Cyanide poisoning occurs when cyanide, a highly toxic chemical, enters the body and disrupts the fundamental process by which cells use oxygen to produce energy. Cyanide works by inhibiting an essential enzyme called cytochrome c oxidase in the mitochondria, which blocks cellular respiration. This means that even though oxygen may be present in the blood, cells cannot use it to generate energy, leading to rapid cell death, especially in organs that require a lot of oxygen like the brain and heart.
There are several ways cyanide can enter the body and cause poisoning:
– **Inhalation of smoke during fires:** When materials such as plastics, wool, or synthetic fibers burn, they can release hydrogen cyanide gas. This is a common cause of cyanide poisoning in fire victims, alongside carbon monoxide poisoning. The inhaled cyanide gas quickly enters the bloodstream through the lungs and exerts its toxic effects[1].
– **Industrial exposure:** Cyanide is used in various industrial processes, including mining (especially gold mining), electroplating, and the manufacture of plastics and chemicals. Workers in these industries may be exposed to cyanide through inhalation, skin contact, or accidental ingestion if safety protocols are not followed properly[1].
– **Ingestion of cyanide-containing substances:** Certain plants, seeds, and foods naturally contain cyanogenic compounds that can release cyanide when metabolized. For example, bitter almonds, cassava, and some fruit pits contain these compounds. Improper preparation or accidental ingestion can lead to cyanide poisoning.
– **Chemical accidents or intentional poisoning:** Cyanide can be involved in chemical spills or used maliciously as a poison. It can be absorbed through the skin, inhaled, or ingested, depending on the form and exposure route.
Once cyanide enters the body, it binds to cytochrome c oxidase in the mitochondria, preventing cells from using oxygen to produce ATP, the energy currency of the cell. This forces cells into anaerobic metabolism, leading to the buildup of lactic acid and metabolic acidosis. The brain and heart, highly dependent on aerobic metabolism, are the first to suffer damage, causing symptoms such as headache, dizziness, confusion, shortness of breath, rapid heart rate, seizures, and potentially respiratory failure and death if untreated[1].
Cyanide poisoning also causes damage to various organs beyond the immediate cellular respiration block. For example, exposure to sodium cyanide has been shown to cause liver toxicity, with elevated liver enzymes indicating hepatocellular injury. This reflects the systemic impact cyanide can have on the body’s organs[2].
The severity of cyanide poisoning depends on the dose and route of exposure. The lethal dose of hydrogen cyanide gas is very low, less than 5 mg per kilogram of body weight, and acute poisoning can occur with doses as low as 0.5 to 3.5 mg per kilogram[1]. Blood lactate levels can be used to gauge the severity of poisoning, with higher levels indicating more severe toxicity.
Treatment for cyanide poisoning must be immediate and involves administering specific antidotes that neutralize cyanide. Common antidotes include hydroxocobalamin, which binds cyanide to form a non-toxic compound excreted in urine, and sodium thiosulfate, which helps convert cyanide to thiocyanate, a less toxic substance eliminated by the kidneys. Supportive care such as oxygen therapy is also critical to help maintain tissue oxygenation while the antidotes work[1].
Preventing cyanide poisoning involves careful handling and storage of cyanide-containing chemicals, using protective equipment in industrial settings, and following strict safety protocols. Awareness of the risk of cyanide release during fires is also important for emergency responders and healthcare providers.
In summary, cyanide poisoning is caused by exposure to cyanide compounds through inhalation, ingestion, or skin contact, leading to inhibition of cellular respiration and rapid cel
