Prognostic factors of hyperbaric oxygen therapy for patients with delayed encephalopathy after acute carbon monoxide poisoning

Huang, Feifei; Yang, Lin; Tan, Zhimin; Yang, Bangmin; Liu, Pingqiong; Li, Zuomin; Shi, Wei; Peng, Kun; Yuan, Jing; He, Qing; Yang, Li; Li, Xinyu; Li, Can; Chen, Dezhong; Peng, Zhengrong

doi:10.1016/j.heliyon.2022.e12351

Cited by 3 publications

(2 citation statements)

References 18 publications

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“…However, its pathogenesis remains undetermined. Therefore, there is no definitive treatment modality against etiology, and the present clinical treatment is primarily symptomatic [13][14][15] . In this study, the incidence of DEACMP was estimated to be 21.68% during follow-up, and most patients presented symptoms after a pseudo-healing period of 2-52 days following acute poisoning, which is essentially consistent with the results of a prior study 13 .…”

Section: Discussionmentioning

confidence: 99%

Analysis of factors associated with the development of delayed encephalopathy following acute carbon monoxide poisoning

Liu,

Wang,

Lian

et al. 2024

Sci Rep

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In this study, we analyzed the factors influencing the development of delayed encephalopathy in patients with acute carbon monoxide poisoning (ACOP) (DEACMP) following conventional treatment such as hyperbaric oxygen therapy (HBOT). Between January 2012 and January 2022, we retrospectively analyzed 775 patients with ACOP, who were admitted to the Second Department of Rehabilitation Medicine and received HBOT in the Second Hospital of Hebei Medical University. These patients were divided into the non-DEACMP and DEACMP groups based on their follow-up; we then compared the general data, clinical characteristics, admission examination, and treatment between the two groups to identify risk factors for the development of DEACMP. The DEACMP group comprised of 168 cases, while the non-DEACMP group consisted of 607 cases. Univariate analysis showed that there were 20 possible prognostic factors in the non-DEACMP and DEACMP groups. The results of multivariable regression analyses suggested that the occurrence of DEACMP was significantly correlated with advanced age, the combination of multiple medical histories, the duration of CO exposure, the duration of coma, poisoning degree, the Interval between ACOP and the first HBOT, the total number of HBOTs, and the combination with rehabilitation treatment. DEACMP patients who are older, have more comorbidities, prolonged CO exposure, prolonged coma, severe intoxication, long intervals between ACOP and the first HBOT, fewer HBOT treatments, and who are not treated with a combination of rehabilitative therapies have a poor prognosis.

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Section: Discussionmentioning

confidence: 99%

Analysis of factors associated with the development of delayed encephalopathy following acute carbon monoxide poisoning

Liu,

Wang,

Lian

et al. 2024

Sci Rep

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“…DEACMP patients suffer a series of neurological and psychiatric disorders, including cognitive dysfunction, motor impairment, extrapyramidal systems dysfunction, even consciousness disturbance after a brief lucid period, cortical blindness, depression. DEACMP may be caused by secondary brain tissue damage, due to CO-mediated brain tissue hypoxia, oxygen-based free radicals, and membrane peroxidation, instead of due to direct hypoxia-induced damage [16][17][18][19].…”

Section: Discussionmentioning

confidence: 99%

A patient with toxic encephalopathy associated with acute carbon monoxide poisoning–A clinical case

et al. 2023

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Carbon monoxide (CO) is a colorless, odorless, and lacking in irritative properties gas. It has a higher affinity towards hemoglobin than oxygen and thus the complex carboxyhemoglobin develops. Acute CO poisoning leads to poly-organic insufficiency and the organs that suffer the most are the ones with higher oxygen needs- the brain, the heart and the kidneys. We present a clinical case of 49-year-old woman with a sudden appearance of complaints of dizziness, stiffness throughout the entire body, inability to move. Subsequently she was found by her relatives with disorientated and “foaming around her mouth”. Earlier she had been using a gasoline generator because of a power outage. Her laboratory results came out with higher carboxyhemoglobin (40%), nitrogen waste products and mixed type acidosis. From the conducted brain MRI there were changes, correlating to toxic encephalopathy after acute CO poisoning.

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Edaravone combined with hyperbaric oxygen therapy in delayed encephalopathy after acute carbon monoxide poisoning: A meta-analysis

Zeng,

Li,

Yao

et al. 2024

Journal of Clinical Neuroscience

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Prognostic factors of hyperbaric oxygen therapy for patients with delayed encephalopathy after acute carbon monoxide poisoning

Cited by 3 publications

References 18 publications

Analysis of factors associated with the development of delayed encephalopathy following acute carbon monoxide poisoning

Analysis of factors associated with the development of delayed encephalopathy following acute carbon monoxide poisoning

A patient with toxic encephalopathy associated with acute carbon monoxide poisoning–A clinical case

Edaravone combined with hyperbaric oxygen therapy in delayed encephalopathy after acute carbon monoxide poisoning: A meta-analysis

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