Hyperbaric Oxygen Therapy Did Not Prevent Delayed Neuropsychiatric Sequelae in a Prospective Observational Study With Propensity Score Matching in 224 Patients With Acute Carbon Monoxide Toxicity

Han, Sangsoo; Nah, Sangun; Choi, Sung-Woo; Lee, Young Hwan; Kim, Gi Woon; Cho, Young Soon

doi:10.1016/j.jemermed.2020.10.050

Cited by 10 publications

(4 citation statements)

References 18 publications

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“…Therefore, it is difficult to generalize the results to all CO patients. However, since it is known that individuals who are not indicated for HBOT have a low risk of developing DNS, the results of this study can be considered meaningful [39]. Finally, this was a single-center study; the HBOT protocol may differ among centers, and the racial and regional characteristics of patients may also influence outcomes.…”

Section: Discussionmentioning

confidence: 98%

Correlation between Time to Hyperbaric Oxygen Therapy and Delayed Neurological Sequelae in Acute Carbon Monoxide Poisoning Patients

Choi,

Nah,

Han

2024

Diagnostics

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Carbon monoxide (CO) is one of the most common causes of intoxication. Delayed neurologic sequelae (DNS) have a major impact on prognosis of CO poisoning patients. Hyperbaric oxygen therapy (HBOT) is widely used to treat DNS. However, there is no consensus regarding the optimal timing of HBOT. This prospective study enrolled patients who visited the hospital from November 2019 to October 2022. The cutoff value for the latency to HBOT after CO exposure was determined, and the area under the receiver operating characteristic curve (AUC) was estimated. In total, 167 patients were divided into non-DNS and DNS groups. The initial Glasgow Coma Scale (GCS) score, CO exposure time, latency to HBOT after CO exposure, median length of hospital stay (p < 0.001) and creatine kinase (p = 0.016) showed significant differences. A GCS score ≤ 9 had an odds ratio (OR) of 5.059 (95% confidence interval [CI]: 1.602–15.976, p = 0.006), and latency to HBOT after CO exposure ≥ 200 min had an OR of 18.971 (95% CI: 4.310–83.508, p < 0.001). The AUC was 0.8235 (95% CI: 0.7504–0.8966). A GCS score ≤ 9 and latency to HBOT ≥ 200 min may be significant risk factors for DNS.

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Section: Discussionmentioning

confidence: 98%

Correlation between Time to Hyperbaric Oxygen Therapy and Delayed Neurological Sequelae in Acute Carbon Monoxide Poisoning Patients

Choi,

Nah,

Han

2024

Diagnostics

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“…Hyperbaric oxygen (HBO) therapy has been considered one of the effective treatment options in eliminating COHb to alleviate tissue hypoxia and ischemia after ACMP [42]. However, HBO treatment does not reduce the incidence of DEACMP [43]. The reason for this phenomenon might ascribe to excessive ROS production due to reoxygenation is that patients are removed from CO-enriched environment.…”

Section: Discussionmentioning

confidence: 99%

Targeting Ferroptosis Promotes Functional Recovery Through Mitigating White Matter Injury Following Acute Carbon Monoxide Poisoning

Wang

Xiong

Yin

et al. 2023

Preprint

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Survivors suffering from acute carbon monoxide poisoning (ACMP) are apt to develop white matter injury (WMI). While, the mechanism that ACMP evokes WMI remains unclear. Given that ferroptosis plays an evident role in igniting oligodendrocyte damage to deteriorate WMI, exploring regimens to attenuate ferroptosis is a feasible approach to alleviate WMI post-ACMP. Here, the results indicated that ACMP induced WMI to evoke motor impairment resulting from the surplus iron and reactive oxygen species (ROS) accumulation after ACMP. And, the administration of ferrostatin-1 reduced iron and ROS deposition to repress ferroptosis, thereafter reducing WMI to promote motor recovery. Furthermore, the result demonstrated that the nuclear factor erythroid-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling pathway was involved in attenuating ferroptosis resulting from the application of ferrostatin-1. The present study offers a rationale that targeting ferroptosis to alleviate WMI is a feasible therapeutic strategy for ACMP.

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“…Hyperbaric oxygen (HBO) therapy is thought to be essential for preventing neurological sequelae in patients with CO poisoning [28]. However, the results have been con icting and the effects of HBO therapy for patients with CO poisoning remains contentious [29,30]. A recent study suggests that HBO treatment with inconsistent protocols showed no advantages over NBO treatment in the prevention of DNS or the improvement in LNS after CO poisoning, and multiple HBO sessions on the rst day of hospitalization were associated with a greter incidence of DNS [31].…”

Section: Discussionmentioning

confidence: 99%

Risk factors and Outcome Analysis of Delayed Neurological Sequelae in elderly patients with carbon monoxide poisoning

Xue

et al. 2023

Preprint

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Objective Carbon monoxide (CO) poisoning is one of the common causes of poisoning in patients and can result in significant neurological sequelae. However, few studies have focused on the elderly population. Method We retrospectively reviewed elderly (age≥60 years) with CO poisoning from non-fire accidents and non-suicid at at the 6th medical center PLA general hospital in China from 2013 to 2023. We analyzed the patients’ epidemiological characteristics and outcome; identified the risk factors for patients who developed delayed neurological sequelae (DNS) and long-term neurological sequelae (LNS); compared the data of patients who received hyperbaric oxygen (HBO) to those who received normobaric oxygen (NBO) therapy. Result A total of 167 elderly patients were enrolled. The annual case number decreased from 2013 to 2023, particularly during the cold months (November to February). The most common source of exposure was coal heating (89.8%). The most common presenting symptoms were consciousness changes (86.8%). Eighty-eight patients (52.3%) developed DNS, of which sixty-nine patients (78.4%) converted to LNS. The most common imaging manifestations were hypoxic ischemic damage in the basal ganglia (54.3%) and demyelination in white matter (45.7%). After multivariate analysis, initial GCS score and coma time were the independent risk factor for patients with DNS (p＜0.001). Interestingly, myocardial injury was more common in non DNS elderly patients than in DNS patients (p＜0.001); only coma time was an independent risk factor for patients with LNS (p＜0.001). There was no significant difference between HBO (p=0.196) and NBO (p=0.379) in the occurrence of DNS and LNS in elderly patients with CO poisoning. Conclusion: Only initial GCS score and coma time are the risk factors of DNS for elderly patients, and coma time alone is a high-risk factor for poor prognosis of CO poisoning in the elderly. Moreover, HBO is not superior to NBO in elderly patients with CO poisoning. Special attention should be given and follow-up should be performed to elderly patients, particularly those have longer coma time and CO exposure time, and lower initial GCS score in acute CO poisoning.

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Hyperbaric Oxygen Therapy Did Not Prevent Delayed Neuropsychiatric Sequelae in a Prospective Observational Study With Propensity Score Matching in 224 Patients With Acute Carbon Monoxide Toxicity

Cited by 10 publications

References 18 publications

Correlation between Time to Hyperbaric Oxygen Therapy and Delayed Neurological Sequelae in Acute Carbon Monoxide Poisoning Patients

Correlation between Time to Hyperbaric Oxygen Therapy and Delayed Neurological Sequelae in Acute Carbon Monoxide Poisoning Patients

Targeting Ferroptosis Promotes Functional Recovery Through Mitigating White Matter Injury Following Acute Carbon Monoxide Poisoning

Risk factors and Outcome Analysis of Delayed Neurological Sequelae in elderly patients with carbon monoxide poisoning

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