In the recent past, there has been renewed focus on delayed encephalopathy (DE) that develops after carbon monoxide (CO) poisoning. In the medical space, the disorder is framed as delayed encephalopathy after acute carbon monoxide poisoning (DEACMP). The former is the most severe complication that results from CO poisoning. If unattended to in good time, it leads to disability. Some of the symptoms of DE include loss of memory and concentration, dementia, learning disability, aphasia, apraxia, persistent headaches and migraines, and agnosia. In severe cases, the cerebral cortex is damaged which leads to cerebral dysfunction, seizures and comas. In the long run, the quality of life of those suffering from the disorder depreciates. HBOT is one of the treatment options that is explored in treatment of DE. The latter improves outcome when used alongside medication such as glucocorticoids. Other forms of treatment which are used alongside HBOT include supportive care and rehabilitation therapy.
Mechanism of Action
HBOT reverses the neurological and psychiatric deficiencies that result from DEACMP. The patients are able to regain their ability to walk, recall, learn and even talk, among other cognitive functions. Also, HBOT prompts angiogenesis which results in increased cerebral vascular density. The latter results in increased supply of oxygen to the brain and body tissues. The ischemic-hypoxic damage to the brain as a result of reduced oxygen carrying capacity by the blood is reversed through increased tissue oxygenation. Immune cytokine stimulation, which controls inflammation is regulated as well. Inflammation, which is heightened by CO poisoning is reduced since lesser cytokines are released into the bloodstream. Axoneuron damage that results from CO poisoning is reversed; functioning of the neuron is kept at optimal levels. The diffuse brain damage is addressed to avoid severity.
Also, HBOT prevents oxidative stress thus stopping the action of leukocyte beta-2 integrins. The result is reduced immune-mediated damage to brain and body tissues. Increased tissue oxygenation also reverses the binding between CO and cytochrome-c oxidase. The binding affects cellular respiration and therefore metabolism. Through the reversed process, the metabolism of cerebral cells is restored as well. HBOT improves the outcome and quality of life led by those who suffer from DE. They are able to get back to depending on themselves and sustaining their social connections. Application of HBOT reduces the lengthy treatment time period and high costs associated with the disorder.
References
Cao, H., Tan, X., Liu, Z., Zhao, L., Chi, L., Li, M., Liu, C., & Li, H. (2021). The effect of adding transcranial direct current stimulation to hyperbaric oxygen therapy in patients with delayed encephalopathy after carbon monoxide poisoning: A randomised controlled trial. Frontiers in Neurology, 12(9), 42–49. https://doi.org/10.3389/fneur.2021.719765
Huang, F., Yang, L., Tan, Z., Yang, B., Liu, P., Li, Z., Shi, W., Peng, K., Yuan, J., He, Q., Yang, L., Li, X., Li, C., Chen, D., & Peng, Z. (2022). Prognostic factors of hyperbaric oxygen therapy for patients with delayed encephalopathy after acute carbon monoxide poisoning. Heliyon, 8(12), 132–139. https://doi.org/10.1016/j.heliyon.2022.e12351
Zhang, L., Sun, Q., Xin, Q., Qin, J., Zhang, L., Wu, D., Gao, G., & Xia, Y. (2021). Hyperbaric oxygen therapy mobilized circulating stem cells and improved delayed encephalopathy after acute carbon monoxide poisoning with up-regulation of brain-derived neurotrophic factor. The American Journal of Emergency Medicine, 42(4), 95–100. https://doi.org/10.1016/j.ajem.2021.01.021
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