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Carbon Monoxide Poisoning (carbon + monoxide_poisoning)
Selected AbstractsHyperbaric Oxygen Does Not Prevent Neurologic Sequelae after Carbon Monoxide PoisoningACADEMIC EMERGENCY MEDICINE, Issue 1 2002Benjamin Gilmer MS Abstract Delayed neurologic sequelae occur in up to 40% of severe carbon monoxide (CO) poisonings. Conflicting clinical data support the efficacy of hyperbaric oxygen (HBO) therapy in the acute treatment of CO poisoning. Objective: To determine whether oxygen therapy reduces neurologic sequelae after CO poisoning in mice. Methods: Male Swiss-Webster mice were exposed to CO at 1,000 ppm for 40 minutes and then 50,000 ppm until loss of consciousness (LOC) (4-9 additional minutes). Total time of both phases of CO exposure was 40-49 minutes. Treatment included HBO with 3 atmospheres (ATA) 100% oxygen, normobaric oxygen (NBO) with 1 ATA 100% oxygen, or ambient air 15 minutes after LOC. All animals underwent passive avoidance training and memory was assessed by measuring step-down latency (SDL) and step-up latency (SUL) seven days following CO exposure. Results: Carbon monoxide poisoning induced significant memory deficits (SDLCO= 156 sec; SULCO= 75%) compared with nonpoisoned (NP) animals (SDLNP= 272 sec; SULNP= 100%). Both HBO and NBO did not prevent these neurologic sequelae. Furthermore, no significant neurobehavioral differences were found between HBO and NBO. Histologic examination of the CA1 layer of the hippocampus for pyknotic cells showed significant damage from CO in the air-treated animals (9.6%) but not in the nonpoisoned animals (3.8%). No significant neuroprotection was seen histologically with NBO and HBO compared with ambient air. Conclusions: These results suggest that HBO is not effective in preventing neurologic sequelae in mice and that there is no benefit of HBO over NBO following severe CO neurotoxicity. [source] Characteristics of Headache Associated With Acute Carbon Monoxide PoisoningHEADACHE, Issue 3 2002Neil B. Hampson MD Objective.,To evaluate systematically the characteristics of headache due to acute exposure to carbon monoxide. Background.,Headache is the most commonly reported symptom in acute carbon monoxide poisoning. While it is often described as throbbing and diffuse, a systematic characterization of carbon monoxide-associated headache has never been published. Methods.,Patients referred for hyperbaric oxygen treatment of acute carbon monoxide poisoning were asked whether headache was part of their symptom complex. When present, specific details about the nature of the headache were collected from 100 consecutive patients through use of a standardized questionnaire. Results.,Information on carbon monoxide-associated headache was collected from 34 female and 66 male patients with a mean carboxyhemoglobin level of 21.3%± 9.3%. The most common location for pain was frontal (66%), although more than one location was involved in 58% of patients. Nature of the pain at any time during its course was dull in 72% of patients and sharp in 36%. Headache was throbbing in 41%, continuous in 74%, and intermittent in 16% of those evaluated. Peak intensity of pain did not correlate with the carboxyhemoglobin level. Headache improved prior to hyperbaric oxygen treatment in 72%, resolving entirely in 21%. Of those with residual headache, pain improved with hyperbaric oxygen in 97%, resolving entirely in 44%. Conclusions.,The headache accompanying acute carbon monoxide poisoning is extremely variable in nature. "Classic" throbbing, diffuse headaches were rarely described by patients. There are no patterns which can be considered characteristic to aid in the diagnosis of carbon monoxide-induced headache. Similarly, no trait was identified which might allow elimination of carbon monoxide poisoning from the differential diagnosis of headache. [source] Suicidal Asphyxiation by Inhalation of Automobile Emission without Carbon Monoxide PoisoningJOURNAL OF FORENSIC SCIENCES, Issue 5 2006Stephen J. DeRoux M.D. ABSTRACT: Reported herein is the suicidal asphyxiation of a young man due to exhaustion of oxygen in the interior of a sealed automobile into which the exhaust emissions were diverted. His blood carboxyhemaglobin concentration was less than 5% saturation. The car was equipped with a catalytic converter and when tested, the exhaust carbon monoxide concentration was 0.01%. [source] Pallidoreticular-Rubral Brain Damage on Magnetic Resonance Imaging After Carbon Monoxide PoisoningJOURNAL OF NEUROIMAGING, Issue 2 2002Cristiano Gandini MD [source] Occult Carbon Monoxide Poisoning in ENT Practice: A Word of CautionTHE LARYNGOSCOPE, Issue 1 2003Article first published online: 2 JAN 200 No abstract is available for this article. [source] Hyperbaric Oxygen Does Not Prevent Neurologic Sequelae after Carbon Monoxide PoisoningACADEMIC EMERGENCY MEDICINE, Issue 1 2002Benjamin Gilmer MS Abstract Delayed neurologic sequelae occur in up to 40% of severe carbon monoxide (CO) poisonings. Conflicting clinical data support the efficacy of hyperbaric oxygen (HBO) therapy in the acute treatment of CO poisoning. Objective: To determine whether oxygen therapy reduces neurologic sequelae after CO poisoning in mice. Methods: Male Swiss-Webster mice were exposed to CO at 1,000 ppm for 40 minutes and then 50,000 ppm until loss of consciousness (LOC) (4-9 additional minutes). Total time of both phases of CO exposure was 40-49 minutes. Treatment included HBO with 3 atmospheres (ATA) 100% oxygen, normobaric oxygen (NBO) with 1 ATA 100% oxygen, or ambient air 15 minutes after LOC. All animals underwent passive avoidance training and memory was assessed by measuring step-down latency (SDL) and step-up latency (SUL) seven days following CO exposure. Results: Carbon monoxide poisoning induced significant memory deficits (SDLCO= 156 sec; SULCO= 75%) compared with nonpoisoned (NP) animals (SDLNP= 272 sec; SULNP= 100%). Both HBO and NBO did not prevent these neurologic sequelae. Furthermore, no significant neurobehavioral differences were found between HBO and NBO. Histologic examination of the CA1 layer of the hippocampus for pyknotic cells showed significant damage from CO in the air-treated animals (9.6%) but not in the nonpoisoned animals (3.8%). No significant neuroprotection was seen histologically with NBO and HBO compared with ambient air. Conclusions: These results suggest that HBO is not effective in preventing neurologic sequelae in mice and that there is no benefit of HBO over NBO following severe CO neurotoxicity. [source] Carbon monoxide poisoning of proton exchange membrane fuel cellsINTERNATIONAL JOURNAL OF ENERGY RESEARCH, Issue 8 2001J. J. Baschuk Abstract Proton exchange membrane fuel cell (PEMFC) performance degrades when carbon monoxide (CO) is present in the fuel gas; this is referred to as CO poisoning. This paper investigates CO poisoning of PEMFCs by reviewing work on the electrochemistry of CO and hydrogen, the experimental performance of PEMFCs exhibiting CO poisoning, methods to mitigate CO poisoning and theoretical models of CO poisoning. It is found that CO poisons the anode reaction through preferentially adsorbing to the platinum surface and blocking active sites, and that the CO poisoning effect is slow and reversible. There exist three methods to mitigate the effect of CO poisoning: (i) the use of a platinum alloy catalyst, (ii) higher cell operating temperature and (iii) introduction of oxygen into the fuel gas flow. Of these three methods, the third is the most practical. There are several models available in the literature for the effect of CO poisoning on a PEMFC and from the modeling efforts, it is clear that small CO oxidation rates can result in much increased performance of the anode. However, none of the existing models have considered the effect of transport phenomena in a cell, nor the effect of oxygen crossover from the cathode, which may be a significant contributor to CO tolerance in a PEMFC. In addition, there is a lack of data for CO oxidation and adsorption at low temperatures, which is needed for detailed modeling of CO poisoning in PEMFCs. Copyright © 2001 John Wiley & Sons, Ltd. [source] The dilemma of managing carbon monoxide poisoningEMERGENCY MEDICINE AUSTRALASIA, Issue 2 2004Greg Emerson No abstract is available for this article. [source] Where to now with carbon monoxide poisoning?EMERGENCY MEDICINE AUSTRALASIA, Issue 2 2004Carlos D Scheinkestel Abstract The controversy regarding the role of hyperbaric oxygen (HBO) in the treatment of carbon monoxide (CO) poisoning has been re-ignited following the publication of a further randomized controlled trial by Weaver et al., the results of which appear to conflict with our findings. Comparative analysis suggests that the apparent outcome differences may be secondary to the design, analysis and interpretation of the results of the two studies. Following careful analysis of these two papers and further results from a study by Raphael et al on 385 CO-poisoned patients, we can still find no convincing evidence favouring HBO therapy. Pending further research to determine optimal oxygen therapy for CO-poisoning, current therapy should involve stratifying patients for risk of a poor outcome. This stratification may be aided by the evolving availability of biochemical markers of brain injury and the finding that patients with transient loss of consciousness and poor performance on neuropsychological tests of the supervisory attention system are at higher risk of neuropsychological sequelae. We propose that those patients most at risk be admitted and receive more prolonged normobaric oxygen therapy whilst those with more minor CO-poisoning should be provided with normobaric oxygen of no less than 6 h duration and certainly until sign and symptom free. [source] Characteristics of Headache Associated With Acute Carbon Monoxide PoisoningHEADACHE, Issue 3 2002Neil B. Hampson MD Objective.,To evaluate systematically the characteristics of headache due to acute exposure to carbon monoxide. Background.,Headache is the most commonly reported symptom in acute carbon monoxide poisoning. While it is often described as throbbing and diffuse, a systematic characterization of carbon monoxide-associated headache has never been published. Methods.,Patients referred for hyperbaric oxygen treatment of acute carbon monoxide poisoning were asked whether headache was part of their symptom complex. When present, specific details about the nature of the headache were collected from 100 consecutive patients through use of a standardized questionnaire. Results.,Information on carbon monoxide-associated headache was collected from 34 female and 66 male patients with a mean carboxyhemoglobin level of 21.3%± 9.3%. The most common location for pain was frontal (66%), although more than one location was involved in 58% of patients. Nature of the pain at any time during its course was dull in 72% of patients and sharp in 36%. Headache was throbbing in 41%, continuous in 74%, and intermittent in 16% of those evaluated. Peak intensity of pain did not correlate with the carboxyhemoglobin level. Headache improved prior to hyperbaric oxygen treatment in 72%, resolving entirely in 21%. Of those with residual headache, pain improved with hyperbaric oxygen in 97%, resolving entirely in 44%. Conclusions.,The headache accompanying acute carbon monoxide poisoning is extremely variable in nature. "Classic" throbbing, diffuse headaches were rarely described by patients. There are no patterns which can be considered characteristic to aid in the diagnosis of carbon monoxide-induced headache. Similarly, no trait was identified which might allow elimination of carbon monoxide poisoning from the differential diagnosis of headache. [source] Interrelation between the Poisoning Severity Score, carboxyhaemoglobin levels and in-hospital clinical course of carbon monoxide poisoningINTERNATIONAL JOURNAL OF CLINICAL PRACTICE, Issue 12 2006A. A. CEVIK Summary The aim of the present study is to evaluate the relationship between the Poisoning Severity Score (PSS) and carboxyhaemoglobin (COHb) levels in patients with carbon monoxide poisoning (COP) using outcome as the measure. The study was designed as a retrospective chart review of patients with final diagnosis of COP. Correlation of PSS and COHb levels at presentation was evaluated with collected data. Majority of the cases were grade 1 (minor) PSS (134 cases, 73.6%) and 93.4% of these patients made a complete recovery. There were six deaths (mortality 3.3%) and six in-hospital major complications (IHMCs) (3.3%) (please specify whether the complications were in the patients who died). There is moderate correlation between PSS and outcome (p < 0.001, r = 0.493). Grade 3 (severe) PSS was significantly different from other grades for outcome (six mortalities and three IHMCs). Patients classified as grade 3 and patients who died had a significantly higher mean age (p < 0.05, 41.8 ± 23.6 and p < 0.01, 60.1 ± 20.3, respectively). Mean COHb level of grade 3 (33.2 ± 13.9%) was significantly higher than that of other grades (p < 0.05). COHb levels according to outcome were not different (? within the patients in grade 3). Decreased level of consciousness, acidosis, tachycardia, high glucose and leucocyte levels showed significant relation with higher PSS, COHb level and adverse outcome. We conclude that the PSS is a reliable guide in COP. Value of the PSS in COP may be enhanced if additional factors and investigations are included. [source] Financial Debt and Suicide in Hong Kong SAR,JOURNAL OF APPLIED SOCIAL PSYCHOLOGY, Issue 12 2007Paul S. F. Yip The presence of indebtedness is known to be a risk factor that can trigger stressed persons to contemplate suicide. This study compares the profiles of suicides with and without debt problems based on 2002 Coroner's Court death files. The category of men aged 25,39 has seen a 70% increase in suicide rate since 1997, and the number using carbon monoxide poisoning has increased from 1% of the total deaths in 1997 to about 26% of the total deaths in 2002. Suicides associated with debt problems seem to involve fewer mental and physical problems with formal job attachment than do suicides without debt problems. Gambling is a significant contributing factor to unmanageable indebtedness. [source] Trends in Clinical Toxicology: Advances That May Change Your PracticeBASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 1 2005Sage W. Wiener We review selected articles that have advanced our thinking about consequential issues such as gastrointestinal decontamination, paracetamol poisoning, ethanol withdrawal, cocaine-associated chest pain, carbon monoxide poisoning and over-anticoagulation. [source] Postural stability before and after hyperbaric oxygen treatmentACTA NEUROLOGICA SCANDINAVICA, Issue 6 2005M. F. Tvede Objective,,, The purpose of this study was to determine the effect of hyperbaric oxygenation (HBO) on postural stability in healthy volunteers. The study was performed in accordance with treatment protocols for divers' decompression sickness and carbon monoxide poisoning. Methods,,, Twenty-one healthy male divers, aged 31 ± 6.88 years (mean ± SD), were tested with quantitative Romberg's test before and after HBO (90 min in a pressure chamber at an ambient pressure of 253 kPa, ,15 m of sea water, breathing pure oxygen). The quantitative Romberg's test is a calculation of the average sway for 50 s. Results,,, No difference was found between sway before and after the HBO (P < 0.05), i.e. we were unable to show that the results of quantitative Romberg's test are affected by HBO. Thus, the quantitative Romberg's test may be a valuable tool in evaluating patients with decompressions sickness, carbon monoxide intoxication and other neurological diseases normally treated with HBO. [source] | ||||||||||||||||||||||