Multicenter retrospective analysis of the risk factors for delayed neurological sequelae after acute carbon monoxide poisoning

Zhang, Yongxue; Lu, Qingsheng; Jia, Jing; Xiang, Dekun; Xi, Yanan

doi:10.1016/j.ajem.2020.06.090

Cited by 18 publications

(20 citation statements)

References 16 publications

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“…Patients with carbon monoxide poisoning (COP) commonly have long-term morbidities [35]. High-flow oxygen may be sufficient to treat patients with CO poisoning where hyperbaric oxygen is not available [36].…”

Section: Discussionmentioning

confidence: 99%

Exploring Health Impacts of Occupational Exposure to Carbon Monoxide in the Labour Community of Hattar Industrial Estate

et al. 2022

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This study was designed to assess the health impacts related to noninvasive carbon monoxide saturation (SPCO %) in the blood of respondents. For this purpose, 150 respondents from the labour community of Hattar Industrial Estate (testing site) and 100 respondents from Sultan Pur (control site) were selected. To achieve this objective, a Rad-57 Pulse CO-Oximeter was used for noninvasive carboxyhemoglobin measurement. Carbon monoxide saturation (SPCO%) in the blood of respondents from Hattar Industrial Estate, Haripur, Pakistan has been compared with the WHO’s standard concentration of SPCO% (5%). High saturation of carbon monoxide (carboxyhemoglobin SPCO) in the blood of respondents and disease association have been interpreted in graphs formed on the basis of statistical analysis in terms of frequencies, using statistical software (SPSS), based on demographic entries as well as exposure time of the employees in the processing, food and steel industries. The highest SPCO% measured was 17% in the steel industry and the lowest measured level was 4.2%. Frequencies and percentages of respiratory inflammation, dermatosis, asthma, breathing issues and eye inflammation among respondents were 29%, 35%, 16.7%, 23.5% and 9%, respectively. Prevalence of disease in three different groups of respondents (from three testing sites) was also analyzed on the basis of exposure time (hrs.) to carbon monoxide emissions. Prevalence of disease among the exposed and non-exposed groups was analyzed and showed comparatively lower disease prevalence in the group of respondents who were not exposed to high carbon monoxide emissions. The data of the current study was also subjected to statistical modelling to find the health risk of air pollutants (carbon monoxide) on population health by calculating attributable risk (AR) or attributable proportion (AP). Results indicated that attributable risk of carbon monoxide exposure for respiratory diseases, dermatosis and eye inflammation were 61.12%, 65.77% and 24.95% respectively. Findings of statistical modelling indicated that dermatosis and respiratory diseases were more prevalent in laborers of industrial units than those at control site.

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Section: Discussionmentioning

confidence: 99%

Exploring Health Impacts of Occupational Exposure to Carbon Monoxide in the Labour Community of Hattar Industrial Estate

et al. 2022

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“…Zhang et al 23 found that both the GCS scores on site and in the ED independently predicted DNS. Ku et al 24 also reported similar result that lower GCS scores could be a meaningful predictor for developing DNS.…”

Section: Discussionmentioning

confidence: 99%

Prediction of delayed neuropsychiatric sequelae after carbon monoxide poisoning via serial determination of serum neuron-specific enolase levels

et al. 2021

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Background Neuron-specific enolase (NSE) is released into serum when nerve cells are damaged, and the levels thereof are used to determine neurological prognosis in patients who have suffered cardiac arrest or stroke. Delayed neuropsychiatric sequelae (DNS), a major complication of carbon monoxide poisoning (COP), can be caused by inflammatory response which is a mechanism of neuronal injury in cardiac arrest and stroke. NSE is known as a predictor of neurological prognosis in ischemic brain injury after cardiac arrest, and it is also reported as a predictor of DNS in acute COP. When serum NSE is measured serially in cardiac arrest patients, the best time to predict neurological prognosis is known at 48–72 h, but there are no studies analyzing serial serum NSE in acute COP. Thus, we explored whether serum NSE levels measured three times at 24 h intervals after COP predicted the development of DNS. Methods This prospective observational study was conducted on patients treated for COP from May 2018 to April 2020 in a tertiary care hospital in Korea. Neuron-specific enolase levels were assessed 24, 48, and 72 h after presentation at hospital. We used logistic regression to explore the association between NSE levels and DNS development. Results The NSE level was highest at 48 h, and the difference between the DNS group and the non-DNS group was greatest on the same time point. On multivariable logistic regression analysis, the NSE level at 48 h of >20.98 ng/mL (odds ratio [OR], 3.570; 95% confidence interval [CI], 1.412–9.026; P = .007) and the initial Glasgow Coma Scale (GCS) score of <9 (OR, 4.559; 95% CI, 1.658–0.12.540; P = .003) was statistically significant for DNS development. Conclusion Early identification of those who will experience DNS in acute COP patients is clinically important for deciding treatment. In this study, we revealed that NSE level of >20.98 ng/mL at 48 h time point can be used as an independent predictor of DNS (OR, 3.570; 95% CI, 1.412–9.026; P = .007; AUC, 0.648).

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“…For widespread applicability, we limited variables to known and potential risk factors 6 , 7 , 12 , 13 , 14 , 15 , 16 , 17 , 18 , 19 , 20 and commonly used variables in acute co poisoning. We evaluated patient age, sex, poisoning intentions, co source (ie, charcoal, oil and gas, or fire), drug coingestion, GCS score at the site of rescue or ED arrival, comorbidities (ie, diabetes, hypertension, cardiovascular disorder, and psychiatric disease), current smoking status and alcohol coingestion, interval of loss of consciousness, shock, seizure, and application of HBO (eAppendix 1 in the Supplement ).…”

Section: Methodsmentioning

confidence: 99%

“…Clinical and laboratory variables suggested for predicting poor neurocognitive prognosis 6 , 7 , 12 , 13 , 14 , 15 , 16 , 17 , 18 , 19 , 20 include older age, underlying cardiovascular disease, any interval loss of consciousness, acidosis, Glasgow Coma Scale (GCS) score, serum creatine kinase level, longer co exposure intervals, serum lactate level, and HBO treatment. As there is no validated simple and accurate clinical scoring model for stratifying patients according to their risk of poor neurocognitive prognosis in early phase, we aimed to develop and validate a simple, accurate clinical scoring model for predicting poor neurocognitive outcomes at 1 month after co poisoning.…”

Section: Introductionmentioning

confidence: 99%

Derivation and Validation of a Score for Predicting Poor Neurocognitive Outcomes in Acute Carbon Monoxide Poisoning

et al. 2022

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Key Points Question Can a novel clinical scoring system predict poor neurocognitive outcomes after acute carbon monoxide poisoning? Findings This prognostic study developed and externally validated a prediction model including 5 risk factors associated with poor neurocognitive outcome at 1 month, creatine kinase level, hyperbaric oxygen therapy, Glasgow Coma Scale score, age, and shock (COGAS score), among patients with carbon monoxide poisoning. COGAS score showed excellent discrimination performance. Meaning These findings suggest that use of a reliable prediction model during the early phase of carbon monoxide poisoning could help identify patients at risk of poor neurocognitive sequelae.

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Multicenter retrospective analysis of the risk factors for delayed neurological sequelae after acute carbon monoxide poisoning

Cited by 18 publications

References 16 publications

Exploring Health Impacts of Occupational Exposure to Carbon Monoxide in the Labour Community of Hattar Industrial Estate

Exploring Health Impacts of Occupational Exposure to Carbon Monoxide in the Labour Community of Hattar Industrial Estate

Prediction of delayed neuropsychiatric sequelae after carbon monoxide poisoning via serial determination of serum neuron-specific enolase levels

Derivation and Validation of a Score for Predicting Poor Neurocognitive Outcomes in Acute Carbon Monoxide Poisoning

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