Hyperbaric oxygen therapy for acute domestic carbon monoxide poisoning: two randomized controlled trials: reply to comment by Birmingham and Hoffman

Annane, Djillali; Chevret, Sylvie; Raphaël, Jean Claude

doi:10.1007/s00134-011-2201-9

Cited by 3 publications

(5 citation statements)

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“…The agnostic sentiment of the authors was reiterated in their published reply to criticism of the protocol—“one cannot summarize the mechanisms of carbon monoxide toxicity using neutrophil adherence to the endothelium. For patients and physicians, only clinical outcomes are of interest,”—and then state that their conclusion was in line with a recent Cochrane review 36 …”

Section: Study Maximum O2 Dose Time Tx Initiateda Acute Treatment Pro...supporting

confidence: 59%

“…For patients and physicians, only clinical outcomes are of interest,"-and then state that their conclusion was in line with a recent Cochrane review. 36 With the critical issue of dose in mind, the RCT by Scheinkestel et al 26 does raise the question of HBOT efficacy. While done with an acute dose of 2.8 ATA, the authors failed to include delay to initiation of treatment in their multivariable analysis (mean HBOT delay of 7.3 h), 69% of the study group attempted suicide (important because depression had a negative impact on the outcome neuropsychological testing 37 ), and only 46% of patients were evaluated at the 1 month follow-up.…”

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confidence: 99%

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Hyperbaric oxygen should be used for carbon monoxide poisoning

Sethuraman

Thom

2022

Brit J Clinical Pharma

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This short review addresses the mechanisms of injury mediated by carbon monoxide (CO) and current information on efficacy of hyperbaric oxygen therapy (HBOT). Recent clinical series involving large, country‐wide databases and prospective randomized trials are summarized. We conclude that there is an abundance of basic science and preclinical and clinical research supporting the use of HBOT for acute CO poisoning. With appropriate consideration for pathology and therapeutic mechanisms, HBOT at a dose of 2.5–3.0 atm absolute is a necessary treatment for this toxidrome.

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Section: Study Maximum O2 Dose Time Tx Initiateda Acute Treatment Pro...supporting

confidence: 59%

mentioning

confidence: 99%

Hyperbaric oxygen should be used for carbon monoxide poisoning

Sethuraman

Thom

2022

Brit J Clinical Pharma

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“…Several studies have reported that hyperbaric oxygen therapy is an effective treatment for CO poisoning (4–6). Furthermore, the addition of dexamethasone (7) or N -butylphthalide (8) to hyperbaric oxygen therapy may also exert beneficial effects.…”

Section: Introductionmentioning

confidence: 99%

Utility of brain CT for predicting delayed encephalopathy after acute carbon monoxide poisoning

Hao

et al. 2019

Exp Ther Med

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Delayed encephalopathy after acute carbon monoxide poisoning (DEACMP) is a serious complication that occurs several days or weeks after carbon monoxide (CO) intoxication. This study identified computed tomography (CT) findings in the prediction of DEACMP development. Adults with CO poisoning admitted to Beijing Chaoyang Hospital, Shenyang Ninth People's Hospital, Shanxi Second People's Hospital and Shandong Provincial Hospital in China from January 2013 to January 2016 were retrospectively analyzed. Baseline demographic and clinical characteristics were extracted from the medical records. Brain CT imaging was carried out within 24 h of admission, and an integrated CT score was calculated to semi-quantify lesion severity. Patients were followed-up for 6 months. Baseline characteristics and CT findings were compared among patients who developed DEACMP (DEACMP group) and those who did not (non-DEACMP group). The receiver operating characteristic (ROC) curve analysis was used to examine the utility of integrated CT score for predicting DEACMP. Among the 123 patients included in the analysis, 27 (22.0%) developed DEACMP. The DEACMP and non-DEACMP groups did not differ with regard to age, sex and carboxyhemoglobin (COHb) level at admission. However, compared with the non-DEACMP group, the patients in the DEACMP group had longer onset time of symptoms and duration of exposure to CO, higher acute physiology and chronic health evaluation-II (APACHE-II) score, lower Glasgow Coma Scale (GCS) score, and there was a higher proportion of patients with severe symptoms and brain CT abnormalities (81.5 vs. 51.0%; P<0.05). Integrated CT score in the DEACMP group was significantly higher than that in the non-DEACMP group (73.63 vs. 51.39; P<0.01). ROC curve was used to analyze the utility of integrated CT score in the prediction of DEACMP. The area under the ROC curve was 0.700 (95% confidence interval, 0.584–0.817; P<0.01). In conclusion, brain integrated CT score has the potential to identify DEACMP in patients.

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“…L'étude qui vient de paraître de l'équipe d'Annane [51] ne remet pas en cause les résultats de l'étude marquante de Weaver et al Le protocole à 2 ATA a été repris avec, cette fois, une distinction pour la perte de connaissance, d'une séance vs zéro et pour le coma, d'une séance vs deux. L'étude est négative avec même un effet potentiellement néfaste pour les patients ayant reçu deux séances d'OHB.…”

Section: • Diminution Des Lésions D'ischémie-reperfusionunclassified

“…Cependant, si on reprend les patients des deux études de cette équipe ayant utilisé le même protocole avec une OHB à 2 ATA et si on rassemble leurs données sur la récupération complète, on ne trouve plus de différence significative en défaveur de deux séances par rapport à une (p = 0,23 test de Fischer). Il faut aussi avoir à l'esprit que dans l'étude d'Annane et al, le groupe comateux traité par une séance d'OHB, 10 % des patients n'avaient en fait pas présenté de coma et donc étaient probablement moins graves [51].…”

Section: • Diminution Des Lésions D'ischémie-reperfusionunclassified

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

et al. 2011

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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 ané-mique 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 : détoxifica-tion plus rapide des protéines héminiques, effet antioxydant et amélioration de la physiologie cérébrale (diminution de la pression intracrânienne, diminution de l'oedème et préserva-tion 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. Pour citer cette revue : Réanimation 20 (2011). Mots clés Oxygénothérapie hyperbare · Intoxication au monoxyde de carboneAbstract 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 p...

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Hyperbaric oxygen therapy for acute domestic carbon monoxide poisoning: two randomized controlled trials: reply to comment by Birmingham and Hoffman

Cited by 3 publications

References 5 publications

Hyperbaric oxygen should be used for carbon monoxide poisoning

Hyperbaric oxygen should be used for carbon monoxide poisoning

Utility of brain CT for predicting delayed encephalopathy after acute carbon monoxide poisoning

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

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