Cases reported "Carbon Monoxide Poisoning"

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1/143. 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.
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2/143. 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.
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3/143. 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.
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4/143. 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.
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5/143. 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.
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6/143. 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.
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7/143. 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.
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keywords = tic disorder, tic
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8/143. Acute carbon monoxide poisoning as the cause of rhabdomyolysis and acute renal failure.

    Acute renal failure (ARF) is a severe complication of acute CO poisoning which, combined with other organ lesions, may result in lethal outcome. In all vague cases of ARF with nontraumatic rhabdomyolysis, CO poisoning should be considered as a possible etiologic factor. The diagnosis is made on the basis of several simple laboratory tests: determination of carboxyhemoglobin concentration, demonstration of myoglobin in urine or pigment granulated cylindres in urinary sediment, positive orthotoluidine test, and high CPK values originating from skeletal musculature. Many authors report on excellent prognosis in ARF due to nontraumatic rhabdomyolysis of various causes. Our case report shows that the prognosis of CO poisoned patient greatly depends on timely and appropriate treatment, severity of damage to other organs, and success of the treatment of complications such as hospital infections.
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9/143. The brain lesion responsible for parkinsonism after carbon monoxide poisoning.

    BACKGROUND: Parkinsonism is a common neurological sequela of carbon monoxide (CO) poisoning, but its pathophysiological mechanism has yet to be clarified. OBJECTIVES: To describe a married couple who were both affected by CO poisoning, but only 1 of whom developed CO-induced parkinsonism, and to discuss the possible underlying pathophysiological mechanism of CO-induced parkinsonism by comparing the neuroimaging findings of these patients. DESIGN AND SETTING: Case report from a clinical neurology department. patients: A married couple experienced CO poisoning simultaneously. One month later, only the husband gradually developed delayed sequelae, including parkinsonism and intellectual impairment. On detailed neurological examination, the husband showed mild but definite rigidity and bradykinesia, while no parkinsonian signs were observed in the wife. Neuropsychological examination revealed impaired memory and attention in both patients, but they were more severe in the husband than in the wife. magnetic resonance imaging scans of the patients' brains disclosed diffuse high-intensity white matter signals in both patients and bilateral pallidal necrosis in the wife. dopamine transporter imaging showed that the degree of dopamine neuronal loss was comparable between these patients. magnetic resonance spectroscopy revealed more severe white matter damage in the husband than in the wife. Thirteen months later, neurological and neuropsychological examinations showed complete recovery from parkinsonism as well as intellectual impairment. Follow-up magnetic resonance spectroscopy also suggested remarkable improvements in white matter damage. CONCLUSION: These results support the role of white matter damage in producing parkinsonism after CO poisoning and highlight the possible usefulness of magnetic resonance spectroscopy in predicting delayed sequelae in patients after CO poisoning. Arch Neurol. 2000;57:1214-1218
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keywords = tic
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10/143. Occupational intoxication with carbon monoxide.

    The most important safety measure for prevention of CO poisoning is the installation of automatic systems that signal high CO concentrations in the work environment. public health measures that include stringent pollution control, introduction of low-cost CO monitors, and public education aimed at the high-risk population (e.g., new workers, drivers) should decrease the number of deaths from CO poisoning and should save productive years of life. Toxicity of CO is a consequence of tissue hypoxia created by the displacement of oxygen from hemoglobin and the subsequent impairment of oxygen release to the tissues. Early symptoms of CO intoxication are insidious and can resemble other diseases; physical examination may be unremarkable. For these reasons, many cases of CO poisoning are not readily recognized.
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