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EM TopicsCyanide poisoning

EM · Cyanide poisoning

Cyanide poisoning

Also known as Cyanide toxicity · Histotoxic hypoxia · Smoke inhalation cyanide · Cytochrome oxidase poisoning

Cyanide poisoning — the histotoxic toxin that halts cellular respiration by binding the ferric iron of cytochrome c oxidase (complex IV), shutting oxidative phosphorylation and forcing every tissue into anaerobic metabolism. The emergency source is the enclosed-space house fire (cyanide released from burning plastics, wool and polyurethane), and the patient is the unconscious fire survivor with soot in the mouth, a high lactate and a metabolic acidosis out of proportion to the carboxyhaemoglobin level — co-existing carbon monoxide is the rule. The clinical signs are rapid collapse, seizure and coma, an initial hypertension then bradycardic cardiovascular collapse, and the rare cherry-red skin from venous oxygen that the tissues cannot extract. Management is 100 per cent oxygen, empirical hydroxocobalamin 70 mg per kilogram (adult 5 g) intravenously — the preferred antidote because it does not cause hypotension or methaemoglobinaemia — and sodium thiosulfate intravenously. The smoke-inhalation kit (amyl or sodium nitrite) is avoided because methaemoglobinaemia worsens the co-existent carbon monoxide poisoning. ACEM-primary, globally tagged.

medium18 referencesUpdated 26 July 202617 min readSource-verified · Sept 2026

Checked against its sources on 5 Sept 2026

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Red flags

  • An unconscious patient from an enclosed-space house fire with plastics has combined cyanide and carbon monoxide poisoning plus an inhalation airway injury — treat both toxins empirically before any cyanide level returns
  • A venous or arterial lactate at or above 10 mmol per litre in a fire survivor is the bedside surrogate for cyanide — give hydroxocobalamin empirically
  • Hydroxocobalamin is the antidote of choice in the hypotensive or fire-inhalation patient because it avoids both the methaemoglobinaemia and hypotension of the nitrite kit and the serious cobalt toxicity of dicobalt edetate when cyanide is absent
  • Never give the sodium or amyl nitrite kit to a smoke-inhalation patient — induced methaemoglobinaemia worsens the co-existent carbon monoxide poisoning and the already-compromised oxygen delivery
  • Cyanide produces histotoxic hypoxia — the blood is well oxygenated but the tissues cannot use the oxygen, so the venous oxygen is abnormally high and the skin may be cherry-red
  • The bitter-almond smell appeared in only 15 per cent of published cases and cherry-red skin in 11 per cent — their absence never excludes cyanide
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Related topics

  • Carbon monoxide poisoning
  • Burn management in the emergency department
  • Coma and GCS assessment
  • Upper airway obstruction in the emergency department
  • The toxidrome approach and the general management of the poisoned patient
  • Salicylate poisoning
Study tools

Your progress

Saved on this device.

Target exams

ACEMFRCEMABEMFRCPCCCFPEMEBEEM

Red flags

  • An unconscious patient from an enclosed-space house fire with plastics has combined cyanide and carbon monoxide poisoning plus an inhalation airway injury — treat both toxins empirically before any cyanide level returns
  • A venous or arterial lactate at or above 10 mmol per litre in a fire survivor is the bedside surrogate for cyanide — give hydroxocobalamin empirically
  • Hydroxocobalamin is the antidote of choice in the hypotensive or fire-inhalation patient because it avoids both the methaemoglobinaemia and hypotension of the nitrite kit and the serious cobalt toxicity of dicobalt edetate when cyanide is absent
  • Never give the sodium or amyl nitrite kit to a smoke-inhalation patient — induced methaemoglobinaemia worsens the co-existent carbon monoxide poisoning and the already-compromised oxygen delivery
  • Cyanide produces histotoxic hypoxia — the blood is well oxygenated but the tissues cannot use the oxygen, so the venous oxygen is abnormally high and the skin may be cherry-red
  • The bitter-almond smell appeared in only 15 per cent of published cases and cherry-red skin in 11 per cent — their absence never excludes cyanide
The one-line answer

Cyanide is the histotoxic toxin — it does not stop oxygen reaching the cell, it stops the cell using it, by binding the ferric iron (Fe³⁺) of cytochrome c oxidase (complex IV) and freezing oxidative phosphorylation. The unconscious patient dragged from an enclosed-space house fire, with soot in the mouth and a venous lactate at or above 10 mmol per litre, gets empirical hydroxocobalamin 5 g intravenously before any cyanide level returns; the nitrite kit is withheld in smoke inhalation because methaemoglobinaemia worsens the co-existent carbon monoxide.[1][4][7]

Meet the patient

A 52-year-old man is dragged unconscious from an enclosed-space house fire started by a polyurethane mattress. He arrives with soot in the mouth and nostrils, singed nasal hair and a hoarse voice, GCS 6, a blood pressure that has fallen from 168 to 84, and a venous lactate of 13.6 mmol per litre with a metabolic acidosis out of all proportion to the carboxyhaemoglobin of 28 per cent.[1]

Two questions decide his first hour: is this the fire survivor with the high lactate? (give hydroxocobalamin now) and is carbon monoxide riding with the cyanide? (treat both toxins in parallel).[1][4] Hold those two questions and the rest of the topic slots in behind them.

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References18ShowHide
  1. [1]Baud FJ, Barriot P, Toffis V, et al. Elevated blood cyanide concentrations in victims of smoke inhalation N Engl J Med, 1991.PMID 1944484
  2. [2]Beasley DM, Glass WI. Cyanide poisoning: pathophysiology and treatment recommendations Occup Med (Lond), 1998.PMID 10024740
  3. [3]Borron SW, Baud FJ, Barriot P, Imbert M, Bismuth C. Prospective study of hydroxocobalamin for acute cyanide poisoning in smoke inhalation Ann Emerg Med, 2007.PMID 17481777
  4. [4]Reade MC, Davies SR, Morley PT, Dennett J, Jacobs IC; Australian Resuscitation Council. Review article: management of cyanide poisoning Emerg Med Australas, 2012.PMID 22672162
  5. [5]Borron SW, Baud FJ. Antidotes for acute cyanide poisoning Curr Pharm Biotechnol, 2012.PMID 22352728
  6. [6]Parker-Cote JL, Rizer J, Vakkalanka JP, et al. Challenges in the diagnosis of acute cyanide poisoning Clin Toxicol (Phila), 2018.PMID 29417853
  7. [7]Hall AH, Saiers J, Baud F. Which cyanide antidote? Crit Rev Toxicol, 2009.PMID 19650716
  8. [8]Hall AH, Dart R, Bogdan G. Sodium thiosulfate or hydroxocobalamin for the empiric treatment of cyanide poisoning? Ann Emerg Med, 2007.PMID 17098327
  9. [9]MacLennan L, Moiemen N. Management of cyanide toxicity in patients with burns Burns, 2015.PMID 24994676
  10. [10]Fortin JL, Desmettre T, Manzon C, et al. Cyanide poisoning and cardiac disorders: 161 cases J Emerg Med, 2010.PMID 20185266
  11. [11]Schaffer DH, Poole ND, Traylor J. Cyanide Toxicity StatPearls [Internet], 2025.PMID 29939573
  12. [12]Marrs TC, Thompson JP. The efficacy and adverse effects of dicobalt edetate in cyanide poisoning Clin Toxicol (Phila), 2016.PMID 27352227
  13. [13]Culnan DM, Craft-Coffman B, Bitz GH, et al. Carbon monoxide and cyanide poisoning in the burned pregnant patient: an indication for hyperbaric oxygen therapy Ann Plast Surg, 2018.PMID 29461288
  14. [14]Grandas F, Artieda J, Obeso JA. Clinical and CT scan findings in a case of cyanide intoxication Mov Disord, 1989.PMID 2733710
  15. [15]Coentrão L, Moura D. Acute cyanide poisoning among jewelry and textile industry workers Am J Emerg Med, 2011.PMID 20825788
  16. [16]Curry SC, Carlton MW, Raschke RA. Prevention of fetal and maternal cyanide toxicity from nitroprusside with coinfusion of sodium thiosulfate in gravid ewes Anesth Analg, 1997.PMID 9141943
  17. [17]Jin WY, Huang DC, Guo J, et al. Evidence for Hydroxocobalamin in Cyanide Toxicity Caused by Smoke Inhalation: An Updated Systematic Review. Emerg Med Int, 2025.PMID 41497958
  18. [18]Dean BS, Verdile VP, Krenzelok EP. Coma reversal with cerebral dysfunction recovery after repetitive hyperbaric oxygen therapy for severe carbon monoxide poisoning Am J Emerg Med, 1993.PMID 8043054
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Related topics

  • Carbon monoxide poisoning
  • Burn management in the emergency department
  • Coma and GCS assessment
  • Upper airway obstruction in the emergency department
  • The toxidrome approach and the general management of the poisoned patient
  • Salicylate poisoning