Real-world effectiveness of hyperbaric oxygen therapy for delayed neuropsychiatric sequelae after carbon monoxide poisoning.
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ABSTRACT:
SUBMITTER: Liao SC
PROVIDER: S-EPMC8479087 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Carbon monoxide (CO) has been the leading cause of poisoning mortality in many countries and hyperbaric oxygen (HBO) is a widely accepted treatment for CO poisoning. However, some patients with CO poisoning will still develop neurocognitive sequelae regardless of HBO therapy, which can persist since CO poisoning or be present days to weeks after a recovery from CO poisoning. HBO has been used in the prevention and treatment of neurocognitive sequelae after CO poisoning, and some mechanisms are also proposed for the potential neuroprotective effects of HBO on the neurocognitive impairment after CO poisoning, but there is still controversy on the effectiveness of HBO on neurocognitive sequelae after CO poisoning. In this paper, we briefly introduce the neurocognitive sequelae after CO poisoning, summarize the potential predictive factors of neurocognitive sequelae, and discuss the use of HBO in the treatment and prevention of neurocognitive sequelae after CO poisoning.
| S-EPMC7871936 | biostudies-literature
Project description:BACKGROUND:Poisoning with carbon monoxide (CO) remains an important cause of accidental and intentional injury worldwide. Several unblinded non-randomized trials have suggested that the use of hyperbaric oxygen (HBO) prevents the development of neurological sequelae. This has led to the widespread use of HBO in the management of patients with carbon monoxide poisoning. OBJECTIVES:To examine randomised trials of the efficacy of hyperbaric oxygen (HBO) compared to normobaric oxygen (NBO) for the prevention of neurologic sequelae in patients with acute carbon monoxide poisoning. SEARCH STRATEGY:We searched the following electronic databases; Cochrane Injuries Group Specialised Register (searched June 2010), Cochrane Central Register of Controlled Trials (The Cochrane Library 2010, Issue 2), MEDLINE (Ovid SP) 1950 to June 2010, EMBASE (Ovid SP) 1980 to June 2010, ISI Web of Science: Science Citation Index Expanded (SCI-EXPANDED) 1970 to June 2010, ISI Web of Science: Conference Proceedings Citation Index-Science (CPCI-S) 1990 to June 2010. SELECTION CRITERIA:All randomised controlled trials of HBO compared to NBO, involving non-pregnant adults who are acutely poisoned with carbon monoxide (regardless of severity). DATA COLLECTION AND ANALYSIS:Two authors independently extracted from each trial information on: the number of randomised patients, types of participants, the dose and duration of the intervention, and the prevalence of neurologic symptoms at follow-up. MAIN RESULTS:Seven randomised controlled trials of varying quality were identified; one was excluded because it did not evaluate clinical outcomes. Of the six remaining trials involving 1361 participants, two found a beneficial effect of HBO for the reduction of neurologic sequelae at one month, while four others did not. One of these is an incomplete publication (an abstract of an interim analysis). Although pooled random effects meta-analysis does not suggest a significant benefit from HBOT (OR for neurological deficits 0.78, 95%CI 0.54 to 1.12), significant methodologic and statistical heterogeneity was apparent among the trials, and this result should be interpreted cautiously. Moreover, design or analysis flaws were evident in all trials. Importantly, the conclusions of one positive trial may have been influenced by failure to adjust for multiple hypothesis testing, while interpretation of the other positive trial is hampered by a high risk of bias introduced during the analysis including an apparent change in the primary outcome. Both were also stopped early 'for benefit', which is likely to have inflated the observed effect. In contrast three negative trials had low power to detect a benefit of HBO due to exclusion of severely poisoned patients in two and very poor follow-up in the other. One trial that was said to be finished around eight years ago has not reported the final analysis in any forum. AUTHORS' CONCLUSIONS:Existing randomised trials do not establish whether the administration of HBO to patients with carbon monoxide poisoning reduces the incidence of adverse neurologic outcomes. Additional research is needed to better define the role, if any, of HBO in the treatment of patients with carbon monoxide poisoning. This research question is ideally suited to a multi-center randomised controlled trial.
| S-EPMC7066484 | biostudies-literature
Project description: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.
| S-EPMC6211110 | biostudies-literature
Project description:ObjectiveDelayed neuropsychiatric sequelae (DNS) are serious complications of carbon monoxide (CO) poisoning that adversely affect poisoned patients' quality of life as well as socioeconomic status. This study aimed to determine clinical predictors of DNS in patients with CO poisoning.MethodsThis retrospective study included all CO-poisoned patients admitted to the emergency department (ED) of Linkou Chang Gung Memorial Hospital in Taiwan from 1 January 2009 to 31 December 2015. The medical records of all patients with CO poisoning were carefully reviewed, and relevant data were abstracted into a standardised form. Univariate and multivariate logistic regression models were used to identify predictors of DNS after CO poisoning. Receiver operating characteristic (ROC) curve analysis was used to determine the ideal cut-off value for continuous variables that predict the development of DNS.ResultsA total of 760 patients with CO poisoning were identified during the study period. Among them, 466 were eligible for the analysis of predictors of DNS. In multivariate analysis, Glasgow Coma Scale <9 (odds ratio [OR], 2.74; 95% confidence interval [CI], 1.21-6.21), transient loss of consciousness (OR, 3.59; 95% CI, 1.31-9.79), longer duration from CO exposure to ED presentation (OR, 1.05; 95% CI, 1.03-1.08), and corrected QT (QTc) prolongation (OR, 2.61; 95% CI, 1.21-5.61) were found to be associated with a higher risk of DNS. The area under the ROC curve (AUC) for QTc interval measured within 6?h after exposure best predicted the development of DNS, with a result of 0.729 (95% CI 0.660-0.791). Moreover, the best cut-off value of the QTc interval was 471?ms, with a sensitivity of 53.3% and a specificity of 85.1%.ConclusionsWe identified several potential predictors of DNS following CO poisoning. Among them, QTc prolongation found within 6?h after exposure is a novel predictor of DNS, which may be helpful in the future care of patients with CO poisoning.
| S-EPMC6176310 | biostudies-literature
Project description:AbstractThis study aimed at assessing which one of the 2 therapies is better for treating carbon monoxide (CO) poisoning from the perspective of reducing delayed neuropsychologic sequelae (DNS).We used Taiwan's National Health Insurance Research Database (NHIRD) to conduct a nationwide population-based cohort study to assess which therapy is better for CO poisoning patients. To accurately identify patients with DNS, the definition of DNS is included neurological sequelae, and cognitive and psychological sequele. The independent variable was therapy and the dependent variable was DNS occurred within 1 year after discharge from a medical institution. The control variables were age, gender, the severity of CO poisoning, and comorbidities present before CO poisoning admission.The risk of developing DNS in patients treated with Hyperbaric Oxygen (HBO) was 1.87-fold (P < .001) than normobaric oxygen (NBO) therapy. The severity of CO poisoning and comorbidities were also found to have significant influences on the risk of developing DNS.HBO may be a risk therapy for treating CO poisoning.
| S-EPMC7808522 | biostudies-literature
Project description:AbstractSmoking is a well-known risk factor for cardio-cerebrovascular disease. However, several studies have reported the "smoker's paradox" whereby smokers have a better prognosis for cardio-cerebrovascular diseases. Similar to cardio-cerebrovascular diseases, hypoxia is one of the major mechanisms of injury in carbon monoxide (CO) poisoning. This study investigated the association between smoking and delayed neuropsychiatric sequelae (DNS) in acute CO poisoning.This study involved patients with CO poisoning treated at a university hospital in Bucheon, Korea between September 2017 and March 2020. The exclusion criteria were age <18 years, discharge against medical advice, loss to follow-up, persistent neurological symptoms at discharge, transfer from another hospital 24 hours after exposure, and transfer from another hospital after hyperbaric oxygen therapy. Logistic regression analysis was performed to find factors associated with DNS.Two hundred sixty three patients visited the hospital due to CO poisoning and of these, 54 were excluded. DNS was evaluated up to 3 months after discharge, and until this time, DNS occurred in 35 (16.8%) patients. And the incidence rate of DNS was lower in smokers than non-smokers (15, 12% vs 20, 23.8%, P = .040). Multivariable logistic regression analysis revealed that CO exposure time (odds ratio [OR] 1.003; confidence interval [CI] 1.001-1.005; P = .003), the Glasgow coma scale (GCS) (OR 0.862; CI 0.778-0.956; P = .005), and pack-years (OR 0.947; CI 0.903-0.993; P = .023) were statistically significant for DNS development.These results indicate that more pack-years smoked were associated with reduced risk of the development of DNS in acute CO poisoning, and that CO exposure time and GCS is a predictive factor for DNS occurrence.
| S-EPMC8137110 | biostudies-literature
Project description:BackgroundThe 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.MethodsWe 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.ResultsA 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).ConclusionsThe 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.
| S-EPMC8213185 | biostudies-literature
Project description:Delayed neuropsychological sequelae (DNS) are the most severe and clinically intractable complications following acute carbon monoxide (CO) poisoning. Symptoms of DNS often resemble those of Parkinson's disease (PD), suggesting shared neurological deficits. Furthermore, Parkinson protein 2 (PARK2) mutations are associated with PD and other neurodegenerative diseases. The association signal was detected between PARK2 and DNS after acute CO poisoning in our DNA pooling base genome-wide association study.Two PARK2 single nucleotide polymorphisms (SNPs), rs1784594 (C/T allele) and rs1893895 (G/A allele), selected from DNA pooling base genome-wide association study, were genotyped by in 514 CO poisoning patients using polymerase chain reaction restriction fragment length polymorphisms (PCR-RFLPs). The patient group consisted of 231 patients with DNS and 283 patients with no signs of lasting neurological damage (control population).The frequency of the rs1784594 T allele was significantly lower in the DNS population (OR?=?1.42, 95%CI: 1.08?-?1.87), as was the TT vs. CC genotype (OR?=?1.95, 95%CI: 1.15?-?3.23) and the TT vs. CT?+?CC frequency (OR?=?1.68, 95%CI: 1.32?-?2.49) compared to controls. Association analysis revealed a significant association between DNS and rs1784594 (P?<?0.01) but not rs1893895 (P?>?0.05). In female cases, the T allele frequency of rs1784594 was significantly lower in DNS patients compared to female controls (OR?=?1.48, 95%CI: 1.01?-?2.17).These data suggest that the allelic variant of rs1784594 is a risk factor for DNS following acute CO poisoning, especially in females. The PARK2 protein may modulate the susceptibility to DNS, underscoring the importance of examining the relationship between other PARK2 polymorphisms and clinical outcome following CO poisoning.
| S-EPMC3849006 | biostudies-literature
Project description:Delayed neurologic sequelae (DNS) are recurrent-transient neuropsychiatric consequences of carbon monoxide (CO) intoxication. Pathologically DNS features damages to the brain white matter. Here we test a hypothesis that direct cytotoxicity of CO to oligodendrocytes plays a role in the development of DNS. In an in vitro model of CO poisoning with the carbon monoxide releasing molecule-2 (CORM-2) as a CO donor, we show that CORM-2 at concentrations higher than 200 µM significantly inhibited viability and caused significant death of PC12 cells. Similar minimum toxicity concentration was observed on primary brain cells including neurons, astrocytes, and microglia. Interestingly, oligodendrocytes showed cytotoxicity to CORM-2 at a much lower concentration (100 µM). We further found that CORM-2 at 100 µM inhibited proteolipid protein (PLP) production and reduced myelin coverage on axons in an in vitro model of myelination. Our results show that direct cytotoxicity is a mechanism of CO poisoning and DNS may result from a high susceptibility of oligodendrocytes to CO poisoning.
| S-EPMC7438756 | biostudies-literature
Project description:ObjectivesCarbon 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.MethodsThis 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.ResultsDuring 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.ConclusionsHigher 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.
| S-EPMC7799805 | biostudies-literature