Friday, October 15, 2004

Clinical nabifestation

The clinical manifestation of acute cyanide poisoning varies in both time and intensity depending upon the magnitude of exposure3,4,10. Hydrocyanic acid is absorbed from any mucous surface and enters the system just as easily by way of the nose and throat as by the stomach10. Various non-specific signs and symptoms like headache, dizziness, nausea, vomiting, confusion, coma and incontinence of faeces and urine occur. Physiologically a series of events like dyspnoea, incoordination of movement, cardiac irregularities, convulsive seizures, coma and respiratory failure may occur leading to death. These signs are not specific for cyanide poisoning, which makes the distinction from other types of poisoning very difficulties without a history of exposure3,4.

On a military battlefield, casualties will be from exposure to cyanide gas; this can be fatal within minutes after exposure to high concentrations. An initial hypercapnea (15 sec after exposure), due to the effect of cyanide on the chemoreceptor bodies, is closely followed by a loss of consciousness (30 sec after exposure). This progress to apnea (3-5 min after exposure), cessation of cardiac activity (5-8 min after exposure), and death3.

After exposure to lower concentrations, or exposure to lethal amounts via the oral or percutaneous routes, the effects are slower to develop. Foe example, after ingestion of a lethal dose of a cyanide salt, the casualty might have 15 to 30 minutes of survival time during which an antidote could be administrated1,3,4,7,9.
Because the toxic effect of cyanide is to block tissue uptake and utilization of oxygen, the casualty is transiently flushed and may have other, related signs of poor tissue oxygen extraction. For example, funduscopic examination shows an equally bright red color for retinal arteries and veins because of venous blood is also responsible foe a “cherry-red” skin color, but this sign may not always be present3.

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