Cases reported "carbon monoxide poisoning"

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1/269. The role of catalytic converters in automobile carbon monoxide poisoning: a case report.

    Inhaling motor vehicle exhaust fumes is a common method used by people attempting to commit suicide; however, the decreased carbon monoxide concentrations found in the exhaust of late-model automobiles equipped with catalytic converters are changing the clinical presentation of exhaust inhalation. ( info)

2/269. carbon monoxide poisoning causes optic neuropathy.

    PURPOSE: To describe the electrophysiological and psychophysical effects of carbon monoxide (CO) poisoning on visual function. methods: Three patients are presented who suffered CO poisoning, two due to suicide attempts and one in the course of a road traffic accident. After a full ocular examination, Goldmann visual fields, flash and pattern visual evoked potentials (VEPs) and flash and pattern electroretinograms (ERGs) were tested. RESULTS: electrophysiology showed reduced or absent N95 components of the pattern ERG and delayed, reduced VEPs. A positive-negative-positive (PNP) VEP waveform was seen in two cases. In one case, where presentation occurred at an early stage, visual and electrophysiological function was improved with hydroxycobalamine. CONCLUSIONS: The combination of ERG and VEP findings suggest that CO poisoning can cause a toxic optic neuropathy that may have a similar aetiological mechanism to that in tobacco amblyopia. Early treatment with hydroxycobalamine may be of some benefit. ( info)

3/269. MRI, quantitative MRI, SPECT, and neuropsychological findings following carbon monoxide poisoning.

    Carbon monoxide (CO) poisoning has been shown to result in neuropathologic changes and cognitive impairments due to anoxia and other related biochemical mechanisms. The present study investigated brain-behaviour relationships between neuropsychological outcome and SPECT, MRI, and Quantitative magnetic resonance imaging (QMRI) in 21 patients with CO poisoning. Ninety-three per cent of the patients exhibited a variety of cognitive impairments, including impaired attention, memory, executive function, and mental processing speed. Ninety-five per cent of the patients experienced affective changes including depression and anxiety. The results from the imaging studies revealed that 38% of the patients had abnormal clinical MRI scans, 67% had abnormal SPECT scans, and 67% had QMRI findings including hippocampal atrophy and/or diffuse cortical atrophy evidenced by an enlarged ventricle-to-brain ratio (VBR). Hippocampal atrophy was also found on QMRI. SPECT and QMRI appear to be sensitive tools which can be used to identify the neuropathological changes and cerebral perfusion defects which occur following CO poisoning. Cerebral perfusion defects include frontal and temporal lobe hypoperfusion. Significant relationships existed between the various imaging techniques and neuropsychological impairments. The data from this study indicate that a multi-faceted approach to clinical evaluation of the neuropathological and neurobehavioural changes following CO poisoning may provide comprehensive information regarding the neuroanatomical and neurobehavioural effects of CO poisoning. ( info)

4/269. An unusual case of carbon monoxide poisoning.

    Carbon monoxide, a gas originating from incomplete combustion of carbon-based fuels, is an important cause of human deaths. In this paper, we describe an unusual carbon monoxide poisoning in a dwelling without obvious sources of combustion gases, for which two adults had to be treated in a hyperbaric chamber. Carbon monoxide readings were taken in the house and in the neighboring homes. methane gas and nitrogen oxide levels were also monitored in the house air. soil samples were collected around the house and tested for hydrocarbon residues. The investigation revealed the presence of a pocket of carbon monoxide under the foundation of the house. The first readings revealed carbon monoxide levels of 500 ppm in the basement. The contamination lasted for a week. The investigation indicated that the probable source of contamination was the use of explosives at a nearby rain sewer construction site. The use of explosives in a residential area can constitute a major source of carbon monoxide for the neighboring populations. This must be investigated, and public health authorities, primary-care physicians, governmental authorities, and users and manufacturers of explosives must be made aware of this problem. ( info)

5/269. Neuropsychiatric aspects of carbon monoxide poisoning: a review and single case report suggesting a role for amphetamines.

    Sublethal exposure to carbon monoxide (CO) can result in severe neurologic and psychiatric complications. Once in the body, CO can wreak havoc on virtually every organ system, with the brain being the most vulnerable to the damaging effects. Neuropathological injury is frequently widespread, and while white matter injury is most common, both gray and white matter injury occurs. Consequently, no neurologic or psychiatric syndrome is pathognomonic for CO poisoning. There are currently no effective treatments for the delayed neuropsychiatric sequelae of CO poisoning, and medical management focuses on correcting immediate symptoms through the use of oxygen, hyperbaric oxygen therapy, and supportive measures. Preliminary data suggest, however, that dopaminergic agents may be useful for the treatment of some of the delayed sequelae of CO neurotoxicity. To our knowledge, ours is the first case report in which dextroamphetamine (DAMP), a potent dopaminergic agent, has been used for treating the neuropsychiatric symptoms of CO poisoning. Our data demonstrate that it is effective in shortening cognitive and motor recovery time, that psychostimulant actions occur slightly sooner than locomotor effects, and that theraputic benefit is most dramatic within the first ten days of use. Therefore, DAMP appears to be a pharmacological agent that can be combined with supportive interventions to reverse, attenuate, or symptomatically improve the delayed sequelae that occur in these patients. ( info)

6/269. brain CT and MRI findings after carbon monoxide toxicity.

    The neuropathologic sequelae of carbon monoxide (CO) toxicity have been well described in postmortem examinations. globus pallidus damage as well as diffuse white matter lesions and encephalopathic changes occur. brain CT has provided imaging correlates to the premortem changes. MRI is more sensitive and provides more specificity. Cerebral edema changes may occur early with subsequent demonstration of globus pallidus lesions and white matter changes. globus pallidus lesions in many cases do not correlate directly to clinical status and outcome; however, the presence of diffuse white matter disease is a more reliable index of both. These changes are seen in patients in both accidental exposures to CO and in suicide attempts. ( info)

7/269. Recurrent acute life-threatening events and lactic acidosis caused by chronic carbon monoxide poisoning in an infant.

    Acute severe carbon monoxide poisoning is usually easy to recognize and diagnose. However, chronic or less severe exposure may produce more subtle symptoms. We report on a 31/2-year-old girl who was admitted to the hospital several times with acute, life-threatening events, acidosis, and flu-like symptoms. The diagnosis was elusive, but after careful questioning of family members and a home visit, chronic carbon monoxide poisoning was diagnosed. ( info)

8/269. Four deaths due to carbon monoxide poisoning in car washes.

    In a period of 13 months, three separate incidents of lethal carbon monoxide (CO) poisoning in closed car wash bays resulted in the deaths of 4 white men aged 20 to 36 years. Each man appears to have been intoxicated with mind-altering substances, which may impair judgment, perception of outside conditions, and self-awareness. All four died in winter months. For three men, the deaths were ruled accidental, and for the remaining man, the previous deaths appear to have provided a model for suicide. Warning signs may not be effective to prevent future CO deaths in car washes because of the possible role of intoxication. Mechanical or electronic methods to prevent a bay door from closing completely may be preferable. ( info)

9/269. Delayed transient loss of consciousness in acute carbon monoxide intoxication.

    In acute carbon monoxide intoxication the presence of altered consciousness, ranging from transient loss of consciousness to coma, represents a poor prognostic factor and modifies the approach to therapy. Transient loss of consciousness is, as a rule, contemporaneous to the exposure, generally occurring at the scene of the intoxication. We report an unusual case of delayed transient loss of consciousness, occurring in the absence of any other evident aetiology, in one member of an orchestra composed of 110 members after a mass carbon monoxide poisoning. ( info)

10/269. Variability of neuropsychological deficits associated with carbon monoxide poisoning: four case reports.

    Carbon monoxide (CO) poisoning is associated with variable neuropsychological deficits, depending on levels of CO exposure and individual differences. Studies to date have reported variable findings, as their subjects have been exposed to different levels of CO from different poisoning sources. Four unique case studies are presented, all of whom experienced the same level of CO poisoning (17-29%) in the same accident. Two of the individuals were brothers with an identical genetic disorder (i.e. syndactylism) and the other two were brother/sister. The results indicated: (1) variable neuropsychological deficits despite similar levels of CO poisoning; (2) consistent estimated decline in intelligence; (3) similar memory decline for the two brothers, but not for the brother and sister; and (4) consistent late-onset emotional-behavioural difficulties. The results also suggested that the neuropsychological and emotional-behavioural deficits had an impact on the individual's ability to work. ( info)
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