Cyanide Toxicity Treatment & Management

  • Author: Inna Leybell, MD; Chief Editor: Asim Tarabar, MD   more...
 
Updated: Nov 1, 2011
 

Approach Considerations

Administer hydroxocobalamin (Cyanokit) or the Cyanide Antidote Kit if a diagnosis of cyanide toxicity is strongly suspected, without waiting for laboratory confirmation.

Hydroxocobalamin, routinely used in Europe, has been approved by the US Food and Drug Administration (FDA) for treating known or suspected cyanide poisoning. Hydroxocobalamin combines with cyanide to form cyanocobalamin (vitamin B-12), which is renally cleared.[7, 8]

The Cyanide Antidote Kit contains amyl nitrite pearls, sodium nitrite, and sodium thiosulfate. Amyl and sodium nitrites induce methemoglobin in red blood cells, which combines with cyanide, thus releasing cytochrome oxidase enzyme. Inhaling crushed amyl nitrite pearls is a temporizing measure before IV administration of sodium nitrite.

Sodium thiosulfate enhances the conversion of cyanide to thiocyanate , which is renally excreted. Thiosulfate has a somewhat delayed effect and thus is typically used with sodium nitrite for faster antidote action.

Special concerns in pregnancy

Fetal demise is possible in cyanide poisoning. Aggressive support and antidotal treatment of the mother is paramount. An obstetric evaluation following stabilization of the mother is essential. Therapeutic abortion may be indicated in the presence of fetal demise.

Transfer

Avoid transfer of patients with acute cyanide toxicity. However, transfer the patient if antidotes and intensive care are unavailable and if rapid, appropriate medical transport can be assured.

Provide medical stabilization (eg, airway, hemodynamic parameters) before transfer. Ideally, transfer patients to a regional toxicology treatment center.

Consultations

Consult a medical toxicologist for confirmation of the diagnosis, for recommendations regarding the most effective available antidotal therapy, and for insight as to potential sources of poisoning (eg, industrial) that may place others at risk.

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Prehospital Care

Certain cyanide compounds can be absorbed dermally; gloves and other forms of skin protection should be worn.

Aggressive airway management with delivery of 100% oxygen can be lifesaving. (Although theoretically useless, supportive care with administration of oxygen alone has proven effective in a number of poisonings.) It can also treat concomitant carbon monoxide exposure pending the levels.

Prehospital treatment also includes the following:

  • Intubation - Intubate the patient if he or she is unconscious or the airway cannot be protected
  • Monitoring and fluids - Institute cardiac monitoring and an intravenous line; administer fluids and vasopressors for hypotension
  • Sodium bicarbonate - Administer sodium bicarbonate if the patient is unconscious or hemodynamically unstable and acidotic (elevated lactate levels)
  • Antidotes - Administer cyanide antidotes in the prehospital setting if the diagnosis is relatively certain; such treatment generally should involve online medical control
  • Anticonvulsants - These may be needed for generalized seizures
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Emergency Department Care

Initial emergency department care for patients with cyanide exposure is identical to that provided in the prehospital phase.

Provide supportive care, including the following:

  • Airway control, ventilation, 100% oxygen delivery
  • Crystalloids and vasopressors, as needed, for hypotension
  • Sodium bicarbonate titrated according to arterial blood gas (ABG) and serum bicarbonate level

Decontaminate the patient with removal of clothing/skin flushing and/or activated charcoal (1g/kg), as appropriate. Activated charcoal should be given after oral exposure in alert patients who are able to protect the airway or after endotracheal intubation in unconscious patients. Remember to protect the health-care provider from potential contamination.

Administer hydroxocobalamin (Cyanokit) or the Cyanide Antidote Kit if the diagnosis is strongly suspected, without waiting for laboratory confirmation.

Cyanokit

Hydroxocobalamin (Cyanokit), routinely used in Europe, has been approved by the US Food and Drug Administration (FDA) for treating known or suspected cyanide poisoning.[7, 8]

Hydroxocobalamin combines with cyanide to form cyanocobalamin (vitamin B-12), which is renally cleared. Hydroxocobalamin administration resulted in faster improvement in mean arterial pressure but similar mortality and serum acidosis, as compared with sodium nitrite, in animals.[9]

Coadministration of sodium thiosulfate (through a separate line or sequentially) has been suggested to have a synergic effect on detoxification.

Adverse effects of hydroxocobalamin administration include transient hypertension (a benefit in hypotensive patients), reddish brown skin, mucous membrane and urine discoloration, and rare anaphylaxis and anaphylactoid reactions. It also interferes with co-oximetry (about a 5% increase in carboxyhemoglobin levels) and blood chemistry testing (bilirubin, creatinine kinase and possibly liver enzymes, creatinine, phosphorus, glucose, magnesium, and iron levels) due to its bright red color.[10] It can also interfere with hemodialysis.[11]

Certain medications should not be administered simultaneously or through the same line as hydroxocobalamin, including diazepam, dopamine, dobutamine, and sodium thiosulfate.

Cyanide Antidote Kit

The Cyanide Antidote Kit contains amyl nitrite pearls, sodium nitrite, and sodium thiosulfate. Amyl and sodium nitrites induce methemoglobin in red blood cells, which combines with cyanide, thus releasing cytochrome oxidase enzyme. Inhaling crushed amyl nitrite pearls is a temporizing measure before IV administration of sodium nitrite.

Sodium thiosulfate enhances the conversion of cyanide to thiocyanate, which is renally excreted. Thiosulfate has a somewhat delayed effect and thus is typically used with sodium nitrite for faster antidote action.

Avoid the sodium nitrite portion of the cyanide kit in patients with smoke inhalation unless carboxyhemoglobin concentration is very low (< 10%). The induction of methemoglobinemia from the nitrites, in addition to present carboxyhemoglobinemia, significantly reduces the oxygen-carrying capacity of blood. Vasodilatation leading to hypotension is another adverse effect of the Cyanide Antidote Kit.

Appropriate dosing of sodium nitrite has not been established in children, who may develop excessive methemoglobinemia and/or hypotension.

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Inpatient and Outpatient Care

Inpatient care

Patients generally require admission to the ICU for continuous cardiac monitoring, respiratory and cardiovascular support, and frequent neurologic evaluation.

Rapid manifestation of acute poisoning from hydrogen cyanide (HCN) gas and soluble salts causes principal acute care concerns of hemodynamic instability and cerebral edema. Conversely, acute poisoning from cyanogens (nitriles) and poorly soluble salts may not manifest or become life threatening for several hours after exposure.

Monitor disease resolution by clinical criteria, serial plasma lactate concentrations, and arterial and venous blood gases. Perform serial electrocardiograms (ECGs) for patients with cardiac dysrhythmias or complaints of chest pain.

Discharge the patient when neurologic and cardiovascular status has normalized and acidosis and other metabolic abnormalities have resolved.

Outpatient care

Reevaluate patients within 7-10 days of discharge to monitor for onset of delayed neurologic manifestations (eg, Parkinson-like syndrome, neuropsychiatric sequelae).

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Deterrence and Prevention

Smoke alarms significantly reduce incidence of serious smoke inhalation injury. Workplaces using cyanides should have engineering controls in place to avoid inadvertent exposures. Workers should be provided with personal protective equipment and training; they should be instructed to avoid contact between cyanide salts and mineral acids or other compounds with low pH.

Determine blood cyanide concentrations or thiocyanate concentrations in patients receiving sodium nitroprusside at high doses or for more than 5 days. Alternatively, coadminister sodium thiosulfate or hydroxocobalamin to reduce the risk of iatrogenic cyanide poisoning.

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Contributor Information and Disclosures
Author

Inna Leybell, MD  Clinical Assistant Professor, Department of Emergency Medicine, NYU Langone Medical Center

Inna Leybell, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Student Association/Foundation, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Coauthor(s)

Stephen W Borron, MD, MS, FAAEM, FACEP, FAACT, FACMT  Professor of Emergency Medicine and Medical Toxicology, Division of Medical Toxicology, Department of Emergency Medicine, Paul L Foster School of Medicine, Texas Tech University Health Sciences Center; Associate Medical Director, West Texas Regional Poison Center

Stephen W Borron, MD, MS, FAAEM, FACEP, FAACT, FACMT is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Emergency Physicians, American College of Medical Toxicology, American College of Occupational and Environmental Medicine, American Industrial Hygiene Association, and European Association of Poisons Centres and Clinical Toxicologists

Disclosure: Meridian Pharmaceuticals Consulting fee Consulting

Carlos J Roldan, MD, FAAEM  Assistant Professor, Department of Emergency Medicine, University of Texas Health Science Center at Houston Medical School; Consulting Staff, Department of Emergency Medicine, Memorial Hermann Hospital and Lyndon Baines General Hospital

Carlos J Roldan, MD, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Pain Society, American Society of Regional Anesthesia and Pain Medicine, International Association for the Study of Pain, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

Asim Tarabar, MD  Assistant Professor, Director, Medical Toxicology, Department of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital

Disclosure: Nothing to disclose.

Additional Contributors

Frederic J Baud, MD Director, Professor, Toxicological and Medical Intensive Care Unit, Hôpital Lariboisiere of Paris, France

Disclosure: Nothing to disclose.

John G Benitez, MD, MPH, FACMT, FAACT, FACPM, FAAEM, Associate Professor, Department of Medicine, Medical Toxicology, Vanderbilt University Medical Center; Managing Director, Tennessee Poison Center

John G Benitez, MD, MPH, FACMT, FAACT, FACPM, FAAEM, is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American College of Medical Toxicology, American College of Preventive Medicine, Society for Academic Emergency Medicine, Undersea and Hyperbaric Medical Society, and Wilderness Medical Society

Disclosure: Nothing to disclose.

Robert S Hoffman, MD, FAACT, FACMT Associate Professor, Departments of Emergency Medicine and Medicine, Clinical Pharmacology, New York University School of Medicine, Consulting Staff, Department of Emergency Services, Bellevue and New York University Hospital

Robert S Hoffman, MD, FAACT, FACMT is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Emergency Physicians, American College of Medical Toxicology, American College of Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

David C Lee, MD Research Director, Department of Emergency Medicine, Associate Professor, North Shore University Hospital and New York University Medical School

David C Lee, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Medical Toxicology, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

John T VanDeVoort, PharmD Regional Director of Pharmacy, Sacred Heart & St. Joseph's Hospitals

John T VanDeVoort, PharmD is a member of the following medical societies: American Society of Health-System Pharmacists

Disclosure: Nothing to disclose.

References
  1. 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].

  2. National Cancer Institute. Cancer topics: Laetrile/Amygdalin. 11/21/2005;[Full Text].

  3. 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].

  4. 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].

  5. 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].

  6. 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].

  7. 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].

  8. 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].

  9. 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].

  10. 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].

  11. Sutter M, Tereshchenko N, Rafii R, Daubert GP. Hemodialysis Complications of Hydroxocobalamin: A Case Report. J Med Toxicol. Mar 30 2010;[Medline].

  12. Hall AH, Saiers J, Baud F. Which cyanide antidote?. Crit Rev Toxicol. 2009;39(7):541-52. [Medline].

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