Cyanide poisoning Flashcards
How does cyanide produce toxicity?
CN group - mitochondrial toxin
Binds to Fe3+ on cytochrome oxidase 3a - INHIBITS OXIDATIVE PHOSPHORYLATION ( no aerobic metabolism)
What are potential sources of cyanide? (5)
Industrial: electroplating, photography, jewelery plating, ore extraction, metal refinery, fertilizer
Fires: combustion of materials ie. wool, silk, polyurethane, polyacrylonitrites, synthetic rubber
Medical: sodium nitroprusside
Diet: fruit pits (apricot, cherry, bitter almond, peach)
What are 5 scenarios where you must consider cyanide toxicity?
house fire (think unexplained acidosis, coma)
vehicle fire
sudden collapse of laboratory or industrial worker
ingestion of artificial nail remover
nitroprusside drips
What are 4 potential route of cyanide toxicity?
inhalational
dermal
ingestion
parenteral
What are the clinical manifestations of cyanide toxicity?
CNS – Headache, anxiety, confusion, vertigo, coma, seizures
CVS – Initial tachycardia and hypertension, then bradycardia and hypotension, atrioventricular block, ventricular dysrhythmias
RESP – Initial tachypnea then bradypnea, pulmonary edema
GI – Vomiting, abdominal pain
SKIN – Flushing (cherry-red color), cyanosis (late finding), irritant dermatitis (itching, erythema, edema, vesicles resulting from skin exposure)
RENAL – Renal failure
HEPATIC– Hepatic necrosis
OTHER – Rhabdomyolysis, bright red venules seen on funduscopy
What does blood look like in a CN poisoned patient
Arterial and venous blood is the same color - due to tissue’s inability to utilize oxygen
What are important investigations in CN poisoning?
No single confirmatory test
CN levels will not return in acute setting
ABG - rule out CO poisoning, see acute lactic acidosis
ScVO2 >90%
What are 3 management priorities in CN toxicity
- Physiologic support (100% O2, fluids, pressors)
- Decontamination (clothes, skin, GI)
- Antidotes
A - Induce methemoglobinemia with Lilly Kit = amyl nitrate, sodium nitrite, sodium thiosulfate
B - hydroxycolbalamin
What is the antidote of choice in fire victims with CN toxicity
Hydroxycolbalamin
avoid inducing methemoglobinemia in CO poisoning, already shifts oxyhemoglobin dissociation curve to the left, would exacerbate poor O2 offloading
What are other differential considerations in a patient who collapses suddenly after exposure to gas?
carbon monoxide hydrogen sulfide phosphine arsine methane
What is the dosing of hydroxycolbalamin?
Hydroxocobalamin 70 mg/kg up to 5 g IV (5 g is standard adult dose) Sodium thiosulfate (25 percent): 1.65 mL/kg up to 50 mL IV, may repeat once (maximum dose 12.5 g)
How does hydroxycolbalamin work as an antidote?
Precursor of Vit B12
Colbalt molecule inside
Binds with cyanide to form cyanocolbalamin (stable, benign compound excreted in urine)
higher affinity for cyanide than cytochrome oxidase
How does the Lilly kit work?
- Induces methemoglobinemia with amyl nitrite and sodium nitrite
Cyanide binds preferentially to methemoglobin over cytochrome oxidase (forms cyanomethemoglobin less toxic) - Sodium thiosulfate gives sulfur ions needed for rhonadase enzyme conversion in the rate limiting step
Forms thiocyanide, excreted in urine
Dosing of the Lilly kit?
Amyl nitrite (AN):
- Crush glass pearls under nose or put in ambu bad or face
mask, only use when IV access is delayed (sodium nitrite is
preferred)
Sodium Nitrite (SN):
- 10 ml of 3% solution over 2-4 min
- Monitor BP and treat hypotension by slowing infusion, giving crystalloids and vasopressors
- Check MetHb level after 30 min (goal is 20-30%)
Sodium Thiosulfate (STS): 50 mL of a 25 percent solution, or 12.5 g
Why is hydroxycolbalamin preferred in pediatric patients?
Younger patients have an oxyhemoglobin dissociation curve shifted to the left - any further shift left (with methemoglobinemia) can be disastrous
