scholarly journals Use of hyperbaric oxygen therapy for preventing delayed neurological sequelae in patients with carbon monoxide poisoning: A multicenter, prospective, observational study in Japan

PLoS ONE ◽  
2021 ◽  
Vol 16 (6) ◽  
pp. e0253602
Author(s):  
Motoki Fujita ◽  
Masaki Todani ◽  
Kotaro Kaneda ◽  
Shinya Suzuki ◽  
Shinjiro Wakai ◽  
...  
Keyword(s):  
Carbon Monoxide ◽  
Observational Study ◽  
Hyperbaric Oxygen ◽  
Prospective Observational Study ◽  
Carbon Monoxide Poisoning ◽  
Clinical Treatment ◽  
Co Poisoning ◽  
Neurological Sequelae ◽  
Factors Associated ◽  
Multicenter Prospective Observational Study

Background The purpose of this study was to clarify the practical clinical treatment for acute carbon monoxide (CO) poisoning in Japan and to investigate the efficacy of hyperbaric oxygen (HBO2) therapy in preventing delayed neurological sequelae (DNS) in the acute phase of CO poisoning. Methods We conducted a multicenter, prospective, observational study of acute CO poisoning in Japan. Patients with acute CO poisoning were enrolled and their treatment details were recorded. The primary endpoint was the onset of DNS within 2 months of CO exposure. Factors associated with DNS were assessed with logistic regression analysis. Results A total of 311 patients from 57 institutions were registered and 255 were analyzed: 171 received HBO2 therapy (HBO2 group) and 84 did not (normobaric oxygen [NBO2] group). HBO2 therapy was performed zero, once, twice, or three times within the first 24 h in 1.8%, 55.9%, 30.9%, and 11.3% of the HBO2 group, respectively. The treatment pressure in the first HBO2 session was 2.8 ATA (47.9% of the HBO2 group), 2.0 ATA (41.8%), 2.5 ATA (7.9%), or another pressure (2.4%). The incidence of DNS was 13/171 (7.6%) in the HBO2 group and 3/84 (3.6%) in the NBO2 group (P = 0.212). The number of HBO2 sessions in the first 24 h was one of the factors associated with the incidence of DNS (odds ratio, 2.082; 95% confidence interval, 1.101–3.937; P = 0.024). Conclusions The practical clinical treatment for acute CO poisoning, including HBO2 therapy, varied among the institutions participating in Japan. HBO2 therapy with inconsistent protocols showed no advantage over NBO2 therapy in preventing DNS. Multiple HBO2 sessions was associated with the incidence of DNS.

scholarly journals Variability in Treatment for Carbon Monoxide Poisoning in Japan: A Multicenter Retrospective Survey

2018 ◽  
Vol 2018 ◽  
pp. 1-5
Author(s):  
Motoki Fujita ◽  
Yasutaka Oda ◽  
Kotaro Kaneda ◽  
Yoshikatsu Kawamura ◽  
Takashi Nakahara ◽  
...  
Keyword(s):  
Carbon Monoxide ◽  
Observational Study ◽  
Online Survey ◽  
Prospective Observational Study ◽  
Carbon Monoxide Poisoning ◽  
Co Poisoning ◽  
Neurological Sequelae ◽  
Retrospective Survey ◽  
Consciousness Disturbance ◽  
Long Time

Background. The aim of this study was to identify practice differences in the treatment of carbon monoxide (CO) poisoning with or without hyperbaric oxygen (HBO2) therapy in Japan. Materials and Methods. Using an online survey website (Google form), we created a questionnaire and invited interested institutions to join the COP-J Study, a prospective observational study of CO poisoning in Japan. Results. Forty-eight (63%) of 76 institutions replied to the questionnaire. Thirty-three institutions (69%) administered HBO2 therapy to patients with CO poisoning, and 15 institutions (31%) did not. Consciousness disturbance on arrival, exposure to CO for a long time, and elevation of arterial carboxyhemoglobin (CO-Hb) were the major indications for HBO2 therapy. The maximum therapeutic pressures were 2.0, 2.5, and 2.8 atmospheres absolute (ATA) at 19 (58%), 6 (18%), and 8 (24%) institutions, respectively. The number of HBO2 sessions on the first day was 1–3, and 1–7 sessions were administered on days 2–7. Seventeen (35%) institutions treated patients with delayed neurological sequelae (DNS) and 15 of them used HBO2 therapy for DNS. Conclusions. This survey indicates that HBO2 therapy for CO poisoning was varied in both the indications and practice regimens used in Japan.

Current and research therapies for the prevention and treatment of delayed neurological syndrome associated with carbon monoxide poisoning: A narrative review

2020 ◽  
Vol 39 (6) ◽  
pp. 765-772
Author(s):  
B del Moral-Barbudo ◽  
R Blancas ◽  
D Ballesteros-Ortega ◽  
M Quintana-Díaz ◽  
Ó Martínez-González
Keyword(s):  
Carbon Monoxide ◽  
Hyperbaric Oxygen ◽  
Carbon Monoxide Poisoning ◽  
Narrative Review ◽  
Co Poisoning ◽  
Common Environment ◽  
Neurological Sequelae ◽  
Neurological Syndrome ◽  
Oxygen Administration ◽  
Prevention And Treatment

Severe carbon monoxide (CO) poisoning causes fulminant deaths in common environment as well as neurological sequelae to survivors. Prevention of delayed neurological syndrome (DNS) after exposure to CO, the most important sequela, is based up to date on hyperbaric oxygen administration. Nevertheless, its use remains controversial due to the lack of evidence regarding its efficacy. The aim of this review is to report therapies under investigation for preventing or improving DNS, some of them with promising results in humans.

scholarly journals Effect of ethanol in carbon monoxide poisoning and delayed neurologic sequelae: A prospective observational study

PLoS ONE ◽  
2021 ◽  
Vol 16 (1) ◽  
pp. e0245265
Author(s):  
Sungwoo Choi ◽  
Sangsoo Han ◽  
Sangun Nah ◽  
Young Hwan Lee ◽  
Young Soon Cho ◽  
...  
Keyword(s):  
Carbon Monoxide ◽  
Observational Study ◽  
Prospective Observational Study ◽  
Neuroprotective Effect ◽  
Carbon Monoxide Poisoning ◽  
Co Poisoning ◽  
Ethanol Level ◽  
Neurologic Sequelae ◽  
Gcs Score ◽  
Delayed Neurologic Sequelae

Objectives Carbon monoxide (CO) is one of the most common poisoning substances, which causes mortality and morbidity worldwide. Delayed neurologic sequelae (DNS) have been reported to occur from several days to months after exposure to CO. Thus, there is a need for prevention, recognition, and treatment of DNS. Patients with CO poisoning as a component of intentional suicide often also consume ethanol, but there is debate regarding its role in DNS. We explored whether ethanol has a neuroprotective effect in CO poisoning. Methods This prospective observational study included patients who visited the emergency department from August 2016 to August 2019 due to CO poisoning. After treatment of acute CO poisoning, patients were interviewed by telephone to ascertain whether DNS had occurred within 2 weeks, 1 month, and 3 months from the time of CO exposure. Results During the study period, 171 patients were enrolled. 28 patients (16.37%) developed DNS. The initial Glasgow Coma Scale (GCS) scores were 15 (10.5–15) for the non-DNS group and 10 (7–15) for the DNS group (p = 0.002). The ethanol levels were 11.01 ± 17.58 mg/dL and 1.49 ± 2.63 mg/dL for each group (p < 0.001). In multivariate logistic regression analysis, the GCS score had an odds ratio of 0.770 (p < 0.001) and the ethanol level had 0.882 (p < 0.030) for onset of DNS. Conclusions Higher ethanol level and higher initial GCS score were associated with lower incidence of DNS. Ethanol could have a neuroprotective effect on the occurrence of DNS in CO poisoning patients.

Neurological Sequelae of Carbon Monoxide Poisoning: Role of Hyperbaric Oxygen

1995 ◽  
Vol 4 (3-4) ◽  
pp. 134-139
Author(s):  
Raffaella Butera ◽  
Stefano M. Candura ◽  
Carlo Locatelli ◽  
Concettina Varango ◽  
Bin Li ◽  
...  
Keyword(s):  
Carbon Monoxide ◽  
Hyperbaric Oxygen ◽  
Carbon Monoxide Poisoning ◽  
Neurological Sequelae

scholarly journals Real-world effectiveness of hyperbaric oxygen therapy for delayed neuropsychiatric sequelae after carbon monoxide poisoning

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Shu-Chen Liao ◽  
Shih-Chieh Shao ◽  
Kun-Ju Yang ◽  
Chen-Chang Yang
Keyword(s):  
Carbon Monoxide ◽  
Hyperbaric Oxygen ◽  
Real World ◽  
Roc Curve ◽  
Hyperbaric Oxygen Therapy ◽  
Oxygen Therapy ◽  
Carbon Monoxide Poisoning ◽  
Chang Gung Memorial Hospital ◽  
Co Poisoning ◽  
Delayed Neuropsychiatric Sequelae

AbstractTo assess real-world effectiveness of hyperbaric oxygen therapy (HBOT) on delayed neuropsychiatric sequelae (DNS) after carbon monoxide (CO) poisoning we conducted a retrospective review of patients with CO poisoning admitted to Linkou Chang-Gung Memorial Hospital, Taiwan’s largest medical center, during 2009–2015. We included patients developing DNS after CO poisoning and compared improvements in neuropsychiatric function, with and without HBOT, after 12 months post-DNS to understand differences in recovery rates. DNS improvement-associated factors were also evaluated. We used receiver operating characteristic (ROC) curve analysis to assess the role of time elapsed between DNS diagnosis and HBOT initiation in predicting DNS improvement. A total of 62 patients developed DNS, of whom 11 recovered while the rest did not. Possible factors predicting DNS improvement included receiving HBOT post-DNS (72.7% vs 25.5%; P = 0.006), and treatment with more than three HBOT sessions during acute stage CO poisoning (81.8% vs 27.5%; P = 0.003). The relevant area under the ROC curve was 0.789 (95% CI 0.603–0.974), and the best cut-off point was 3 days post-DNS diagnosis, with 87.5% sensitivity and 61.5% specificity. Early HBOT in patients who developed DNS after CO poisoning significantly improved their DNS symptoms, with treatment effects sustained for 1 year after DNS diagnosis.

Carbon monoxide poisoning can act as a stress test to reveal underlying coronary artery disease: case report

2020 ◽  
pp. 151-169
Author(s):  
Lindell K. Weaver ◽  
◽  
Keyword(s):  
Carbon Monoxide ◽  
Hyperbaric Oxygen ◽  
Carbon Monoxide Poisoning ◽  
Stress Test ◽  
The United States ◽  
Brain Inflammation ◽  
Smoke Inhalation ◽  
Co Poisoning ◽  
Exposure Limits ◽  
Disease Case

Despite established exposure limits and safety standards as well as the availability of carbon monoxide (CO) alarms, each year 50,000 people in the United States visit emergency departments for CO poisoning. Carbon monoxide poisoning can occur from brief exposures to high levels of CO or from longer exposures to lower levels. Common symptoms can include headaches, nausea and vomiting, dizziness, general malaise, and altered mental status. Some patients may have chest pain, shortness of breath, and myocardial ischemia, and may require mechanical ventilation and treatment of shock. Individuals poisoned by CO often develop brain injury manifested by neurological problems, including cognitive sequelae, anxiety and depression, persistent headaches, dizziness, sleep problems, motor weakness, vestibular and balance problems, gaze abnormalities, peripheral neuropathies, hearing loss, tinnitus, Parkinsonian-like syndrome, and other problems. In addition, some will have cardiac issues or other ailments. While breathing oxygen hastens the removal of carboxyhemoglobin (COHb), hyperbaric oxygen (HBO2) hastens COHb elimination and favorably modulates inflammatory processes instigated by CO poisoning, an effect not observed with breathing normobaric oxygen. Hyperbaric oxygen improves mitochondrial function, inhibits lipid peroxidation transiently, impairs leukocyte adhesion to injured microvasculature, and reduces brain inflammation caused by the CO-induced adduct formation of myelin basic protein. Based upon three supportive randomized clinical trials in humans and considerable evidence from animal studies, HBO2 should be considered for all cases of acute symptomatic CO poisoning. Hyperbaric oxygen is indicated for CO poisoning complicated by cyanide poisoning, often concomitantly with smoke inhalation.

Emerging Cellular-Based Therapies in Carbon Monoxide Poisoning

2021 ◽  
Author(s):  
David H. Jang ◽  
Sarah Piel ◽  
John C. Greenwood ◽  
Johannes K. Ehinger ◽  
Todd J. Kilbaugh
Keyword(s):  
Carbon Monoxide ◽  
Hydrogen Sulfide ◽  
Active Site ◽  
Carbon Monoxide Poisoning ◽  
Co Poisoning ◽  
Multiple Sources ◽  
Engine Exhaust ◽  
Neurological Sequelae ◽  
Carbon Compounds ◽  
House Fires

Carbon monoxide (CO) is an odorless and colorless gas has multiple sources that include engine exhaust, faulty furnaces and other sources of incomplete combustion of carbon compounds such as house fires. The most serious complications for survivors of consequential CO exposure is persistent neurological sequelae occurring in up to 50% of patients. CO inhibits mitochondrial respiration by specifically binding to the heme a3 in the active site of CIV like hydrogen sulfide, cyanide and phosphides. While hyperbaric oxygen remains the cornerstone for treatment, it has variable efficacy requiring new approaches to treatment. There are a paucity of cellular-based therapies in the area of CO poisoning, there have been recent advancements that include antioxidants and a mitochondrial substrate prodrug. The succinate prodrugs derived from chemical modification of succinate are endeavored to enhance delivery of succinate to cells, increasing uptake of succinate into the mitochondria, and providing metabolic support for cells. The therapeutic intervention of succinate prodrugs is thus potentially applicable to patients with CO poisoning via metabolic support for fuel oxidation and possibly improving efficacy of HBO therapy.

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