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Problems for Discussion - 3 - Carbon Monoxide

Carbon monoxide (CO) occurs naturally as a by-product of haemoglobin catabolism but only reaches toxic levels following exogenous absorption. The commonest external source is the incomplete combustion of organic fuels: wood, charcoal, coal or petroleum. Previously, exposure to car exhaust was a common source of exposure but improvements in vehicle emission controls makes this a far less frequent cause of CO poisoning. Another source of carbon monoxide poisoning is the paint-stripping agent, methylene chloride. It can be absorbed by ingestion, inhalation or across the skin and then undergoes hepatic metabolism to form CO.

CO is carried in the blood carried to haemoglobin as COHb. Whilst COHb cannot carry oxygen the functional hypoxia produced by CO poisoning is unlikely to be the cause of morbidity. An additional effect may include the binding to and inactivation of mitochondrial cytochrome oxidase producing cellular hypoxia. Another potential mechanism is free radical oxygen injury secondary to nitric oxide release from platelets which causes leucocyte binding to endothelial cells resulting in peroxidative tissue damage. The target organs of CO poisoning are principally the heart and brain. Of particular concern is the potential for delayed neurotoxicity including parkinsonism, memory and concentration impairment.

The management of CO poisoning remains a matter of considerable controversy. The administration of 100% oxygen will displace CO from haemoglobin and decrease the effective T ½ from 4 hours to 40 minutes. The administration of hyperbaric oxygen (HBO) at 2.5 atmospheres of pressure will decrease the effective T ½ to approximately 20 minutes and has been suggested to decrease the risk of delayed neuropsychiatric sequelae. Clinical trials assessing the effectiveness of HBO in reducing these sequelae have produced conflicting results.

The role of HBO in the acute management of patients with severe CO poisoning, such as coma, seizures, severe metabolic acidosis or cardiac dysfunction or pregnant patients is also unclear as controlled clinical trials have tended to exclude this group of patients. If easily available the use of HBO is generally recommended for these patients as it is the most effective mechanism for treating hypoxia.


  1. Understand the possible mechanism by which CO may cause toxicity.
  2. Detail the range of toxicity of CO poisoning.
  3. Understand how to assess the severity of CO poisoning.
  4. Outline the options for the management of CO poisoning.
  5. Discuss the role of hyperbaric oxygen in the management of CO poisoning including the potential benefits and adverse effects.
  6. Understand the potential chronic complications of CO poisoning.


  1. Langford RM, Armstrong RF.Algorithm for managing injury from smoke inhalation.BMJ. 1989 Oct 7;299(6704):902-5. (fulltext)
  2. Weaver LK, Hopkins RO, Chan KJ, Churchill S, Elliott CG, Clemmer TP, Orme JF Jr, Thomas FO, Morris AH Hyperbaric Oxygen for Acute Carbon Monoxide Poisoning N Engl J Med 347:1057, October 3, 2002 (fulltext) plus correspondence (fulltext)
  3. Scheinkestel CD, Bailey M, Myles PS, et al. Hyperbaric or normobaric oxygen for acute carbon monoxide poisoning: a randomised controlled clinical trial. MJA. 1999;170:203-210. (fulltext)
  4. Weaver LK, Hopkins RO, Chan KJ, et al. Hyperbaric oxygen for acute carbon monoxide poisoning. N Eng J Med. 2002;347:1057-1067.
  5. Thom SR. Hyperbaric oxygen for acute carbon monoxide poisoning. N Eng J Med. 2002;347:1105-1106.
  6. Scheinkestel CD, Jones K, Myles PS, et al. Where to now with carbon monoxide poisoning? Emerg Med Australasia. 2004;16:151-154.
  7. Emerson G. The dilemma of carbon monoxide poisoning. Emerg Med Australasia. 2004;16:101-102.
  8. Weaver LK, Hopkins RO, Chan KJ, et al. Carbon Monoxide Research Group, LDS Hospital, Utah in reply to Scheinkestel et al. and Emerson: The role of hyperbaric oxygen in carbon monoxide poisoning. Emerg Med Australasia. 2004;16:394-399.
  9. Juurlink DN, Buckley NA, Stanbrook MB, et al. Hyperbaric oxygen for carbon monoxide poisoning. The Cochrane Database of Systematic Reviews. 2005, Issue 1. Art. No.: CD002041.pub2. DOI: 10.1002/14651858.CD002041.pub2.


A 57-year-old male is brought to hospital by ambulance after being found unresponsive in his car, with the engine running, in the family garage. A plastic hose was placed from the exhaust into the vehicle cabin. An empty packet of temazepam and a bottle of whisky were found on the floor of the car. On arrival at hospital the ambulance officers report he is responding appropriately and opening his eyes to pain and is non-verbal. His HR is 90/min, BP 120/80, and RR 14/min. An IV line has been placed and he is on high flow oxygen by facemask. His family are in transit.

  1. What additional information do you require?
  2. What initial management is necessary?
  3. What information would you want from his family?
  4. What investigations are indicated?
  5. How would you proceed with further management?


A 35- year-old man is brought to hospital after collapsing at work. He was cutting cement slabs in a basement using a portable petrol generator and an electric saw. On being brought to the outside he awoke and vomited. He was transported to hospital and arrived within 10 minutes. On arrival his was complaining of a headache but no other symptoms. On assessment he was noted to be awake and alert with normal vital signs. Examinations of cranial and peripheral nerves were normal.

  1. What other aspects of the history and examination are important?
  2. What investigations are indicated and why?
  3. What are the options for management and how would these be indicated?
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