Duration Of Carbon Monoxide Exposure Research Articles

Carboxyhemoglobin half-life toxicokinetic profiles during and after normobaric oxygen therapy: On a swine model

Investigations on acute carbon monoxide (CO) poisoning struggle to highlight a relevant discriminant criterion related to CO poisoning severity for predicting complications, such as delayed neurological syndromes. In this context, it remains difficult to demonstrate the superiority of one method of oxygen (O2) administration over others or to identify the optimal duration of normobaric 100% oxygen (NBO) treatment. Myoglobin, as hemoglobin, are a potential binding site for CO, which could be a source of extravascular CO storage that impacts the severity of CO poisoning. It is not possible in routine clinical practice to estimate this potential extravascular CO storage. Indirect means of doing so that are available in the first few hours of poisoning could include, for example, the carboxyhemoglobin half-life (COHbt1/2), which seems to be influenced itself by the level and duration of CO exposure affecting this store of CO within the body. However, before the elimination of CO can be assessed, the COHbt1/2 toxicokinetic model must be confirmed: research still debates whether this model mono- or bi-compartmental. The second indirect mean could be the assessment of a potential COHb rebound after COHb has returned to 5% and NBO treatment has stopped. Moreover, a COHb rebound could be considered to justify the duration of NBO treatment. On an experimental swine model exposed to moderate CO poisoning (940 ppm for ±118 min until COHb reached 30%), we first confirm that the COHb half-life follows a bi-compartmental model. Secondly, we observe for the first time a slight COHb rebound when COHb returns to 5% and oxygen therapy is stopped. On the basis of these two toxicokinetic characteristics in favor of extravascular CO storage, we recommend that COHbt1/2 is considered using the bi-compartmental model in future clinical studies that compare treatment effectiveness as a potential severity criterion to homogenize cohorts of the same severity. Moreover, from a general toxicokinetic point of view, we confirm that a treatment lasting less than 6 hours appears to be insufficient for treating moderate CO poisoning.

Clinical factors for delayed neuropsychiatric sequelae from acute carbon monoxide poisoning: a retrospective study.

Delayed neuropsychiatric sequelae (DNS), which seriously affect the daily lives of patients, are the most common complications of carbon monoxide (CO) poisoning. No uniform screening tool is available for identifying high-risk groups. Therefore, in this study, we aimed to explore whether conventional laboratory indicators and imaging data from primary hospitals could predict the occurrence of DNS. This retrospective observational study was conducted in a single-center primary hospital from January 1, 2021 to May 31, 2023. Participants included patients aged >18 years with acute CO poisoning. Patients with complete recovery in the acute phase were followed up by telephone and outpatient visits, and the presence of DNS was determined according to the occurrence of new neurological symptoms within 6 weeks after discharge. We obtained demographic, laboratory, and imaging data from the medical records and performed a univariate analysis. A multivariate logistic regression model was used to identify independent clinical predictors of DNS. A total of 73 patients were included in the study, of whom 25 (34.2%) developed DNS. Multivariate logistic regression analysis revealed that a longer duration of CO exposure (adjusted odds ratio (AOR): 1.262, 95% confidence interval (CI): 1.069-1.490) and the presence of acute brain lesions on diffusion-weighted imaging (DWI) (AOR: 5.117, 95% CI: 1.430-18.315) were independent risk factors for DNS. Receiver operating characteristic analyses of the duration of CO exposure were performed (area under the curve (AUC): 0.825; 95% CI: 0.731-0.918) with a cut-off value of 5.5 h, and DNS was predicted with a sensitivity of 96% and a specificity of 66.7%. High cranial DWI signal within 24 h and duration of poisoning longer than 5.5 h are independent predictors of DNS. The predictive effects of conventional laboratory indicators require further standardized and large-sample studies.

Predicting acute brain lesions on magnetic resonance imaging in acute carbon monoxide poisoning: a multicenter prospective observational study

An acute brain lesion (ABL) identified by brain magnetic resonance imaging (MRI) after acute carbon monoxide (CO) poisoning is a strong prognostic factor for the development of delayed neuropsychiatric syndrome (DNS). This study aimed to identify predictors of ABLs on MRI in patients with acute CO poisoning. This was a multicenter prospective registry-based observational study conducted at two tertiary hospitals. A total of 1,034 patients were included. Multivariable logistic regression analysis showed that loss of consciousness (LOC) (adjusted odds ratio [aOR] 2.68, 95% Confidence Interval [CI]: 1.49–5.06), Glasgow Coma Scale (GCS) score < 9 (aOR 2.41, 95% CI: 1.49–3.91), troponin-I (TnI) (aOR 1.22, 95% CI: 1.08–1.41), CO exposure duration (aOR 1.09, 95% CI: 1.05–1.13), and white blood cell (WBC) (aOR 1.05, 95% CI: 1.01–1.09) were independent predictors of ABLs on MRI. LOC, GCS score, TnI, CO exposure duration, and WBC count can be useful predictors of ABLs on MRI in patients with acute CO poisoning, helping clinicians decide the need for an MRI scan or transfer the patient to an appropriate institution for MRI or hyperbaric oxygen therapy.

How to Decide Oxygen Therapy in Childhood Carbon Monoxide Poisoning?

Carbon monoxide poisoning is an important cause of morbidity and mortality all over the world. In our study, it was aimed to determine the clinical and laboratory parameters that may be effective in deciding the need for hyperbaric oxygen therapy in the management of cases. From January 2012 to the end of December 2019, 83 patients who applied to a university hospital pediatric emergency department in İstanbul with the diagnosis of carbon monoxide poisoning were included. Demographic characteristics, carbon monoxide source, exposure duration, treatment approach, physical examination findings, Glasgow Coma Score, laboratory results, electrocardiogram, cranial imaging, and chest x-ray were evaluated from the records. The median age of the patients was 56 (37.0-100.0) months and 48 (57.8%) of them were male. The median time of exposure to carbon monoxide was 5.0 (0.5-3.0) hours in those who received hyperbaric oxygen therapy and was significantly higher than those who received normobaric oxygen therapy (P < .001). Myocardial ischemia, chest pain, pulmonary edema, and renal failure were not detected in any of the cases. The median lactate level was detected as 1.5 (1.0-2.15) mmol/L in those who received normobaric oxygen therapy and 3.7 (3.17-4.62) mmol/L in those who received hyperbaric oxygen therapy, and the difference between them was statistically significant (P < .001). A guideline containing precise clinical and laboratory parameters for hyperbaric oxygen therapy in children has not been developed yet. In our study, carbon monoxide exposure duration, carboxyhemoglobin levels, neurological symptoms, and lactate levels were found to be guiding parameters in determining the need for hyperbaric oxygen therapy.

Neurological sequelae in acute carbon monoxide poisoning: Aprospective observational study with MRI data.

Acute carbon monoxide (CO) poisoning survivors may experience persistent neurological sequelae (PNS) and delayed neurological sequelae (DNS). This study evaluated the clinical features, laboratory results, acute brain lesions (ABLs) on diffusion-weighted imaging (DWI) at presentation, and long-term outcomes and explored differences between patients with PNS and DNS. The study included 443 patients who had experienced CO poisoning, underwent DWI and completed 1-year follow-ups. The demographics, comorbidities, symptomatology, laboratory results, ABLs on DWI at presentation, and long-term outcomes were compared between patients with PNS and those with DNS. The 42 (9.5%) and 96 (21.7%) patients with PNS and DNS, respectively, showed no significant differences in demographics, duration of CO exposure, initial conscious level, symptomatology, and laboratory results. ABLs on DWI were observed in 33 patients (33/42) with PNS and 62 patients (62/96) with DNS. The most common region of ABLs was the globus pallidus (60.6% and 56.6% in PNS and DNS, respectively). The proportion of ABLs present and lesion distribution did not differ significantly between the two groups. At 1year, a significantly higher proportion of patients in the PNS group showed a good outcome (defined as modified Rankin Scale [mRS] scores of 0-2, 81%) compared with the DNS group (81% vs. 56.3%, p=.047). Demographics, clinical features, laboratory results, and acute brain lesions on MRI at presentation did not differ between the PNS and DNS groups. However, the long-term outcome of PNS was better than that of DNS.

Clinical predictors of delayed neurological sequelae in charcoal-burning carbon monoxide poisoning.

The main objective of the treatment of acute carbon monoxide (CO) poisoning is to prevent delayed neurological sequelae (DNS). However, today there is still no objective screening tool to identify patients at high risk of developing DNS. The aim of this study was to identify clinical factors that could predict DNS after acute charcoal-burning CO poisoning. This prospective observational study was conducted from September 1, 2019 to August 31, 2020 in a single academic medical center. Patients older than 18 years of age suffering from charcoal-burning CO poisoning were included in the study. After acute recovery, patients were followed up for six weeks to investigate for DNS development. The clinical predictors of DNS were determined using a multivariate logistic regression model. Of the 217 patients-113 males (52.1%), median age 37.0 (27.5-51.5) years-included, 49 (22.6%) developed DNS. The multivariate logistic regression analysis revealed the independent predictors of DNS as a lower initial Glasgow Coma Scale (GCS) score (adjusted odds ratio (AOR): 0.73, 95% confidence interval (CI): 0.62-0.87), a longer duration of CO exposure (AOR: 2.18, 95% CI: 1.65-2.88), and the presence of acute brain lesions with high signal intensity on diffusion-weighted imaging (AOR: 5.22, 95% CI: 1.50-18.08). The created multivariate regression model predicted DNS development with high accuracy (area under the curve: 0.93, 95% CI: 0.89-0.97). A low initial GCS score, longer exposure to CO and abnormal findings on diffusion-weighted magnetic resonance imaging can assist in the early identification of patients at high risk of DNS development.

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

Delayed neurological sequelae (DNS) is a devastating consequence following acute carbon monoxide (CO) poisoning. This study aims at exploring the independent predictors of DNS in patients with CO exposure. Data of patients with diagnosis of CO poisoning was retrospectively collected and reviewed in 5 regional medical facilities. Patients were classified into the DNS group and non-DNS group according to clinical findings during a follow-up period of 6months. Demographic characteristics, co-morbidities, clinical manifestations, and treatment strategies were compared to identify possible correlative factors. Multivariate analysis was performed to determine the independent predictors of DNS. We screened 1129 patients and enrolled 326 cases (158 males, average age 44.56±16.08years) in the analysis. Thirty-seven (11.35%) developed DNS at a median interval of 33days. Uni-variable analysis identified older age, higher body mass index, hypertension, loss of consciousness, longer CO exposure, lower Glasgow Coma Scale (GCS) on-site/at emergency room, and elevation of lactate as relevant factors for DNS; while multivariable logistic regression revealed that older age (OR=1.11; p<0.001), longer duration of CO exposure (OR=1.54; p=0.023), GCS on-site (OR=2.06; p<0.001), and GCS at emergency room (OR=1.33; p=0.048) were independent predictors for DNS. Our multicenter study demonstrated older age, longer duration of CO exposure, and GCS score were independent predictors of DNS in COP patients. GCS scored on-site might be a more sensitive and specific parameter compared with GCS evaluated at the emergency room. Further prospective studies in a larger patient cohort are warranted to draw a comprehensive conclusion.

Predictors of Delayed Neurological Sequelae after Acute Carbon Monoxide Poisoning at Zagazig University Hospitals

Background: Carbon monoxide (CO) is an odorless, tasteless and colorless gas that causes a potentially fatal illness with a tremendous burden due to significant mortality and morbidity. Carbon monoxide poisoning leads to the development of delayed neurological sequelae (DNS). Aim: To assess the possible risk factors that can predict the development of DNS after acute CO poisoning. Subjects and methods: The patients were recruited between January 2018 and December 2018. The study included 37 cases with acute CO poisoning. The medical history was taken thoroughly. Patients underwent general and neurological clinical assessments with laboratory investigations, including arterial blood gases (ABG), carboxyhemoglobin (COHb), cardiac enzymes, and serum lactate. At the time of admission, all patients were subjected to an electrocardiogram (ECG) and brain imaging (CT or MRI) of the brain. They were followed up three and six months after discharge for complete neurological examination and cognitive functions assessment using the Mini-Mental State Examination (MMSE). Results: Two patients died, both presenting with coma and hemodynamic instability. Five cases were excluded due to a lack of comprehension and refusal to follow-up. Out of the 30 patients who completed the follow-up, 67% survived with no complication, while DNS developed in 33% of the patients. Several predictors for development of DNS were identified. They included lower Glasgow coma score, duration of CO exposure, high COHb level, decrease in blood pH, elevated serum levels of creatine kinase and lactate, and abnormalities in brain structure. The time of DNS development extended to six months post-exposure. Conclusion: We conclude that several clinical and laboratory parameters can predict DNS. Recommendations: proper and accurate clinical and laboratory evaluation of any suspected case of acute CO poisoning should be performed especially those parameters proved to be predictors for DNS. The follow-up of cases should continue at least for six months post-exposure.

Exposure Duration and History of Hypertension Predicted Neurological Sequelae in Patients with Carbon Monoxide Poisoning.

Carbon monoxide poisoning (COP) accounts for a large number of emergency department visits worldwide and is fatal in many cases. In surviving patients, neurological sequelae (NS) attributable to cerebral hypoxia are the most devastating outcome, but reliable predictors are limited. Therefore, we conducted a study to identify predictors of NS in patients with COP and evaluate their effects. In this retrospective case-control study, we identified patients with COP in a medical center in Southern Taiwan between January 2005 and December 2014. Cases were patients with NS, and controls were patients without NS. We obtained information on potential predictors of NS from medical records and evaluated their association with NS, including demographic characteristics, exposure source, suicide attempts, duration of exposure (by tertile), histories, symptoms, signs, laboratory data, treatment, and the length of hospital stay. We included 371 patients with COP. Of them, 93 developed NS, and their mean ages (41.4 ± 14.7 years vs. 39.7 ± 14.2 years) and proportions of males (59.1% vs. 58.6%) were similar to those in the 298 controls. Multivariate logistic regression showed that a history of hypertension (adjusted odds ratio = 2.1; 95% confidence interval = 1.0, 4.5) and a longer duration of carbon monoxide exposure (adjusted odds ratio = 1.7; 95% confidence interval = 1.1, 2.8; the longest tertile [>5 hours] vs. the other two tertiles [≤5 hours]) were independent predictors for NS, but not the level of carboxyhemoglobin. This study identified two independent predictors for NS that may be useful for public healthcare workers and physicians in predicting outcomes and deciding on treatment strategies for COP patients.

Clinical Predictors of Acute Brain Injury in Carbon Monoxide Poisoning Patients With Altered Mental Status at Admission to Emergency Department.

Objective screening tool for patients at a high risk of developing acute brain injury (ABI) is necessary for the proper treatment of carbon monoxide (CO) poisoning patients. The aim of this study is to identify clinical factors that could predict ABI due to CO poisoning in patients with an altered mental status. A prospectively collected CO poisoning registry at a single academic medical center was retrospectively analyzed. CO poisoning patients with an altered mental status at the emergency department, defined as unalert on the alert/responsive to voice/responsive to pain/unresponsive scale and underwent diffusion-weighted magnetic resonance imaging (DW-MRI) between January 1, 2013, and December 31, 2015, were included. ABI was defined as the presence of acute hypoxic brain lesions. Clinical predictors of ABI were identified by multivariate logistic regression analysis. Of 180 patients, 67 (37.2%) had ABI as revealed by DW-MRI. Multivariate analysis showed that CO exposure duration>5 hours (adjusted odds ratio [AOR]= 7.082; 95% confidence interval [CI]= 3.463-15.014; p<0.001) defined as the time between CO exposure and rescue, abnormal white blood cell count (AOR= 2.568, 95% CI= 1.188-5.700, p=0.02), and abnormal creatinine concentration (AOR= 2.667, 95% CI= 1.110-6.605, p=0.03) were predictors of ABI. CO exposure duration had the highest predictive value (area under the curve, 0.815), and the optimal cutoff value was 5 hours. Moreover, increasing exposure durations (quartile) indicated a stepwise increase in the risk of ABI. In CO poisoning patients with an altered mental status, CO exposure duration was useful for predicting ABI, which may help clinicians or paramedics identify high-risk patients and provide treatment on priority.

LAMANYA PAPARAN KARBON MONOKSIDA TERHADAP PROFIL ENZIM ALANIN AMINOTRANFERASE

Background: Carbon Monoxide (CO) is a gas compound that is colorless, odorless and tasteless. Carbon monoxide comes from incomplete combustion such as burning firewood.Firewood is the main fuel used in tofu manufacturing in tofu factories. Wood-burning smoke in the tofu plant contains CO gas capable of polluting the air, so it can cause disturbance in the form of reddish eyes, quick thirst, headache and shortness of breath. This disorder can occur in exposed to factory workers who are exposed to CO. Carbon Monoxide enters the body at a certain level of exposure causing changes in some of the body's molecules and ultimately disrupts the functioning of the body. One of the organs involved changes due to excessive CO exposure is the liver characterized by increased levels of enzyme Alanin Aminotransferase (ALT). Research Objectives: To analyze the duration of carbon monoxide exposure to the enzyme profile Alanin Aminotranferase. Method: Using Cross Sectional design with 34 respondents. serum of factory workers know checked ALT levels using Mindray BA-88Aspeculator. Data were analyzed using Spearman Correlation test. Result: Exposure time of CO to factory worker to know obtained mean (4.06 years), median (4.00 years), minimum value (1 year) and maximum (7 years). Levels of ALT enzyme in factory workers know obtained mean (33,82 U / L), median (33.00 U / L), minimum value (8 U / L) and maximum value (56 U / L). There is a long relationship of CO exposure to ALT levels (r = 0.783; p &lt;0.001; n = 34). Conclusion: The longer the factory workers know exposed to CO, the higher the ALT level. Factory workers know to reduce carbon monoside exposure by changing jobs and pay attention to the use of personal protective equipment when working.

Serum neuron-specific enolase levels at presentation and long-term neurological sequelae after acute charcoal burning-induced carbon monoxide poisoning

Objective: This study aimed to investigate whether clinical parameters and serum neuron-specific enolase (NSE) levels measured at emergency department (ED) presentation help stratify the risk of acute or delayed persistent severe neurological sequelae after acute carbon monoxide (CO) poisoning induced by charcoal burning.Methods: This retrospective study included 236 patients who suffered from CO poisoning. Demographic information, serum NSE levels measured in the ED, treatment, clinical course, and long-term neurological outcomes were recorded.Results: The median serum NSE level at presentation was 15.5 (10.9–22.7) ng/mL. No differences were observed in the duration of CO exposure; the initial Glasgow Coma Scale (GCS) score; the levels of arterial HCO3−, white blood cells (WBCs), C-reactive protein (CRP) or troponin I; or the frequency of abnormal diffusion-weighted imaging finding at presentation among the groups with different serum NSE levels at presentation. The incidences of acute and delayed persistent neurologic sequelae assessed at 22.3 months after acute charcoal CO poisoning were 5.1% and 8.5%, respectively. No difference in the NSE level was observed between patients stratified according to long-term neurological status. According to the multinomial logistic regression analysis, age, serum CRP levels and the initial GCS score were risk factors for the two types of persistent severe neurological sequelae, whereas troponin I levels were associated only with the acute persistent severe neurological sequelae. However, the adjusted NSE level was not a risk factor for any persistent neurological sequelae.Conclusions: Serum NSE levels at presentation were not correlated with the risk of acute or delayed persistent neurological sequelae. Further studies with blood sampling at optimal time points and serial measurements should be conducted. Age, initial GCS score, and CRP levels may be risk factors for persistent severe neurological sequelae.

Neuropsychological Evaluation of Children and Adolescents With Acute Carbon Monoxide Poisoning.

Carbon monoxide (CO) poisoning is a worldwide health problem. We have limited information regarding psychological adversities of CO poisoning in children and adolescents. The aim of this study was (1) to investigate the effects of severe CO poisoning on cognitive functions, mood, and behaviors in children and adolescents and (2) to identify factors related to occurrence of neuropsychological symptoms. This study included pediatric patients, who were evaluated after CO poisoning at the Department of Child and Adolescent Psychiatry between January 2012 and April 2013. The patients were evaluated at 2 time points. The first evaluation was done when they were discharged from emergency department, and the second evaluation was done 1 month after CO poisoning. Turkish versions of internationally recognized tests were used to evaluate anxiety, depressive symptoms, attention, visual-spatial skills, memory, and behaviors of patients. Twenty-seven patients were analyzed. The mean age of the patients was 11.8 ± 2.7 years (range, 6-18 years). The mean carboxyhemoglobin level was 31.5% ± 7.8% (range, 19%-51%) dir. Delayed neurological sequel was observed in only 1 patient, who had headache and tinnitus. We found that carboxyhemoglobin level was not correlated with later neuropsychiatric test scores. However, we found a correlation between history of loss of consciousness and anxiety symptom level, hyperbaric oxygen (HBO) therapy session and behavioral problems, and time to HBO therapy and attention problems. We suggest that CO exposure duration, history of loss of consciousness, time to HBO therapy, and the number of HBO therapy session affect neuropsychological symptom levels and occurrence of attention and behavioral problems.

Carbon monoxide poisoning increases Tpeak-Tend dispersion and QTc dispersion : cardiovascular topic

SummaryObjectiveCarbon monoxide (CO) poisoning leads to cardiac dysrhythmia. Increased heterogeneity in ventricular repolarisation on electrocardiogram (ECG) shows an increased risk of arrhythmia. A number of parameters are used to evaluate ventricular repolarisation heterogeneity on ECG. The aim of our study is to investigate the effect of acute CO poisoning on indirect parameters of ventricular repolarisation on ECG.MethodsSixty-seven patients were included in this case–control study. Thirty patients with acute CO poisoning were assigned to group 1 (19 females, mean age: 30.8 ± 11.3 years). A control group was formed with patients without known cardiac disease (group 2, n = 37; 25 females, mean age: 26.0 ± 5.2 years). Twelve-lead ECG and serum electrolyte levels were recorded in all patients. Also, carboxyhaemoglobin (COHb) levels were recorded in group 1. Tpeak–Tend (TpTe) interval, TpTe dispersion, TpTe/QT ratio, QT interval and QTd durations were measured as parameters of ventricular repolarisation. Corrected QT (QTc) and QTc dispersion (QTcd) intervals were determined with the Bazett’s formula.ResultsThe mean COHb level in group 1 was 27.6 ± 7.4% and mean duration of CO exposure was 163.5 ± 110.9 min. No statistically significant difference was found in age, gender, serum electrolytes or blood pressure levels between the groups. QRS, QT, QTc, TpTe interval and TpTe/QT ratio were similar between the groups (p > 0.05). QTcd (65.7 ± 64.4 vs 42.1 ± 14.2 ms, p = 0.003) and TpTe dispersion (40.5 ± 14.8 vs 33.2 ± 4.9 ms, p = 0.006) were significantly longer in group 1 than group 2. COHb level was moderately correlated with TpTe dispersion (r = 0.29; p = 0.01).ConclusionTo our knowledge, this is the first study to investigate TpTe interval and dispersion in CO poisoning. Our results showed that TpTe dispersion and QTc dispersion increased after CO poisoning.

Unintentional domestic non-fire related carbon monoxide poisoning: Data from media reports, UK/Republic of Ireland 1986–2011

Context. Gathering information on the circumstances that give rise to unintentional domestic non-fire related carbon monoxide poisoning and the associated morbidity and mortality is not straightforward because the diagnosis is so often missed in life. Methods. We searched Newsbank and related databases (at least 332 sources, UK and Republic of Ireland) for reports of domestic carbon monoxide poisoning, 1986–end 2011 inclusive. The search terms were ‘carbon monoxide AND (house* OR home* OR caravan* OR tent*) NOT (work OR fire OR suicide*)’. Newsbank includes full-text articles from 19 UK national newspapers and over 140 UK & Irish regional and local newspapers and periodicals. Results and discussion. There were reports of 348 incidents (880 victims: 334 male, 352 female, 194 sex not stated). Reports of incidents increased from 1986 (1) to 2011 (28). There were 298 deaths (169 male, 124 female, 5 sex not reported). The likelihood of a fatal outcome increased with age for both males and females (28%, 1–9 years; 71%, 80 + years). The source of carbon monoxide was often a central heating or water boiler (48% of 244 incidents). Many incidents (49%) occurred in private dwellings. However, incidents in caravans, tents, sheds and outhouses had a much higher death rate. If a victim was discovered alive chances of survival were relatively good (87%), even if found unconscious. The estimated duration of carbon monoxide exposure ranged from minutes to years in both fatal and non-fatal incidents. Pets were recorded in 31 incidents (17 died). In 5 cases, carbon monoxide poisoning was identified through illness or death of a pet. Prosecutions were recorded in 49 incidents and at least 7 custodial (prison) sentences resulted, with 34 further convictions resulting in a fine. Charges were preferred against either an installer/maintenance engineer (42%), or the landlord (31%). Conclusion. Deaths and permanent injuries from unintentional domestic non-fire related carbon monoxide poisoning continue. Survival rates are relatively high if poisoning is diagnosed in life, but warning signs are often missed and inappropriate behavior such as placing barbecues in tents and failure to perform proper safety checks by gas appliance fitters still kills.

The usefulness of the serum s100b protein for predicting delayed neurological sequelae in acute carbon monoxide poisoning

Context. Some patients with acute carbon monoxide poisoning will experience delayed neurological sequelae. Several factors associated with delayed neurological sequelae have been reported, but these factors are unsatisfactory for the assessment of unconscious patients. Objective. The aim of this study was to assess the usefulness of the serum S100B protein as a biochemical marker for predicting delayed neurological sequelae. Materials and methods. In this retrospective study, we evaluated the data for patients who visited an emergency medical center once during a period of 7 months. The enrollment criteria were the diagnosis of acute carbon monoxide poisoning and the measurement of the serum S100B level. A standardized extraction using medical records was performed. Result. A total of 71 patients were enrolled, and 10 patients (14.1%) presented delayed neurological sequelae. The delayed neurological sequelae group had a longer duration of carbon monoxide exposure, a longer duration of loss of consciousness, and a worse mental status (p-value < 0.001). In addition, the S100B protein levels were higher in the delayed neurological sequelae group (0.891 vs. 0.063, p-value < 0.001). Multiple logistic regression analysis showed that only the serum S100B protein level was independently associated with the development of delayed neurological sequelae (OR, 120.594; 95% CI, 4.194–3467.220), and a serum S100B protein level of more than 0.165 μg/L predicted the development of delayed neurological sequelae (sensitivity 90%, specificity 87%). Discussion and conclusion. In the present study, the level of serum S100B protein was found to be useful for evaluating acute CO poisoning patients and was found to be an independent predictor of the development of DNS after acute CO poisoning.

Delayed neuropsychological sequelae after carbon monoxide poisoning: predictive risk factors in the Emergency Department. A retrospective study

BackgroundDelayed neuropsychological sequelae (DNS) commonly occur after recovery from acute carbon monoxide (CO) poisoning. The preventive role and the indications for hyperbaric oxygen therapy in the acute setting are still controversial. Early identification of patients at risk in the Emergency Department might permit an improvement in quality of care. We conducted a retrospective study to identify predictive risk factors for DNS development in the Emergency Department.MethodsWe retrospectively considered all CO-poisoned patients admitted to the Emergency Department of Careggi University General Hospital (Florence, Italy) from 1992 to 2007. Patients were invited to participate in three follow-up visits at one, six and twelve months from hospital discharge. Clinical and biohumoral data were collected; univariate and multivariate analysis were performed to identify predictive risk factors for DNS.ResultsThree hundred forty seven patients were admitted to the Emergency Department for acute CO poisoning from 1992 to 2007; 141/347 patients participated in the follow-up visit at one month from hospital discharge. Thirty four/141 patients were diagnosed with DNS (24.1%). Five/34 patients previously diagnosed as having DNS presented to the follow-up visit at six months, reporting a complete recovery. The following variables (collected before or upon Emergency Department admission) were associated to DNS development at one month from hospital discharge in the univariate analysis: CO exposure duration >6 hours, a Glasgow Coma Scale (GCS) score <9, seizures, systolic blood pressure <90 mmHg, elevated creatine phosphokinase concentration and leukocytosis. There was no significant correlation with age, sex, voluntary exposure, headache, transient loss of consciousness, GCS between 14 and 9, arterial lactate and carboxyhemoglobin concentration. The multivariate analysis confirmed as independent prognostic factors GCS <9 (OR 7.15; CI 95%: 1.04-48.8) and leukocytosis (OR 3.31; CI 95%: 1.02-10.71).ConclusionsOur study identified several potential predictive risk factors for DNS. Treatment algorithms based on an appropriate risk-stratification of patients in the Emergency Department might reduce DNS incidence; however, more studies are needed. Adequate follow-up after hospital discharge, aimed at correct recognition of DNS, is also important.

Cardiovascular Effects of Carbon Monoxide Poisoning

Carbon monoxide (CO) poisoning is an important health problem. Cardiac abnormalities may occur in patients with CO poisoning; however, the severity and duration of cardiac abnormalities are not well known. In this study, cardiac structures and function in CO poisoning were evaluated prospectively. Twenty patients were enrolled in the study. Echocardiographic examination was performed in all patients on admission, at 24 hours, and within the first week. B-type natriuretic peptide and carboxyhemoglobin levels were measured. Patients with increased cardiac markers underwent coronary angiography. Cardiac markers were high in 6 patients. Patients with high cardiac markers had significantly higher carboxyhemoglobin levels and longer exposure to CO. Left ventricular ejection fraction (LVEF) was <45% in 8 patients (group I) on admission and >55% in 7 patients in group I 24 hours after echocardiography. A significant negative correlation was found between B-type natriuretic peptide and LVEF on admission (r = -0.586, p <0.01). The decrease in LVEF was also negatively correlated with carboxyhemoglobin level and CO exposure duration. All angiograms showed normal coronary arteries. In conclusion, despite normal coronary arteries, myocardial dysfunction may occur in patients with CO poisoning. LV systolic function might be normal or mildly to severely impaired. However, most of the myocardial dysfunction dissipates at 24 hours in patients with CO poisoning.

Intravascular Neutrophil Activation Due to Carbon Monoxide Poisoning

We hypothesized that platelet-neutrophil interactions occur as a result of acute carbon monoxide (CO) poisoning, and subsequent neutrophil activation triggers events that cause neurologic sequelae. To identify platelet-neutrophil interactions and neutrophil activation in patients and in animal models, and to establish the association between these intravascular events and changes linked to CO-mediated neurologic sequelae in an animal model. Blood was obtained from 50 consecutive patients. Abnormalities were variable depending on the carboxyhemoglobin level at study admission and duration of CO exposure. Platelet-neutrophil aggregates were detected and plasma myeloperoxidase (MPO) concentration was significantly elevated in those with confirmed CO poisoning. Among patients exposed to CO for over 3 h, flow cytometry scans of neutrophils revealed increased surface expression of CD18 and, in some groups, MPO on the cell surface. Animal models revealed consistent evidence of platelet-neutrophil aggregates, neutrophil activation and surface MPO, and plasma MPO elevation. MPO was deposited along the brain vascular lining and colocalized with nitrotyrosine. CO poisoning caused abnormalities in the charge pattern of myelin basic protein (MBP), changes linked to adaptive immunologic responses responsible for neurologic sequelae in this model. Changes did not occur in thrombocytopenic rats, those receiving tirofiban to inhibit platelet-neutrophil interactions, or those receiving L-nitroarginine methyl ester to inhibit nitric oxide synthesis. Alterations in MBP did not occur in CO-poisoned knockout mice lacking MPO. Acute CO poisoning causes intravascular neutrophil activation due to interactions with platelets. MPO liberated by neutrophils mediates perivascular oxidative stress, which is linked to immune-mediated neurologic sequelae.

Analysis of factors that influence rates of carbon monoxide uptake, distribution, and washout from blood and extravascular tissues using a multicompartment model

To better understand factors that influence carbon monoxide (CO) washout rates, we utilized a multicompartment mathematical model to predict rates of CO uptake, distribution in vascular and extravascular (muscle vs. other soft tissue) compartments, and washout over a range of exposure and washout conditions with varied subject-specific parameters. We fitted this model to experimental data from 15 human subjects, for whom subject-specific parameters were known, multiple washout carboxyhemoglobin (COHb) levels were available, and CO exposure conditions were identical, to investigate the contributions of exposure conditions and individual variability to CO washout from blood. We found that CO washout from venous blood was biphasic and that postexposure times at which COHb samples were obtained significantly influenced the calculated CO half times (P < 0.0001). The first, more rapid, phase of CO washout from the blood reflected the loss of CO to the expired air and to a slow uptake by the muscle compartment, whereas the second, slower washout phase was attributable to CO flow from the muscle compartment back to the blood and removal from blood via the expired air. When the model was used to predict the effects of varying exposure conditions for these subjects, the CO exposure duration, concentration, peak COHb levels, and subject-specific parameters each influenced washout half times. Blood volume divided by ventilation correlated better with half-time predictions than did cardiac output, muscle mass, or ventilation, but it explained only approximately 50% of half-time variability. Thus exposure conditions, COHb sampling times, and individual parameters should be considered when estimating CO washout rates for poisoning victims.