Derangement of PaCO2 requires physician attention in acute carbon monoxide poisoning

2020 ◽  
Vol 39 (5) ◽  
pp. 642-652
Author(s):  
JM Moon ◽  
BJ Chun ◽  
YS Cho
Keyword(s):  
Carbon Monoxide ◽  
Incidence Rate ◽  
Linear Trend ◽  
Carbon Monoxide Poisoning ◽  
Metabolic Changes ◽  
Secondary Response ◽  
Co Poisoning ◽  
Significant Linear Trend ◽  
Arterial Blood ◽  
The Mean

The objective was to describe the prevalence of derangement of the partial pressure of arterial carbon dioxide (PaCO2) and to determine the association between PaCO2 and adverse cardiovascular events (ACVEs) in carbon monoxide (CO)-poisoned patients. Additionally, we evaluated whether the derangement of PaCO2 was simply secondary to metabolic changes. This retrospective study included 194 self-breathing patients after CO poisoning with an indication for hyperbaric oxygen therapy and available arterial blood gas analysis at presentation and 6 h later. The incidence rate of hypocapnia at presentation after acute CO poisoning was 67.5%, and the mean PaCO2 during the first 6 h was 33 (31–36.7) mmHg. The most common acid–base imbalance in 131 patients with hypocapnia was primary respiratory alkalosis. The incidence rate of ACVEs during hospitalization was 50.5%. A significant linear trend in the incidence of ACVEs was observed across the total range of PaCO2 variables. In multivariate regression analysis, mean PaCO2 was independently associated with ACVEs (odds ratio 0.051; 95% confidence interval 0.004–0.632). PaCO2 derangements were common after acute CO poisoning and were not explainable as a mere secondary response to metabolic changes. The mean PaCO2 during the first 6 h was associated with ACVEs. Given the high incidence of ACVEs and PaCO2 derangement and the observed association between the mean PaCO2 and ACVEs, this study suggests that (1) PaCO2 should be monitored in the acute stage to predict and/or prevent ACVEs and (2) further investigation is needed to validate this result and explore the early manipulation of PaCO2 as a treatment strategy.

How much apoptosis does carbon monoxide poisoning cause? Primary clinical soluble TWEAK protein level study

2019 ◽  
Vol 38 (8) ◽  
pp. 974-982 ◽  
Author(s):  
N Dindar Badem ◽  
E Cömertpay ◽  
F Coşkun
Keyword(s):  
Carbon Monoxide ◽  
Peripheral Blood ◽  
Protein Level ◽  
Cell Apoptosis ◽  
Predictive Value ◽  
Complete Blood Count ◽  
Carbon Monoxide Poisoning ◽  
Control Group ◽  
Co Poisoning ◽  
Arterial Blood

Carbon monoxide (CO) is an important cause of deaths via poisoning. CO poisoning causes inhibition of O2 transport and development of tissue hypoxia, which then causes cell apoptosis. A significant indicator of cell apoptosis, soluble tumor necrosis factor-like weak inducer of apoptosis (sTWEAK) protein, is important for the stimulation of apoptosis. The primary purpose of this study is to determine whether apoptosis occurs during acute CO poisoning and to show that sTWEAK protein is an indicator of apoptosis that can be analyzed as a marker in the peripheral blood sample. The secondary aim is to determine the diagnostic and prognostic values of sTWEAK protein. The study was performed prospectively on 43 patients with CO poisoning and 30 healthy volunteer control individuals. The anamneses were taken from all patients, who also underwent physical examination. Complete blood count, biochemical markers, cardiac enzymes, and arterial blood gas measurements were analyzed. All the patients’ sTWEAK protein levels were also analyzed. The sTWEAK protein level of patients with CO poisoning was 2278 pg/mL (1197–7234), while the level of the control group was 1609 pg/mL (310–3721). The patients’ sTWEAK levels were significantly higher than the controls (area under the curve: 0.77 (0.66–0.89); p < 0.001), and the cutoff value was determined as 1895.50 pg/mL. The cutoff level had a sensitivity of 74.4%, a specificity of 76.7%, a positive predictive value of 82.0%, and a negative predictive value of 67.6%. sTWEAK is a significant indicator of apoptosis in CO poisoning that can be analyzed in the peripheral blood. However, further clinical trials are needed in terms of prognostic criteria.

Atrial fibrillation associated with carbon monoxide poisoning

2019 ◽  
pp. 203-206
Author(s):  
Mevlut Demir ◽  
◽  
Muslum Sahin ◽  
Ahmet Korkmaz ◽  
◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Carbon Monoxide ◽  
Sinus Rhythm ◽  
Partial Pressure ◽  
Motor Vehicle ◽  
Carbon Monoxide Poisoning ◽  
Venous Blood ◽  
Blood Gas ◽  
Arterial Blood Gas ◽  
Arterial Blood

Carbon monoxide intoxication occurs usually via inhalation of carbon monoxide that is emitted as a result of a fire, furnace, space heater, generator, motor vehicle. A 37-year-old male patient was admitted to the emergency department at about 5:00 a.m., with complaints of nausea, vomiting and headache. He was accompanied by his wife and children. His venous blood gas measures were: pH was 7.29, partial pressure of carbon dioxide (pCO2) was 42 mmHg, partial pressure of oxygen (pO2) was 28 mmHg, carboxyhemoglobin (COHb) was 12.7% (reference interval: 0.5%-2.5%) and oxygen saturation was 52.4%. Electrocardiogram (ECG) examination showed that the patient was not in sinus rhythm but had atrial fibrillation. After three hours the laboratory examination was repeated: Troponin was 1.2 pg/ml and in the arterial blood gas COHb was 3%. The examination of the findings on the monitor showed that the sinus rhythm was re-established. The repeated ECG examination confirmed the conversion to the sinus rhythm. He was monitored with the normobaric oxygen administration.

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 Frontal QRS-T angle as a predictive marker for myocardial damage in acute carbon monoxide poisoning

2021 ◽  
pp. 096032712110434
Author(s):  
Yusuf K Tekin ◽  
Gülaçan Tekin ◽  
Naim Nur ◽  
İlhan Korkmaz ◽  
Sefa Yurtbay
Keyword(s):  
Carbon Monoxide ◽  
Creatine Kinase ◽  
Cardiac Troponin ◽  
Troponin I ◽  
Myocardial Damage ◽  
Cardiac Troponin I ◽  
Arterial Oxygen ◽  
Co Poisoning ◽  
Arterial Blood ◽  
Creatine Kinase Mb

Introduction The present study was undertaken to investigate the prognostic value of the frontal QRS-T angle associated with adverse cardiac outcomes in patients with carbon monoxide (CO) poisoning in early stages in the emergency department. Materials and methods The data of 212 patients with CO poisoning who were admitted to the ED between January 2010 and May 2020 were retrospectively analyzed. The frontal QRS-T angle was obtained from the automatic reports of the EKG device. Results Compared to patients without myocardial damage, among patients with myocardial damage, statistically high creatinine, creatine kinase MB, cardiac troponin I, and frontal QRS-T angle values were found ( p < 0.001 for all parameters), while the saturation of arterial blood pH and arterial oxygen values were found to be lower ( p = 0.002 and p < 0.001, respectively). The frontal QRS-T angle values were correlated with creatine kinase, creatine kinase-MB, cardiac troponin I, and oxygen saturation (SpO2) in arterial blood (r = 0. 232, p = 0.001; r = 0. 253, p = < 0.001; r = 0. 389, p = < 0.001; r = −0. 198, p = 0.004, respectively). The optimum cut-off value of the frontal QRS-T angle was found to be 44.5 (area under the curve: 0.901, 95% confidence interval: 0.814–0.988, sensitivity: 87%, specificity: 84%). Conclusions The frontal QRS-T angle, a simple and inexpensive parameter that can be easily obtained from 12-lead surface electrocardiography, can be used as an early indicator in the detection of myocardial damage in patients with CO poisoning.

Brain stem and spinal cord demyelination due to acute carbon monoxide poisoning

2021 ◽  
pp. 247-253
Author(s):  
Yan Lv ◽  
Yv Zhang ◽  
Shuyi Pam ◽  
Keyword(s):  
Spinal Cord ◽  
Carbon Monoxide ◽  
Brain Stem ◽  
Carbon Monoxide Poisoning ◽  
Recovery Period ◽  
Extended Period ◽  
Severe Case ◽  
Co Poisoning ◽  
Secondary Demyelination ◽  
The Brain

Demyelination throughout the brain stem and spinal cord caused by acute carbon monoxide (CO) poisoning has not been previously reported. Magnetic resonance imaging (MRI) has revealed that acute CO poisoning primarily affects the subcortical white matter of the bilateral cerebral hemispheres and basal ganglia. Here we report the case of a patient with delayed neuropsychological sequelae (DNS) due to acute CO poisoning. A 28-year-old man was admitted to our department following a suicide attempt by acute CO poisoning. After a six-month pseudo-recovery period, he was diagnosed with DNS, with MRI evidence of demyelinating change of the bilateral cerebral peduncles. Demyelination was identified throughout the brain stem, expanding from the bilateral cerebral peduncles to the medulla oblongata, occurring approximately six months after poisoning. One and a half years after acute CO poisoning, demyelination of the cervical and thoracic spine was observed, most notable in the lateral and posterior cords. It is evident that previously published research on this topic is extremely limited. Perhaps in severe cases of acute CO poisoning the fatality rate is higher, leading to fewer surviving cases for possible study. This may be because a more severe case of acute CO poisoning would result in the higher likelihood of secondary demyelination. This research indicates that clinicians should be aware of the risk of secondary demyelination and take increased precautions such as vitamin B supplementation and administration of low-dose corticosteroids for an extended period of time in order to reduce the extent and severity of demyelination.

Epidemiological aspects and a current approach to the problem of carbon monoxide poisoning

2020 ◽  
Vol 6 (4) ◽  
pp. 4-9
Author(s):  
Sayit I. Indiaminov ◽  
Antonina A. Kim
Keyword(s):  
Carbon Monoxide ◽  
World Literature ◽  
Carbon Monoxide Poisoning ◽  
Epidemiological Data ◽  
Current Approach ◽  
Co Poisoning ◽  
Fatal Poisoning ◽  
Young Males ◽  
Causes Of Mortality ◽  
Mechanical Asphyxia

Background: Carbon monoxide (CO) poisoning is the leading cause of death from poisoning (accidental and intentional). The number of cases of CO poisoning is increasing day by day. Aims: The aim of the study was to analyze the epidemiological situation of CO poisoning and identify the urgent aspects of this problem. In the article, the author provided a retrospective analysis of 117 cases of CO poisoning, registered in a number of regional branches of the Republican Scientific and Practical Center of the Forensic Medical Examination of Uzbekistan, after he studied and analyzed the world literature on the epidemiology of CO poisoning. It has been revealed that fatal poisoning ranks third after mechanical injuries and mechanical asphyxia and constitutes 6.3% (513 cases) in the range of deaths by violence (8078 cases). Therefore, CO poisoning is considered as one of the most prevailing (51%) causes of mortality. Conclusion: This is a global problem, with young males at risk. Further studies on the current clinical and forensic aspects of CO poisoning are required, and the necessity for regular analysis of epidemiological data for taking comprehensive measures to prevent CO poisoning is emphasized.

scholarly journals Carbon Monoxide Poisoning Effectively Treated with High-flow Nasal Cannula

2019 ◽  
Vol 4 (1) ◽  
pp. 42-45
Author(s):  
Patrick Lee ◽  
Steven Salhanick
Keyword(s):  
Carbon Monoxide ◽  
Carbon Monoxide Poisoning ◽  
High Flow ◽  
Nasal Cannula ◽  
The Novel ◽  
Co Poisoning ◽  
High Flow Nasal Cannula ◽  
Disease States ◽  
Cohb Level ◽  
Potential Option

Carbon monoxide (CO) poisoning is typically treated by administration of oxygen via non-rebreather mask (NRB). High-flow nasal cannula (HFNC) is an alternative to NRB in a variety of disease states. We report a case of the novel use of HFNC in the treatment of acute CO poisoning. A 29-year-old man presented with a carboxyhemoglobin (COHb) level of 29.8%. He was treated with HFNC, and COHb levels declined to 5.4% in 230 minutes. Given several theoretical advantages of HFNC relative to NRB, HFNC is a potential option for use in the treatment of CO poisoning.

Evaluation of oxidative stress and antioxidant parameters in children with carbon monoxide poisoning

2019 ◽  
Vol 38 (11) ◽  
pp. 1235-1243
Author(s):  
O Teksam ◽  
S Sabuncuoğlu ◽  
G Girgin ◽  
H Özgüneş
Keyword(s):  
Oxidative Stress ◽  
Carbon Monoxide ◽  
Carbon Monoxide Poisoning ◽  
Venous Blood ◽  
Treatment Modalities ◽  
Control Group ◽  
Co Poisoning ◽  
Erythrocyte Catalase ◽  
Significant Difference ◽  
Before And After

Objective: In this study, we aimed to investigate oxidative stress and antioxidant parameter levels in patients with carbon monoxide (CO) poisoning. Methods: The study was conducted prospectively between March 1, 2015 and April 30, 2016 in the pediatric emergency department. Eligible patients included children aged 0–18 years old with a diagnosis of CO poisoning. To determination of oxidative stress and antioxidant parameter levels, venous blood with heparinized and urine samples were drawn during the admission and after normobaric oxygen (NBO) and hyperbaric oxygen (HBO) treatment. Results: Forty-seven children with CO poisoning for study group and 29 patients as control group were included to the study. Sixteen patients treated with HBO. Basal plasma malondialdehyde levels were found to be significantly higher in the CO poisoning group when compared with the control group ( p = 0.019). There is no significant difference in oxidative stress and antioxidant parameter levels except erythrocyte catalase enzyme levels in patients treated with NBO when comparing before and after NBO treatment ( p > 0.05). Decreasing of basal erythrocyte catalase enzyme levels were found statistically significant after NBO treatment ( p = 0.04). There was no significant difference in oxidative stress and antioxidant parameter levels in patients treated with HBO before and after therapy ( p > 0.05). Conclusions: CO poisoning is associated with increased lipid peroxidation in children immediately after the poisoning. However, both treatment modalities including NBO or HBO do not have a significant effect on oxidative stress or antioxidant parameter levels.

scholarly journals Storm-Related Carbon Monoxide Poisoning

2013 ◽  
Vol 19 (3) ◽  
pp. 188-199 ◽  
Author(s):  
Scott A. Damon ◽  
Jon A. Poehlman ◽  
Douglas J. Rupert ◽  
Peyton N. Williams
Keyword(s):  
Carbon Monoxide ◽  
Carbon Monoxide Poisoning ◽  
The United States ◽  
Attitudes And Beliefs ◽  
Matrix Approach ◽  
Co Poisoning ◽  
Protective Behaviors ◽  
Home Safety ◽  
Severe Storms ◽  
Summer Storm

Carbon monoxide (CO) poisonings in the United States consistently occur when residents improperly use portable gasoline-powered generators and other tools following severe storms and power outages. However, protective behaviors—such as installing CO alarms and placing generators more than 20 feet away from indoor structures—can prevent these poisonings. This study identified knowledge, attitudes, and beliefs that lead consumers to adopt risk and protective behaviors for storm-related CO poisoning and post-storm generator use. Four focus groups (32 participants in total) were conducted with generator owners in winter and summer storm-prone areas to explore home safety, portable generator use, CO poisoning knowledge, and generator safety messages. Discussions were transcribed, and findings analyzed using an ordered meta-matrix approach. Although most generator owners were aware of CO poisoning, many were unsure what constitutes a safe location for generator operation and incorrectly stated that enclosed areas outside the home—such as attached garages, sheds, and covered porches—were safe. Convenience and access to appliances often dictated generator placement. Participants were receptive to installing CO alarms in their homes but were unsure where to place them. These findings suggest a deficit in understanding how to operate portable generators safely and a need to correct misconceptions around safe placement. In terms of behavioral price, the simple installation and maintenance of inexpensive CO alarms may be the most important strategy for ultimately protecting homes from both storm-related and other CO exposures.

scholarly journals Delayed post-hypoxic leukoencephalopathy: case report with a review of disease pathophysiology

2013 ◽  
Vol 5 (3) ◽  
pp. 13 ◽  
Author(s):  
Michael Andrew Meyer
Keyword(s):  
Carbon Monoxide ◽  
Case Report ◽  
Carbon Monoxide Poisoning ◽  
White Matter Hyperintensity ◽  
Review Of The Literature ◽  
Initial Event ◽  
Fluid Attenuated Inversion Recovery ◽  
Clinical Phenomenon ◽  
The Mean ◽  
Weighted Sequences

Delayed post-hypoxic leukoencephalopathy is a rare clinical phenomenon usually observed in a small number of carbon monoxide poisoning survivors. A similar phenomenon is reported here in a patient who successfully recovered from a large overdose of diazepam and methadone, but then abruptly declined 3 weeks after the initial event. Magnetic resnance revealed confluent white matter hyperintensity on fluid-attenuated inversion recovery and T2 weighted sequences, and spectroscopy revealed elevated peaks in choline, creatinine, and lactate. Analysis and review of the literature suggests this phenomenon occurs on average about 19 days after the initial event. Although the pathophysiology remains obscure, it is noted here that the mean lucid interval coincides approximately with the replacement half-life for myelin related lipids and proteins.

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