Table of Contents

Problems for Discussion - 3- Cyanide

Cyanide is a rapidly toxic agent that is found in liquid and gaseous form. It is used in many chemical compounds including medications and can be found endogenously in plant and bacteria. It is important to know the unique mechanism of action of this poison as delay in treatment can have disastrous consequences to the patient.

Industries that use cyanide include metal extraction and refining, electroplating, photography and fumigation. Suicides are the commonest cause of cyanide poisoning. Deliberate contamination of medications and food has occurred recently. Another source of cyanide includes the combustion of wool, silk, synthetic rubber and polyurethane.

The availability of antidotes to cyanide poisoning varies around the world. In Australia dicobalt edetate IV, sodium nitrite IV and sodium thiosulfate are available. In North America amyl nitrate pearls for inhalation can also used be used. Hydroxocobalamin is widely used in Europe but only has limited availability in North America and Australia.

The management of cyanide poisoning requires firstly the identification of patients who may be at risk of cyanide poisoning and the selection of antidotes. This is complicated by the lack of a readily available assay and the variability of available antidotes. With an understanding of these concepts, you too, will be able to treat that secret agent who is trying to kill himself (or herself) before they reveal the secret plans…

OBJECTIVES

  1. Describe he pathophysiology of cyanide poisoning.
  2. List possible sources of cyanide.
  3. Describe the target organs and clinical presentation of cyanide poisoning.
  4. Discuss the investigations useful in this setting.
  5. Outline the management of cyanide poisoning.
  6. Describe the mechanism of action the classic antidotes for this poison, how it should be given and what circumstances in which it can be dangerous for the patient.
  7. Describe other antidotes for cyanide toxicity available worldwide and their mechanism of action.
  8. Compare these antidotes in terms of costs, availability, side- effects and use with concomitant carbon monoxide poisoning.
  9. Discuss the controversy over permanent neurologic sequelae and vulnerable population after acute cyanide poisoning.

READING

  1. Cyanide
  2. eMedicine Cyanide
  3. Geller RJ, Barthold C, Saiers JA, Hall AH.Pediatric cyanide poisoning: causes, manifestations, management, and unmet needs. Pediatrics. 2006 Nov;118(5):2146-58. (fulltext)
  4. Baud FJ, Borron SW, Bavoux E, Astier A, Hoffman JR.Relation between plasma lactate and blood cyanide concentrations in acute cyanide poisoning.BMJ. 1996 (fulltext)
  5. Bhowmik D, Mathur R, Bhargava Y, et al. Chronic interstitial nephritis following parenteral copper sulfate poisoning. Ren Failure. 2001;23:731-735.
  6. Kilburn KH, McKinley KL. Persistent neurotoxicity from a battery fire: is cadmium the culprit? South Med J. 1996;89:693-8.
  7. Buge A, Supino-Viterbo V, Rancurel G, Pontes C. Epileptic phenomena in bismuth toxic encephalopathy. J Neurol Neurosurg Psychiatr. 1981;44:62-7.
  8. Barnhart S, Rosenstock L. Cadmium chemical pneumonitis. Chest. 1984;86:789-91.
  9. Merchant J, Webby R. Metal fume fever: A case report and literature review. Emerg Med. 2001;13:373-375.
  10. Yeoh MJ, Braitberg G. Carbon monoxide and cyanide poisoning in fire related deaths in Victoria, Australia. J Toxicol Clin Toxicol 2004;42:855-863.
  11. Cummings TF. The treatment of cyanide poisoning. Occup Med (Lond). 2004;54:82-5.
  12. Sauer SW, Keim ME. Hydroxocobalamin: improved public health readiness for cyanide disasters.Ann Emerg Med. 2001 Jun;37:635-41.
  13. Mannaioni G, Vannacci A, Marzocca C, et al. Acute cyanide intoxication treated with a combination of hydroxycobalamin, sodium nitrite, and sodium thiosulfate. J Toxicol Clin Toxicol. 2002;40:181-3.
  14. Baud FJ, Borron SW, Mégarbane B, et al. Value of lactic acidosis in the assessment of the severity of acute cyanide poisoning. Crit Care Med 2002;30:2044-2050.

PROBLEM 1

A 25-year-old female living with her boyfriend working in the mining industry in Western Australia is brought to hospital by ambulance after calling 000 herself. The ambulance arrived at the scene 15 minutes after the call and found the patient unconscious with a RR of 4/min followed rapidly by a cardiac arrest. Cardiopulmonary resuscitation and endotracheal intubation with 100% oxygen were performed. She regained a pulse but was responding only to painful stimuli. On arrival at the hospital, pulse oximetry is non-capturing, she is mottled and cyanosed. Her BP was 40 mmHg and HR 56 beats/min. Arterial blood gas analysis shows: pH 7.15 and HCO3 8 mmol/L.

  1. What would be your next step?
  2. What is your differential diagnosis?
  3. How could you investigate a possible diagnosis of cyanide poisoning?
  4. Outline your further management.

PROBLEM 2

40-year-old male firefighter collapses after going in a warehouse on fire to retrieve another victim. He is unconscious on arrival to the Emergency Department. His HR is 50 beats/min and BP is 60 mmHg systolic. ABG reveals: pH 7.05 and HCO3 10. Oxygen saturation is 80% on a 100% non rebreather mask.

  1. Outline you initial management.
  2. How would you manage this patient particularly in terms of antidote for suspected cyanide poisoning?
  3. Discuss the pros and cons of different antidotes if all were available to you.