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Intoxication au monoxyde de carbone et place de l’oxygénothérapie hyperbare

Carbon monoxide poisoning: what about hyperbaric oxygen?

  • Mise Au Point / Update
  • Published:
Réanimation

Résumé

Le traitement par oxygénothérapie hyperbare (OHB) lors des intoxications au monoxyde de carbone est utilisé depuis plus de 50 ans. Néanmoins, le protocole à appliquer et le sous-groupe de patients pouvant bénéficier de l’OHB restent débattus. La physiopathologie de l’intoxication au monoxyde de carbone est complexe, expliquant la diversité des tableaux cliniques retrouvés neurologiques (troubles de la conscience et syndrome postintervallaire) mais aussi cardiaques (ischémie à coronaires saines notamment). La physiopathologie fait intervenir une hypoxie anémique par formation de carboxyhémoglobine mais aussi une hypoxie hypoxique par blocage de la chaîne respiratoire au niveau de la cytochrome oxydase, un stress oxydatif et des lésions d’ischémie-reperfusion. La carboxyhémoglobine (veineuse ou artérielle) n’est pas à prendre en compte pour le traitement; le dosage de la troponine Ic au moindre doute est souhaitable. Les bases de traitement par l’OHB reposent d’abord sur des arguments physiopathologiques: détoxification plus rapide des protéines héminiques, effet antioxydant et amélioration de la physiologie cérébrale (diminution de la pression intracrânienne, diminution de l’oedème et préservation de la zone de pénombre). Les autres arguments sont issus des essais thérapeutiques randomisés. Quatre des cinq études randomisées utilisant une OHB avec une pression supérieure à 2 ATA étaient positives. Deux études à 2 ATA étaient négatives. Ainsi, les recommandations européennes et américaines suggèrent l’utilisation d’OHB à 2,5 ATA au moins dans les situations à risque de séquelles neurologiques (tout signe neurologique objectif y compris perte de connaissance), en cas d’atteinte cardiaque ou de grossesse. Il faut insister sur un traitement par oxygénothérapie à fort débit pendant 8-12 heures en cas de non-indication de l’OHB.

Abstract

Hyperbaric oxygen (HBO) is used since more than 50 years for carbon monoxide poisoning. However, HBO protocols and indications are still debated. Neurological (coma and delayed neuropsychological sequelae) and cardiac (ischemic changes with normal coronary arteries) clinical scenarios are explained by complex mechanisms. Carboxyhemoglobin formation, cytochrome oxydase inhibition, oxidative stress, as well as ischemia-reperfusion phenomenon are among these mechanisms. Venous and arterial carboxyhemoglobin levels are not correlated with the patient’s final prognosis and thus not mandatory for indicating the treatment. Conversely, troponin IC measurement is strongly recommended if myocardial involvement is suspected. HBO treatment relies on mechanistic bases: earlier detoxification, anti-oxidant properties, and improvement in cerebral physiology (decrease in intracranial pressure and oedema, and ischemic penumbra preservation). Clinical basis is assessed by the results of the randomized clinical trials (RCTs). Four among the 5 RCTs using > 2 ATA OHB protocols were positive. Two RCTs at 2 ATA level were negative. Therefore, international guidelines recommend OHB with at least 2.5 ATA in patients at risk of delayed neuropsychological sequelae, whatever the objective neurological signs are, in pregnant women, and patients with myocardial involvement. If OHB is not required, normobaric oxygen with high flow rates during at least 8-12 hours is mandatory.

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  1. Pôle de réanimation, centre régional d’oxygénothérapie hyperbare, CHRU de Lille, université Lille Nord de France, Lille, France

    R. Favory, J. Poissy, E. Parmentier & D. Mathieu

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  1. R. Favory
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  2. J. Poissy
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  3. E. Parmentier
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  4. D. Mathieu
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Correspondence to R. Favory.

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Favory, R., Poissy, J., Parmentier, E. et al. Intoxication au monoxyde de carbone et place de l’oxygénothérapie hyperbare. Réanimation 20, 493–501 (2011). https://doi.org/10.1007/s13546-011-0327-y

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