Cyanide toxicity is generally considered a rare form of poisoning. However, cyanide exposure is relatively common in patients who have inhaled smoke from residential or industrial fires. In addition, intensive treatment with sodium nitroprusside or long-term intake of cyanide-containing foods can cause cyanide poisoning. Historically, cyanide has been used as a chemical weapon and can be a means of terrorist attacks. Cyanide can cause toxicity by inhalation, ingestion, percutaneous absorption, or parenteral administration, depending on its form. Clinical symptoms vary widely with dose and route of exposure, ranging from mild upper respiratory tract irritation to circulatory collapse and death within minutes. Cyanide poisoning is poisoning from exposure to various forms of cyanide. Early symptoms include headache, dizziness, rapid heart rate, shortness of breath, and vomiting. This phase is followed by seizures, slow heartbeat, hypotension, loss of consciousness, and cardiac arrest. Symptoms usually appear within minutes. Some survivors have long-term neurological problems. Toxic cyanide-containing compounds include hydrogen cyanide gas and various cyanide salts. Poisoning after inhaling smoke from a house fire is relatively common. Other potential routes of exposure include metal polishing workshops, certain pesticides, the drug sodium nitroprusside, and certain seeds such as apples and apricots. Liquid cyanide is absorbed through the skin. Cyanide ions interfere with cellular respiration, making oxygen unavailable to body tissues. Diagnosis is often difficult. Suspicion may occur after a house fire when unconsciousness, low blood pressure, or high lactate levels are present. Blood levels of cyanide can be measured, but it takes time. Levels between 0.5 and 1 mg/L are mild, 1 and 2 mg/L are moderate, 2 and 3 mg/L are severe, and levels above 3 mg/L are generally fatal. If exposure is suspected, the person should be removed from the source of exposure and decontaminated. Treatment includes supportive care and 100% oxygen delivery. Hydroxocobalamin (vitamin B12a) appears to be a useful antidote and is generally the first choice. Sodium thiosulfate can also be given. In the past, cyanide was used in mass suicides and Nazi genocide. Inhaling hydrocyanic acid can lead to coma with seizures, respiratory failure, cardiac arrest, and death within seconds. At low doses, loss of consciousness may be preceded by a perception of general weakness, dizziness, headache, dizziness, confusion, and dyspnea. In the early stages of unconsciousness, breathing is often adequate or even rapid, but the patient's condition progresses toward a deep coma, sometimes with pulmonary edema, and ultimately cardiac arrest. Dark cherry red skin color may be due to increased oxygen saturation of venous hemoglobin. Despite their similar names, cyanide does not directly cause cyanosis. The lethal dose for humans is as low as 1.5 mg/kg body weight. Other sources indicate that the lethal dose for vertebrates is 1-3 mg/kg body weight. Prolonged exposure to low levels of cyanide (e.g., after improper processing of cassava roots, a major food source in tropical Africa) can lead to elevated blood cyanide levels, leading to debility and permanent paralysis. can lead to a variety of symptoms such as Neuropathy, hypothyroidism, miscarriage. Other effects include mild liver and kidney damage.

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