Cyanide Poisoning Flashcards
Cyanide Patho
Binds with high affinity to ferric ion cytochrome a3 (electron transport chain) and therefore stops ATP production regardless of O2. Tissues with high oxygen demand are affected first
Sources of cyanide
Burning, fumigants and fertilizers, vermin exterminations, chemistry laboratories, some plant seeds (cassava, bamboo, apricots, cherries, plums, peaches) dartskies and vehicle exhause
Smokers, cyanide and excretion
2.5X higher in smokers
Detox is metabolism in liver by rhodanese to thiocyanate which is renally excreted
Low exposure symptoms (less than 50ppm)
Anxiety, palpitations, dyspnea and headache
Higher concentrations of cyanide symptoms
Severe dyspnea, coma, seizures, dysrhythmias.
Lethal dose of cyanide gas
200ppm for 30 minutes and 600-700 for 5.
Symptom onset is within minutes
K+ or Na+ cyanide 140-250mg, but as little as 50 can kill a person
Typical cyanide presentation
Altered LOC, hyperventilating, hypotensive, bradycardic and a smell of bitter almonds (only 60-80% can detect)
Delayed cyanide poisoning
Acetronitrile (cosmetic nail remover) and amygdalin from apricot pits slowly release cyanide (delayed onset of symptoms?)
Lab results cyanide poisoning
Elevated anion gap - lactic acidosis from anaerobic metabolism
Metabolic acidosis
Lactate <90mg/dL
Normal O2 sats
Decreased arterial mixed venous oxygen difference - decreased tissue O2 consumption
Whole blood cyanide >0.5mcg/mL Fatal at >2.5 (plasma is 1/10th of whole blood)
TX for cyanide
100% O2
fluid/vasopressors hypotension
Bicarb for acidosis (enhances nitrites and thiosulfate)
Amyl nitrite, 3% sodium nitrite, and 25% sodium thiosulfate
Consult with expert for these
Nitrites physiology
Create methemoglobin, which bind cyanide better than ferric iron of cytochrome oxidase.
Hypotension may occur but is not a contraindication
Pts who also have CO poisoning may suffer as methemoglobin means less hemoglobin for O2 to bind to
Methemglobin
Iron is Fe3+ instead of normal Fe2+ of hemoglobin
Sodium Thiosulfate
Enhances rhodanese which catalyzes transfer of sulfate from sodium thiosulfate to cyanide to form thiocyanate (less toxic, excreted by kidneys)
CAN be used if pts have CO poisoning
Hydroxocobalamin
Cobolt center that binds cyanide and forms cyanocobalamin
Good for when its unknown if it is cyanide, or if theres also CO on board.
Dose is 5G IV over 15 minutes and a second dose of 5g may be repeated.
Hydroxocobalamin sides
transient HTN, reddish discolouration of skin and mucous membranes, rarely anaphylatic reactions
Dimethylaminophenol
Rapidly induces methemglobin. Similar efficiency to sodium nitrite. 250mg IV over 1 minute used with sodium thiosulfate
Dicobalt edetate
Cobalt compound with high affinity for cyanide. Toxic when cyanide is not present.
300mg IV over 1 minute, repeat after 5 minutes
Cobinamide
Precursor to cobalamine, highly effective. Can be given IM
Gastic decontamination
For pts who are alert, have a patent airway, and present within 1 hour of ingestion
What is cyanide
Any chemical compound that contains a cyano group
Where is cyanide found
Acrylic fibers, synthetic rubber and plastics, mining gold and plata, pigment in blueprints and blue jeans. Burning unleashes their cyanidy fury!
Burning these produces cyanide
Wool, nylon, silk, acrylic, polyurethane, other plastics. Suspect cyanide in any pt exposed to combustion
Hydroxocobalamin dosing
5G
SIVP for seizures or arrest
over 15 minutes if not
Second dose OLMC 15 minutes - 2 hours
May interefere with pulse ox and CO ox readings
Don’t mix with other meds (use second line if you can)
