Effects of donepezil on cognition and global functioning in patients with delayed encephalopathy after carbon monoxide poisoning: A case series

Introduction: Carbon monoxide poisoning may occur in several contexts.Material and Methods: Retrospective of 37 carbon monoxide poisoning cases that underwent hyperbaric oxygen during wildfires in Funchal in August 2016.Results: The studied sample included 37 patients, mean age of 38 years, 78% males. Ten were firefighters, four children and two pregnant victims. Neurological symptoms were the most reported. Median carboxyhemoglobin level was 3.7% (IQR 2.7). All received high-flow oxygen from admission to delivery of hyperbaric oxygen. Persistence of symptoms was the main indication for hyperbaric oxygen. Median time to hyperbaric oxygen was 4.8 hours (IQR 9.5), at 2.5 ATA for 90 minutes, without major complications. Discharge in less than 24 hours occurred in 92% of the cases. Thirty days follow-up: five patients presented clinical symptoms of late neurological syndrome; twelve patients were lost to follow-up. Carboxyhemoglobin levels on admission and mean time to hyperbaric oxygen were no different between those who did and did not develop the syndrome at 30 days (p = 0.44 and p = 0.58, respectively).Discussion: Late neurological syndrome at 30 days occurred in 20% and no new cases were reported at 12 months.Conclusion: Use of hyperbaric oxygen appears to have reduced the incidence of the syndrome. This seems to be the first Portuguese series reporting use of hyperbaric oxygen in carbon monoxide poisoning due to wildfires. The authors intend to alert to the importance of referral of these patients because the indications and benefits of this treatment are well documented. This is especially important given the ever-growing issue of wildfires in Portugal.

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Case report about delayed encephalopathy after carbon monoxide poisoning

Journal of the Neurological Sciences ◽

10.1016/j.jns.2021.119026 ◽

2021 ◽

Vol 429 ◽

pp. 119026

Author(s):

Tungalag Enkhbat ◽

Dulamragchaa Purev ◽

Odgerel Ochirkhuu

Keyword(s):

Carbon Monoxide ◽

Case Report ◽

Carbon Monoxide Poisoning ◽

Delayed Encephalopathy

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Altered regional homogeneity in delayed encephalopathy after carbon monoxide poisoning: A resting-state fMRI study

Neuroscience Letters ◽

10.1016/j.neulet.2020.135002 ◽

2020 ◽

Vol 729 ◽

pp. 135002

Author(s):

Kaifu Wu ◽

Meng Liu ◽

Guoshu Zhao ◽

Laichang He ◽

Yongming Tan

Keyword(s):

Carbon Monoxide ◽

Resting State ◽

Carbon Monoxide Poisoning ◽

Resting State Fmri ◽

Regional Homogeneity ◽

Fmri Study ◽

Delayed Encephalopathy

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LRCH1 polymorphisms linked to delayed encephalopathy after acute carbon monoxide poisoning identified by GWAS analysis followed by Sequenom MassARRAY® validation

BMC Medical Genetics ◽

10.1186/s12881-019-0931-7 ◽

2019 ◽

Vol 20 (1) ◽

Cited By ~ 2

Author(s):

Jiapeng Gu ◽

Jiao Zeng ◽

Xi Wang ◽

Xin Gu ◽

Xiaoli Zhang ◽

...

Keyword(s):

Carbon Monoxide ◽

Association Analysis ◽

Carbon Monoxide Poisoning ◽

Genetic Models ◽

Nucleotide Polymorphisms ◽

Sequenom Massarray ◽

Acute Carbon Monoxide Poisoning ◽

Diagnosis And Prognosis ◽

Increased Risk ◽

Delayed Encephalopathy

Abstract Background We explored the association of leucine-rich repeats and calponin homology domain containing 1 (LRCH1) gene polymorphisms with genetic susceptibility to delayed encephalopathy after acute carbon monoxide poisoning (DEACMP), which might provide a theoretical basis for the pathogenesis, diagnosis, and prognosis research of DEACMP. Methods Four single nucleotide polymorphisms, rs1539177 (G/A), rs17068697 (G/A), rs9534475 (A/C), and rs2236592 (T/C), of LRCH1, selected as candidate genes through genome-wide association analysis, were genotyped in 661 patients (DEACMP group: 235 cases; ACMP group: 426 cases) using Sequenom Massarray®. The association analysis of four SNPs and LRCH1 was performed under different genetic models. Results LRCH1 polymorphisms (rs1539177, rs17068697, rs9534475) under additive and dominant genetic models were significantly associated with an increased risk of DEACMP, but no significant association under allele and recessive models was found. The LRCH1 rs2236592 polymorphism was susceptible to DEACMP only under the dominant model (TT/TC + CC, OR = 1.616, 95% CI: 1.092–2.390, P = 0.015784). In addition, the A allele gene of rs9534475 polymorphism in LRCH1 might increase the risk for DEACMP (OR = 1.273, 95% CI: 1.013–1.601, P = 0.038445). Conclusions We found a significant association between the four LRCH1 polymorphisms and DEACMP. The allelic A of rs9534475 polymorphism in LRCH1 might be a risk factor for DEACMP.

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