Medication Summary
Provide oxygen as the initial agent in suspected or confirmed cyanide poisoning. Administer sodium bicarbonate in severe poisoning because of marked lactic acidosis. Decontaminate as appropriate. Upon consideration of cyanide toxicity diagnosis, immediately administer antidotal therapy based on clinical criteria, even if laboratory confirmation of cyanide poisoning has not been received. Administer anticonvulsants as indicated.
A review by Hall et al notes that hydroxocobalamin (Cyanokit) has not been associated with clinically significant toxicity in antidotal doses compared with other cyanide antidotes. Hydroxocobalamin has a rapid onset of action, neutralizes cyanide without interfering with cellular oxygen use, is conducive to prehospital use due it its tolerability and safety profiles, and is safe for use in patients with smoke inhalation.[12]
Cyanide Antidotes
Class Summary
Cyanide is a cellular toxin that binds to cytochrome oxidase, inhibiting cellular respiration. Administer antidotes to accelerate reversal of this activity.
Sodium nitrite and sodium thiosulfate (Nithiodote)
Sodium nitrite is the drug of choice in the United States. It induces methemoglobin formation and vasodilation.
Sodium thiosulfate is a second-line therapy because of its slower mechanism of action. It regenerates sulfur-dependent rhodanese activity. Coadminister sodium thiosulfate with or after sodium nitrite or hydroxocobalamin (Cyanokit). It is a useful adjunct in prolonged (cyanogen) poisonings.
Hydroxocobalamin (Vitamin B12, Cyanokit)
Hydroxocobalamin contains cobalt ion, which is able to bind to cyanide with greater affinity than cytochrome oxidase to form cyanocobalamin (nontoxic), which is excreted in urine. Hydroxocobalamin has few adverse effects, is tolerated by critically ill patients, and is well tolerated by patients with concomitant carbon monoxide poisoning (no effect on the oxygen carrying capacity of hemoglobin). In France, it commonly is used in combination with sodium thiosulfate. Low-dose hydroxocobalamin in combination with sodium thiosulfate has been used successfully to prevent cyanide toxicity due to prolonged sodium nitroprusside infusions.
Amyl nitrite
Amyl nitrite is an alternative temporizing therapy; it may be useful in the absence of IV access (eg, in industrial settings).
Anticonvulsants, Other
Class Summary
Repeated or prolonged, generalized seizures (status epilepticus) indicate anticonvulsant therapy.
Lorazepam (Ativan)
Lorazepam is the drug of choice. It is a sedative hypnotic with a short onset of effects and a relatively long half-life. By increasing the action of gamma-aminobutyric acid (GABA), a major inhibitory neurotransmitter in the brain, lorazepam may depress all levels of the central nervous system, including the limbic and reticular formation.
The drug is an excellent choice when the patient needs to be sedated for longer than 24 hours. It is commonly used prophylactically to prevent delirium tremens.
Midazolam
Midazolam is used as an alternative drug for the termination of refractory status epilepticus. Because it is water soluble, this agent takes approximately 3 times longer than diazepam to peak electroencephalogram (EEG) effects. Therefore, the clinician must wait 2-3 minutes to fully evaluate midazolam's sedative effects before initiating a procedure or repeating the dose. Midazolam has twice the affinity for benzodiazepine receptors that diazepam has. It may be administered intramuscularly if IV access cannot be obtained.
Phenobarbital sodium
Phenobarbital sodium is a second-line drug, after benzodiazepines. It interferes with the transmission of impulses from the thalamus to the brain's cortex. Phenobarbital sodium is used as a sedative.
Alpha/Beta Adrenergic Agonists
Class Summary
These agents augment coronary and cerebral blood flow during the low-flow states associated with cyanide poisoning.
Epinephrine (Adrenalin, EpiPen)
Epinephrine is the drug of choice for treating anaphylactoid reactions. It has alpha-agonist effects that include increased peripheral vascular resistance, reversed peripheral vasodilatation, systemic hypotension, and vascular permeability. Its beta-agonist effects include bronchodilatation, chronotropic cardiac activity, and positive inotropic effects.
Alkalinizing Agents
Class Summary
These agents are used in severe poisoning, which causes marked lactic acidosis.
Sodium bicarbonate (Neut)
Sodium bicarbonate may be required in large doses for alkalization.
Akyildiz BN, Kurtoglu S, Kondolot M, Tunc A. Cyanide poisoning caused by ingestion of apricot seeds. Ann Trop Paediatr. 2010;30(1):39-43. [Medline].
National Cancer Institute. Cancer topics: Laetrile/Amygdalin. 11/21/2005;[Full Text].
Bronstein AC, Spyker DA, Cantilena LR Jr, Green JL, Rumack BH, Heard SE. 2007 Annual Report of the American Association of Poison Control Centers' National Poison Data System (NPDS): 25th Annual Report. Clin Toxicol (Phila). Dec 2008;46(10):927-1057. [Medline]. [Full Text].
Bronstein AC, Spyker DA, Cantilena LR Jr, Green JL, Rumack BH, Giffin SL. 2008 Annual Report of the American Association of Poison Control Centers' National Poison Data System (NPDS): 26th Annual Report. Clin Toxicol (Phila). Dec 2009;47(10):911-1084. [Medline].
Lee J, Mukai D, Kreuter K, et al. Potential interference by hydroxocobalamin on co-oximetry hemoglobin measurements during cyanide and smoke inhalation treatments. Ann Emerg Med. 2007;49(6):802-805. [Medline].
Fortin JL, Desmettre T, Manzon C, Judic-Peureux V, Peugeot-Mortier C, Giocanti JP, et al. Cyanide poisoning and cardiac disorders: 161 cases. J Emerg Med. May 2010;38(4):467-76. [Medline].
Borron SW, Baud FJ, Mégarbane B, Bismuth C. Hydroxocobalamin for severe acute cyanide poisoning by ingestion or inhalation. Am J Emerg Med. Jun 2007;25(5):551-8. [Medline].
Borron SW, Baud FJ, Barriot P, Imbert M, Bismuth C. Prospective study of hydroxocobalamin for acute cyanide poisoning in smoke inhalation. Ann Emerg Med. Jun 2007;49(6):794-801, 801.e1-2. [Medline].
Bebarta VS, Tanen DA, Lairet J, Dixon PS, Valtier S, Bush A. Hydroxocobalamin and sodium thiosulfate versus sodium nitrite and sodium thiosulfate in the treatment of acute cyanide toxicity in a swine (Sus scrofa) model. Ann Emerg Med. 2010;55(4):345-51. [Medline].
Curry SC, Connor DA, Raschke RA. Effect of the cyanide antidote hydroxocobalamin on commonly ordered serum chemistry studies. Ann Emerg Med. Jul 1994;24(1):65-7. [Medline].
Sutter M, Tereshchenko N, Rafii R, Daubert GP. Hemodialysis Complications of Hydroxocobalamin: A Case Report. J Med Toxicol. Mar 30 2010;[Medline].
Hall AH, Saiers J, Baud F. Which cyanide antidote?. Crit Rev Toxicol. 2009;39(7):541-52. [Medline].
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