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For further information, see CMDT Part 40-31: Cyanide Poisoning
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Cyanide is rapidly absorbed by inhalation, skin absorption, ingestion
In gaseous form, hydrogen cyanide is an important component of fire smoke
Cyanide-generating glycosides also found in the pits of apricots and other related plants
Cyanide is generated by breakdown of nitroprusside; poisoning can result from rapid high-dose infusions
Also formed by metabolism of acetonitrile, found in some over-the-counter fingernail glue removers
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Onset of toxicity is nearly instantaneous after inhalation
"Bitter almond" odor may be detected on the victim's breath or in vomitus, although this is not a reliable finding
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Emergency and supportive measures
Remove the patient from exposure, taking care to avoid exposure to rescuers
Stop or slow the nitroprusside infusion rate for suspected cyanide toxicity
Activated charcoal
Due to low affinity for cyanide, the usual doses of 60–100 g are adequate to bind typically ingested lethal doses (100–200 mg)
Do not use for comatose or convulsing patients unless they are endotracheally intubated
In the United States, there are two antidote regimens (eTable 40–1)
Hydroxocobalamin
Nithiodote
Hydroxocobalamin
Preferred regimen; directly binds and detoxifies free cyanide
Adult dose: 5 g intravenously
Note: Causes red discoloration of skin and body fluids that may last several days and can interfere with some laboratory tests
Nithiodote
Contains
Sodium nitrite (to induce methemoglobinemia, which binds free cyanide)
Sodium thiosulfate (to promote conversion of cyanide to the less toxic thiocyanate)
Administer 3% sodium nitrite solution, 10 mL intravenously followed by 25% sodium thiosulfate solution, 50 mL intravenously (12.5 g)
Caution: Nitrites may induce hypotension and dangerous levels of methemoglobin
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