Archived Comments for:
Delayed neuropsychological sequelae after carbon monoxide poisoning: predictive risk factors in the Emergency Department. A retrospective study
Heikki Savolainen, Dept. of Occup.Safety & Hlth., Tampere, Finland
20 August 2011
Dear Editor,
The excellent study on delayed neuropsychological sequels after a grave carbon monoxide poisoning (1) does not offer support for a treatment with hyperbaric oxygen gas. It may even be harmful (2).
It is true that oxygen given under pressure shortens the half-life of the CO in the circulation. At ambient pressure (21 % oxygen) it varies 4-5 h while at a 2 atmosphere pressure 100 % oxygen, it is shortened to 30 min.
The benefit of this can be questioned as the neurological complication characterized by central demyelination (3) coincides with glial cell reaction probably due to peroxidative events in an animal model (4). Thus, large oxygen concentrations could aggravate this.
1 Pepe G et al. Delayed neuropsychological sequelae after carbon monoxide poisoning: predictive risk factors in the emergency department. A retrospective study. Scand J Trauma Resusc Emerg Med 2011; 19:16
2 Scheinkestel CD et al. Hyperbaric or normobaric oxygen for acute carbon monoxide poisoning: a randomised controlled trial. Med J Austr 1999; 170: 203
3 Savolainen H, Elovaara E. Effect of carbon monoxide on protein metabolism in mouse brain. Exp Neurol 1977; 57: 374
4 Savolainen H et al. Biochemical effects of carbon monoxide poisoning in rat brain with special reference to blood carboxyhemoglobin and cerebral cytochrome oxidase activity. Neurosci Lett 1980; 19: 319
Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine
Hyperbaric oxygen could be harmful
20 August 2011
Dear Editor,
The excellent study on delayed neuropsychological sequels after a grave carbon monoxide poisoning (1) does not offer support for a treatment with hyperbaric oxygen gas. It may even be harmful (2).
It is true that oxygen given under pressure shortens the half-life of the CO in the circulation. At ambient pressure (21 % oxygen) it varies 4-5 h while at a 2 atmosphere pressure 100 % oxygen, it is shortened to 30 min.
The benefit of this can be questioned as the neurological complication characterized by central demyelination (3) coincides with glial cell reaction probably due to peroxidative events in an animal model (4). Thus, large oxygen concentrations could aggravate this.
1 Pepe G et al. Delayed neuropsychological sequelae after carbon monoxide poisoning: predictive risk factors in the emergency department. A retrospective study. Scand J Trauma Resusc Emerg Med 2011; 19:16
2 Scheinkestel CD et al. Hyperbaric or normobaric oxygen for acute carbon monoxide poisoning: a randomised controlled trial. Med J Austr 1999; 170: 203
3 Savolainen H, Elovaara E. Effect of carbon monoxide on protein metabolism in mouse brain. Exp Neurol 1977; 57: 374
4 Savolainen H et al. Biochemical effects of carbon monoxide poisoning in rat brain with special reference to blood carboxyhemoglobin and cerebral cytochrome oxidase activity. Neurosci Lett 1980; 19: 319
Competing interests
None