytochrome oxidase, forming nontoxic cyanocobalamin (vitamin B12), which is then excreted in urine. It is generally well tolerated, including in critically ill patients, and does not affect the oxygen-carrying capacity of hemoglobin, making it safe for those with carbon monoxide poisoning. It can be used in combination with sodium thiosulfate for acute cyanide toxicity treatment. However, its disadvantages include the need for a large dose to be effective and its availability in very dilute forms in the U.S. Adverse effects may include transient hypertension, allergic reactions (rarely including anaphylaxis and angioedema), and a reddish discoloration of urine and body fluids. 

Sodium Thiosulfate & Sodium Nitrite (Nithiodote): Sodium nitrite induces methemoglobin formation and vasodilation, while sodium thiosulfate works more slowly by donating sulfur to detoxify cyanide into thiocyanate. Sodium thiosulfate can be used alone in cases of carbon monoxide poisoning when sodium nitrite is contraindicated, or together with hydroxocobalamin for severe cases. The dosage is based on the patient’s hemoglobin levels, with adjustments needed for anemia. If symptoms persist, a second dose may be administered after one hour. 

Amyl Nitrite: Amyl nitrite reacts with hemoglobin to form methemoglobin, which binds with cyanide to form cyanomethemoglobin. It can be inhaled by a spontaneously breathing patient or administered via a bag-valve-mask to an apneic patient as an interim measure until intravenous access is established. The effect lasts about three minutes, and it should be administered in intervals to allow the patient to oxygenate. Rescuers should maintain a safe distance due to the compound’s volatile nature. 

Activated Charcoal (Actidose-Aqua, EZ-Char, Kerr Insta-Char): Though activated charcoal is not very effective in binding cyanide (1g adsorbs only 35mg), it is still used for oral cyanide poisoning. A dose of 1g/kg can bind a potentially lethal dose of cyanide with a low-risk profile, making it useful for oral exposure, especially when administered quickly. 

Sodium Bicarbonate (Neut): Sodium bicarbonate may be needed in large doses for alkalization, particularly to address metabolic acidosis associated with cyanide poisoning. 

Emergency Medicine

Lorazepam (Ativan): Lorazepam is the preferred medication for managing cyanide-induced seizures. It is a sedative hypnotic that acts quickly and has a relatively long half-life. It enhances the action of GABA, an inhibitory neurotransmitter in the brain, which helps depress central nervous system activity, including areas involved in emotions and arousal. 

Pentobarbital (Nembutal): Pentobarbital is a short-acting barbiturate with sedative, hypnotic, and anticonvulsant effects. It works by disrupting the transmission of signals from the thalamus to the cortex. It is used as a second-line treatment for drug-induced seizures. 

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Emergency Medicine

pinephrine (EpiPen, EpiPen Jr, Adrenaclick, Auvi-Q, Adrenalin): Epinephrine is the first-line treatment for anaphylactoid reactions. It works by increasing peripheral vascular resistance and reversing vasodilation, helping to treat systemic hypotension and vascular permeability. Its beta-agonist effects include bronchodilation, increased heart rate, and enhanced heart contractility. 

Emergency Medicine

Airway Management: Intubation may be required for patients with compromised breathing or severe symptoms to ensure proper oxygen delivery. 

Mechanical Ventilation: For patients with respiratory distress or failure, mechanical ventilation supports adequate oxygenation and carbon dioxide removal. 

Decontamination: If cyanide was ingested, removing contaminated clothing and flushing the skin can prevent further absorption of the toxin. 

Continuous Cardiac Monitoring: Continuous ECG monitoring helps detect arrhythmias and ensures cardiovascular stability. 

Emergency Medicine

The management of cyanide toxicity involves distinct phases: 

Pre-hospital Phase: Immediate actions include securing the airway, providing high-flow oxygen, and removing the patient from the cyanide source. If possible, antidotes such as hydroxocobalamin or sodium thiosulfate should be administered. 

Hospital Phase: Upon arrival, further stabilization occurs through airway management, mechanical ventilation if necessary, and intravenous administration of antidotes. Continuous cardiac monitoring and hemodynamic support are critical, and decontamination is performed if cyanide is ingested. 

Post-acute Phase: Following stabilization, patients are closely monitored for complications like delayed neurological effects or pulmonary edema. Continuous care and follow-up evaluations ensure recovery and address any long-term issues.