Serum neuron-specific enolase as an early predictor of delayed neuropsychiatric sequelae in patients with acute carbon monoxide poisoning

2017 ◽  
Vol 37 (3) ◽  
pp. 240-246 ◽  
Author(s):  
YS Cha ◽  
H Kim ◽  
HH Do ◽  
HI Kim ◽  
OH Kim ◽  
...  
Keyword(s):  
Carbon Monoxide ◽  
Troponin I ◽  
Carbon Monoxide Poisoning ◽  
Neuropsychiatric Symptoms ◽  
Neuron Specific Enolase ◽  
Additional Parameter ◽  
Co Poisoning ◽  
Early Predictors ◽  
Delayed Neuropsychiatric Sequelae ◽  
Serum Neuron Specific Enolase

Delayed onset of neuropsychiatric symptoms after apparent recovery from acute carbon monoxide (CO) poisoning has been described as delayed neuropsychiatric sequelae (DNS). To date, there have been no studies on the utility of serum neuron-specific enolase (NSE), a marker of neuronal cell damage, as a predictive marker of DNS in acute CO poisoning. This retrospective observational study was performed on adult patients with acute CO poisoning consecutively treated over a 9-month period. Serum NSE was measured after emergency department arrival, and patients were divided into two groups. The DNS group comprised patients with delayed sequelae, while the non-DNS group included patients with none of these sequelae. A total of 98 patients with acute CO poisoning were enrolled in this study. DNS developed in eight patients. The median NSE value was significantly higher in the DNS group than in the non-DNS group. There was a statistical difference between the non-DNS group and the DNS group in terms of CO exposure time, Glasgow Coma Scale (GCS), loss of consciousness, creatinine kinase, and troponin I. GCS and NSE were the early predictors of development of DNS. The area under the curve according to the receiver operating characteristic curves of GCS, serum NSE, and GCS combined with serum NSE were 0.922, 0.836, and 0.969, respectively. In conclusion, initial GCS and NSE served as early predictors of development of DNS. Also, NSE might be a useful additional parameter that could improve the prediction accuracy of initial GCS.

scholarly journals Predictive Role of QTc Prolongation in Carbon Monoxide Poisoning-Related Delayed Neuropsychiatric Sequelae

2018 ◽  
Vol 2018 ◽  
pp. 1-8
Author(s):  
Shu-Chen Liao ◽  
Yan-Chiao Mao ◽  
Yao-Min Hung ◽  
Ching-Hsing Lee ◽  
Chen-Chang Yang
Keyword(s):  
Carbon Monoxide ◽  
Roc Curve ◽  
Carbon Monoxide Poisoning ◽  
Chang Gung Memorial Hospital ◽  
Qtc Interval ◽  
Continuous Variables ◽  
Co Poisoning ◽  
Qtc Prolongation ◽  
Roc Curve Analysis ◽  
Delayed Neuropsychiatric Sequelae

Objective. Delayed 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. Methods. This 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. Results. A 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%. Conclusions. We 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.

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.

scholarly journals Amantadine Improves Delayed Neuropsychiatric Sequelae of Carbon Monoxide Poisoning: A Case Report

2019 ◽  
Vol 9 (11) ◽  
pp. 292 ◽  
Author(s):  
Tomosuke Nakano ◽  
Toshiki Hasegawa ◽  
Dai Suzuki ◽  
Eishi Motomura ◽  
Motohiro Okada
Keyword(s):  
Carbon Monoxide ◽  
Cognitive Impairment ◽  
Case Report ◽  
Brain Damage ◽  
Carbon Monoxide Poisoning ◽  
Gait Disturbance ◽  
Co Poisoning ◽  
Time And Space ◽  
Urine Incontinence ◽  
Delayed Neuropsychiatric Sequelae

Carbon monoxide (CO) poisoning causes severe brain damage, including delayed neuropsychiatric sequelae (DNS), which occur after a lucid interval following recovery from the insult of acute CO poisoning. We describe a 39-year-old male who developed DNS, including gait disturbance, trunk ataxia, and fecal/urine incontinence, after remission of acute CO poisoning. Furthermore, he showed confusion, with disorientation in terms of time and space. All symptoms, including cognitive impairment, were dramatically improved by amantadine monotherapy. The present case illustrates the possibility of amantadine treatment for cognitive impairment as well as Parkinsonism induced by CO poisoning.

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

2021 ◽  
pp. 096032712110434
Author(s):  
Sangun Nah ◽  
Sungwoo Choi ◽  
Gi Woon Kim ◽  
Ji Eun Moon ◽  
Young Hwan Lee ◽  
...  
Keyword(s):  
Carbon Monoxide ◽  
Logistic Regression ◽  
Cardiac Arrest ◽  
Carbon Monoxide Poisoning ◽  
Tertiary Care ◽  
Neuron Specific Enolase ◽  
Care Hospital ◽  
Delayed Neuropsychiatric Sequelae ◽  
Neurological Prognosis ◽  
Time Point

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).

scholarly journals High-Sensitivity Troponin I and Creatinine Kinase-Myocardial Band in Screening for Myocardial Injury in Patients with Carbon Monoxide Poisoning

Diagnostics ◽  
2020 ◽  
Vol 10 (4) ◽  
pp. 242 ◽  
Author(s):  
June-Sung Kim ◽  
Byuk Sung Ko ◽  
Chang Hwan Sohn ◽  
Youn-Jung Kim ◽  
Won Young Kim
Keyword(s):  
Carbon Monoxide ◽  
Troponin I ◽  
Myocardial Dysfunction ◽  
Carbon Monoxide Poisoning ◽  
Right Ventricular Dysfunction ◽  
High Sensitivity ◽  
Left Ventricular ◽  
Co Poisoning ◽  
High Sensitivity Troponin ◽  
Poor Outcomes

Myocardial dysfunction due to acute carbon monoxide (CO) poisoning is common and associated with poor outcomes. The role of cardiac markers, including creatine kinase-myocardial band (CK-MB), high-sensitivity troponin I (hsTnI), and brain natriuretic peptide (BNP), in identifying patients with CO-induced cardiomyopathy were evaluated. This single-center, retrospective cohort study included 905 consecutive adult patients in the CO poisoning registry from February 2009 to December 2019. Cardiomyopathy was defined as any abnormality on transthoracic echocardiography (TTE), including left ventricular systolic and diastolic dysfunction, right ventricular dysfunction, and wall motion abnormalities. The areas under receiver operating curves (AUCs) for biomarkers were compared. Of the 850 included patients, 101 (11.9%) had CO-induced cardiomyopathy. Initial and peak hsTnI and CK-MB concentrations, and initial BNP concentrations were significantly higher in patients with than without cardiomyopathy (all P-values < 0.01), but the AUCs were higher for hsTnI (0.894) and CK-MB (0.864) than for BNP (0.796). Initial TnI > 0.01 ng/mL and CK-MB > 1.5 ng/mL each had 95% sensitivity and 97% negative predictive value for CO-induced cardiomyopathy. Higher hsTnI or CK-MB levels on admission can identify patients at high-risk of CO-induced cardiomyopathy and can be a screening tool for CO poisoning.

The usefulness of diffusion-weighted magnetic resonance imaging performed in the acute phase as an early predictor of delayed neuropsychiatric sequelae in acute carbon monoxide poisoning

2017 ◽  
Vol 37 (6) ◽  
pp. 587-595 ◽  
Author(s):  
YS Kim ◽  
YS Cha ◽  
MS Kim ◽  
HJ Kim ◽  
YS Lee ◽  
...  
Keyword(s):  
Magnetic Resonance Imaging ◽  
Carbon Monoxide ◽  
Magnetic Resonance ◽  
Carbon Monoxide Poisoning ◽  
Co Poisoning ◽  
Resonance Imaging ◽  
Diffusion Weighted ◽  
Significant Difference ◽  
Delayed Neuropsychiatric Sequelae ◽  
Weighted Magnetic Resonance Imaging

Delayed onset of neuropsychiatric symptoms after apparent recovery from acute carbon monoxide (CO) poisoning has been described as delayed neuropsychiatric sequelae (DNS). No previous study has determined whether early use of diffusion-weighted magnetic resonance imaging (DWI) can predict which patients will develop DNS in the acute CO poisoning. This retrospective observational study was performed on adult patients with acute CO poisoning consecutively treated over a 17-month period. All included patients with acute CO poisoning underwent DWI to evaluate brain injury within 72 h after CO exposure. DWI was evaluated as follows: (1) presence of pathology, (2) number of pathologies, (3) asymmetry, and (4) location of pathology. Patients were divided into two groups. The DNS group was composed of patients with delayed sequelae, while the non-DNS group included patients with no sequelae. A total of 102 patients with acute CO poisoning were finally enrolled in this study. DNS developed in 10 patients (9.8%). Between the DNS group and the non-DNS group, presence of pathology on DWI and initial Glasgow Coma Scale (GCS) showed significant difference. There was also a statistical difference between the non-DNS group and DNS group in terms of CO exposure time, troponin I, rhabdomyolysis, acute kidney injury, and pneumonia. The presence of pathology in DWI and initial GCS (cutoff: <12) at the emergency department served as an early predictors of DNS.

scholarly journals Acute Heart Failure in a Healthy Young Patient after Severe Carbon Monoxide Poisoning

2019 ◽  
Author(s):  
Christos E Lampropoulos ◽  
Evagelia Sklavou ◽  
Charalampos Anastogiannis ◽  
Vasiliki Papanikolaou ◽  
Dimitris Tsilivarakis ◽  
...  
Keyword(s):  
Heart Failure ◽  
Carbon Monoxide ◽  
Troponin I ◽  
Carbon Monoxide Poisoning ◽  
Severe Heart Failure ◽  
Left Ventricular ◽  
Co Poisoning ◽  
Jugular Veins ◽  
X Ray ◽  
Cellular Hypoxia

Introduction: Carbon monoxide (CO) poisoning may cause severe cellular hypoxia. Materials and methods: A 28-year-old male presented reduced levels of consciousness and dyspnoea after CO exposure. Clinical examination revealed tachypnoea, bilateral rales, dilated jugular veins and confusion. Troponin I, lactate and carboxyhaemoglobin levels were increased. Thoracic X-ray depicted pulmonary oedema and an echocardiogram, severe heart failure (HF; EF<25%). He was intubated due to clinical deterioration. Results: He remained intubated for 5 days with excellent improvement of left ventricular function (EF>55%). He was discharged 1 week later with full recovery. Discussion: Acute HF is a rare serious complication of CO poisoning, even in healthy young individuals.

The Evaluation of Myocardial Damage in 83 Young Adults with Carbon Monoxide Poisoning in the East Anatolia Region in Turkey

2006 ◽  
Vol 25 (8) ◽  
pp. 439-446 ◽  
Author(s):  
Sahin Aslan ◽  
Mustafa Uzkeser ◽  
Bedri Seven ◽  
Fuat Gundogdu ◽  
Hamit Acemoglu ◽  
...  
Keyword(s):  
Carbon Monoxide ◽  
Young Adults ◽  
Troponin I ◽  
Complete Blood Count ◽  
Carbon Monoxide Poisoning ◽  
Photon Emission ◽  
Myocardial Damage ◽  
Cardiac Biomarkers ◽  
Emission Computed Tomography ◽  
Co Poisoning

Carbon monoxide (CO) poisoning is the leading cause of death from intoxication. In CO poisoning, it is important to know if there are any symptoms regarding myocardial damage, which are usually unobserved as a result of hypoxia. This study was planned to assess myocardial damage in young healthy patients with CO poisoning. Eighty-three young healthy cases who had been exposed to CO were included in this study. The demographic and clinical characteristics, the origin of CO gas and smoking habits of the patients were recorded. The evaluation of ECG, peripheral ABG, complete blood count and serial cardiac biomarkers (creatine kinase, creatine kinasemyocardial band and troponin I) measurements were performed in all cases. Additionally, echocardiogram (ECHO) and myocardial perfusion single-photon emission computed tomography (SPECT) were performed at the appropriate times in all cases. The mean age of the patients was 27.39 /10.9 years. The main complaint of the patients was loss of consciousness with a 62.7% rate. The average carboxyhaemoglobin level of the patients was 34.49 /15.9%. Sinus tachycardia was present in 26.5% of patients. Diagnostic ischaemic ECG changes were present in 14.4% of patients. In myocardial SPECT, myocardial ischaemic damage was observed in 9 cases, in 6 of whom ECHO findings were also confirmed. Myocar-dial damage due to CO poisoning should not be ignored. If patients are at risk in terms of myocardial damage, further studies, such as ECHO and scintigraphy are needed to determine myocardial damage resulting from CO poisoning. However, in the young adults of the risk group, if the baseline ECG and serial cardiac biomarkers are normal, further studies such as ECHO and scintigraphy, considering the length of exposure and the severity of poisoning, may not be necessary for the evaluation of myocardial damage due to CO poisoning.

scholarly journals Can indicators of myocardial damage predict carbon monoxide poisoning outcomes?

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Hitoshi Koga ◽  
Hideki Tashiro ◽  
Kouta Mukasa ◽  
Tomohiro Inoue ◽  
Aya Okamoto ◽  
...  
Keyword(s):  
Carbon Monoxide ◽  
Qt Interval ◽  
Troponin I ◽  
Morphological Changes ◽  
Carbon Monoxide Poisoning ◽  
Myocardial Damage ◽  
Qt Dispersion ◽  
Ecg Changes ◽  
Corrected Qt Interval ◽  
Logistic Analysis

Abstract Background Carbon monoxide causes electrical, functional, and morphological changes in the heart. It is unclear, however, whether the indicators of myocardial damage can predict the patient’s prognosis after carbon monoxide poisoning. This retrospective study aimed to investigate the relationship between the carboxyhemoglobin level and electrocardiographic (ECG) changes and whether the ECG changes and troponin I levels are related to the patient’s prognosis after carbon monoxide poisoning. Methods Carboxyhemoglobin, troponin I, and ECG parameters were measured in 70 patients with carbon monoxide poisoning. The QT and RR intervals were measured for each ECG lead in all patients, and the corrected QT interval and corrected QT dispersion were calculated. Results The correlation between the maximum corrected QT interval and the carboxyhemoglobin level was significant (P = 0.0072, R2 = 0.1017), as were the relationships between QT dispersion and carboxyhemoglobin (P < 0.001, R2 = 0.2358) and the corrected QT dispersion and carboxyhemoglobin (P < 0.001, R2 = 0.2613). The multivariate logistic analysis showed that the significant predictors of sequential disability were corrected QT dispersion (P = 0.0042), and troponin I level (P = 0.0021). Conclusions Patients’ prognosis following carbon monoxide poisoning can be predicted based on corrected QT dispersion and the troponin I level. Patients with myocardial damage should be monitored not only for their cardiovascular outcome but also for their neurological outcome and their prognosis.

Sign in / Sign up

Export Citation Format

Share Document