Résumé
La prévalence des séquelles neurologiques suite à une exposition au monoxyde de carbone (CO) peut atteindre 50 %. Ces séquelles sont classées en deux catégories : persistantes et retardées. Leur genèse implique non seulement la survenue d’une anoxie prolongée, mais également l’inhibition de la cytochrome-oxydase a3 de la chaîne respiratoire, au sein surtout de la cellule endothéliale cérébrale. L’association de troubles mnésiques et d’anomalies du tonus et de la posture doit faire craindre l’apparition du syndrome neurologique retardé. Le meilleur traitement est la prévention ; l’intérêt de l’oxygénothérapie hyperbare (OHB) reste controversé et n’est justifié à ce jour que pour les formes graves initialement comateuses et chez la femme enceinte.
Abstract
Neuropsychiatric sequelae of carbon monoxide (CO) poisoning occur in up to 50% of all patients presenting with toxic CO levels. Neurological abnormalities include persistent (PNS) and delayed neurological sequelae (DNS) that occur after an asymptomatic period. Multiple hypotheses explain the mechanisms by which CO toxicity leads to cerebral injury including prolonged hypoxemia and dysfunction of intracellular mitochondrial cytochrome oxydase. Neurological examination shows impairments in memory and concentration as well as parkinsonism. Urinary and fecal incontinences represent common problems in severely CO-poisoned patients. No neuroprotective agents have yet demonstrated efficacy in preventing or improving delayed post-anoxic encephalopathy. Data on the effects of hyperbaric oxygen are conflicting because of the absence of any consensual protocol to treat CO poisonings.
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Brahmi, N., M’rad, A., El Ghord, H. et al. Intoxication aiguë au monoxyde de carbone et séquelles neurologiques : de la physiologie à la clinique. Réanimation 20, 452–456 (2011). https://doi.org/10.1007/s13546-011-0274-7
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DOI: https://doi.org/10.1007/s13546-011-0274-7