Cyanide is a rare but potentially deadly poison. It works by making the body unable to use life-sustaining oxygen.
Common possible cause of poisoning is Fire. Smoke inhalation during the burning of common substances such as rubber, plastic, and silk can create cyanide fumes.
Cyanide compounds are used:
- as fumigant rodenticide
- in chemical industry
- used in photography, metallurgy, electroplating, metal cleaning, ore refining, in the synthetic rubber industry, artificial nail removers, and rodenticides
Mechanism of action of cyanide in the body
Cyanide inhibits mitochondrial cytochrome oxidase and hence blocks electron transport, resulting in decreased oxidative metabolism and oxygen utilization. Lactic acidosis occurs as a consequence of anaerobic metabolism. The oxygen metabolism at the cell level is grossly hampered.
Cyanide is rapidly absorbed from the stomach, lungs, mucosal surfaces, and unbroken skin.
Cyanide poisoning can be difficult to detect. The effects of cyanide ingestion are very similar to the effects of suffocation.
The lethal dose of potassium or sodium cyanide is 200 to 300 mg and of hydrocyanic acid is 50 mg. Effects begin within seconds of inhalation and within 30 min of ingestion.
Initial effects of poisoning – include headache, faintness, vertigo, excitement, anxiety, a burning sensation in the mouth and throat, breathing difficulty, increased heart rate, and hypertension. Nausea, vomiting, and sweating are common. A bitter almond odor may be detected on the breath.
Later effects – include coma, convulsions, paralysis, respiratory depression, pulmonary edema, arrhythmias, bradycardia, and hypotension.
Antidotal therapy: Amyl nitrite, sodium nitrite, and sodium thiosulfate (the Lilly cyanide antidote kit) with high-dose oxygen should be given as soon as possible.
The rationale for nitrite therapy is that the Nitrites cause formation of Methemoglobin by combining with the hemoglobin. Methemoglobin has a higher affinity for cyanide than does cytochrome oxidase and thus promotes its dissociation from this enzyme. Thiosulfate reacts with the cyanide as the latter is slowly released from cyanomethemoglobin, forming the relatively nontoxic thiocyanate, which is excreted in the urine.
Amyl nitrite is administered for 30 sec. of each minute. The ampule is broken between two pads of gauze and placed over the airway while the patient breathes spontaneously or is ventilated by a bag-mask unit. A new ampule should be used every 3 min.
Sodium nitrite is administered intravenously as a 3% solution at a rate of 2.5 to 5.0 mL/min up to a total dose of 10 to 15 mL (300 to 450 mg). Sodium thiosulfate is then administered intravenously as a 25% solution at a dose of 50 mL (12.5 g) given over 1 to 2 min.
High dose oxygen is also given.