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 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 Multiple Victims of Carbon Monoxide Poisoning in the Aftermath of a Wildfire: A Case Series

2018 ◽  
Vol 31 (3) ◽  
pp. 146 ◽  
Author(s):  
Luís Ramos dos Santos ◽  
Magna Alves-Correia ◽  
Margarida Câmara ◽  
Manuela Lélis ◽  
Carmo Caldeira ◽  
...  
Keyword(s):  
Carbon Monoxide ◽  
Hyperbaric Oxygen ◽  
Clinical Symptoms ◽  
Carbon Monoxide Poisoning ◽  
Case Series ◽  
Neurological Syndrome ◽  
High Flow Oxygen ◽  
Lost To Follow Up ◽  
Mean Time

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.

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.

The impact of hyperthermia after acute carbon monoxide poisoning on neurological sequelae

2018 ◽  
Vol 38 (4) ◽  
pp. 455-465 ◽  
Author(s):  
JM Moon ◽  
BJ Chun ◽  
SD Lee ◽  
MH Shin
Keyword(s):  
Carbon Monoxide ◽  
Carbon Monoxide Poisoning ◽  
Early Period ◽  
Maximum Temperature ◽  
Co Poisoning ◽  
Neurological Sequelae ◽  
Neurological Outcomes ◽  
Significant Difference ◽  
The Impact

This study investigated whether hyperthermia within the first 24 h after presentation was associated with long-term neurological outcomes after acute carbon monoxide (CO) poisoning. This retrospective study included 200 patients with acute severe CO poisoning. Hyperthermia (≥ 37.5°C) developed during the first 24 h after presentation in 55 (27.5%) patients, and poor long-term neurological sequelae assessed at 23 months after acute CO poisoning developed in 19.5% of the patients. The incidence of poor long-term neurological outcomes was significantly higher in the hyperthermia group than in the normothermia group. Patients with poor long-term neurological outcomes had higher maximum temperatures than patients with good outcomes. No significant difference was found in the time of hyperthermia onset within the first day according to the neurological outcomes. Hyperthermia (adjusted odds ratio (aOR) 5.009 (95% confidence interval (CI) 1.556–16.126)) and maximum temperature (aOR 2.581 (95% CI 1.098–6.063)) within the first 24 h after presentation to the emergency department were independently associated with poor long-term neurological outcomes. Body temperature measurements, which are easily and noninvasively recorded at the bedside in any facility, help to predict the risk for poor long-term neurological outcomes. This study carefully emphasizes fastidious control of pyrexia, particularly during the early period after acute CO poisoning.

scholarly journals Impact of Hyperbaric Oxygen Therapy on Subsequent Neurological Sequelae Following Carbon Monoxide Poisoning

2018 ◽  
Vol 7 (10) ◽  
pp. 349 ◽  
Author(s):  
Chien-Cheng Huang ◽  
Chung-Han Ho ◽  
Yi-Chen Chen ◽  
Chien-Chin Hsu ◽  
Yi-Fong Wang ◽  
...  
Keyword(s):  
Carbon Monoxide ◽  
Hyperbaric Oxygen ◽  
Hyperbaric Oxygen Therapy ◽  
Oxygen Therapy ◽  
Carbon Monoxide Poisoning ◽  
Population Based ◽  
Chronic Obstructive ◽  
Monthly Income ◽  
Neurological Sequelae ◽  
Increased Risk

The purpose of this study was to evaluate the effects of hyperbaric oxygen therapy (HBOT) on reducing neurological sequelae (NS) in patients with carbon monoxide poisoning (COP). Using a nationwide database of insurance claims in Taiwan, we conducted a population-based cohort study to identify 24,046 patients with COP diagnosed between 1999 and 2012, including 6793 (28.2%) patients who received HBOT and 17,253 (71.8%) patients who did not. We followed the two cohorts of patients and compared the occurrence of NS. The two cohorts had similar sex ratios, but patients who received HBOT were younger (34.8 ± 14.8 vs. 36.1 ± 17.2 years, p < 0.001). Patients who received HBOT had a higher risk for NS (adjusted hazard ratio [AHR]: 1.4; 95% confidence interval [CI]: 1.4–1.5), after adjusting for age, sex, underlying comorbidities (hypertension, diabetes, chronic obstructive pulmonary disease, hyperlipidemia, malignancy, coronary artery disease, congestive heart failure, liver disease, renal disease, connective tissue disease, human immunodeficiency virus [HIV] infection, and alcoholism), monthly income, suicide, drug poisoning, and acute respiratory failure. We observed similar findings when we stratified the patients by age, sex, underlying comorbidities, and monthly income. The increased risk was most prominent in the first 2 weeks (AHR: 2.4; 95% CI: 2.1–2.7) and remained significant up to 6 months later (AHR: 1.6; 95% CI: 1.4–1.7). The risk for NS was higher in patients with COP who received HBOT than in those who did not, even after considering the possible impact of longer observation periods on survivors. Further studies that included the potential confounding factors we did not measure are needed to confirm findings in this study.

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