Cases reported "Carbon Monoxide Poisoning"

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1/32. 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.
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2/32. Recognition of chronic carbon monoxide poisoning.

    Chronic exposure to low levels of carbon monoxide can cause vague symptoms that are easily mistaken for other common illnesses. During the past 5 years, three families have contacted the wisconsin Division of public health to report illnesses that may have been caused by chronic exposure to carbon monoxide. Members of these families were diagnosed with a variety of conditions including chronic fatigue syndrome, depression and influenza. Carbon monoxide exposure was not suspected as a cause of these illnesses until heating contractors discovered that gas appliances in these families' homes were not properly vented. These cases serve as reminders that carbon monoxide exposure should be considered in the differential diagnosis of patients who present with chronic symptoms of headache, fatigue, dizziness, nausea and mental confusion--especially when these symptoms onset during the winter heating season.
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3/32. Carbon-monoxide poisoning presenting as an afebrile seizure.

    A 1-year-old male who experienced an afebrile seizure and loss of consciousness caused by carbon-monoxide poisoning is reported. His blood gas analysis revealed an elevated carboxyhemoglobin level (up to 25%) and metabolic acidosis. A cranial computed tomography depicted diffuse swelling of the brain. He was promptly treated with hyperbaric oxygen. He recovered fully 8 hours after the onset of the illness. No neurologic deficit was evident during the 8 months of follow-up. Although seizures are generally regarded as a manifestation of severe and near-fatal carbon-monoxide poisoning, an early diagnosis and aggressive hyperbaric-oxygen therapy could result in a good clinical outcome. In a patient presenting with an afebrile seizure, carbon monoxide poisoning should always be considered as one of the etiologies.
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4/32. Extracorporeal support in an adult with severe carbon monoxide poisoning and shock following smoke inhalation: a case report.

    The objective of this study was to discuss the case of a patient with severe smoke inhalation-related respiratory failure treated with extracorporeal support. The study was set in a 12-bed multi-trauma intensive care unit at a level one trauma center and hyperbaric medicine center. The patient under investigation had carbon monoxide poisoning, and developed acute respiratory distress syndrome and cardiovascular collapse following smoke inhalation. Rapid initiation of extracorporeal support, extreme inverse-ratio ventilation and intermittent prone positioning therapy were carried out. Admission and serial carboxyhemoglobin levels, blood gases, and computerized tomography of the chest were obtained. The patient developed severe hypoxia and progressed to cardiovascular collapse resistant to resuscitation and vasoactive infusions. Veno-venous extracorporeal support was initiated. Cardiovascular parameters of blood pressure, cardiac output, and oxygen delivery were maximized; oxygenation and ventilation were supported via the extracorporeal circuit. Airway pressure release ventilation and intermittent prone positioning therapy were instituted. Following 7 days of extracorporeal support, the patient was decannulated and subsequently discharged to a transitional care facility,neurologically intact. smoke inhalation and carbon monoxide poisoning may lead to life-threatening hypoxemia associated with resultant cardiovascular instability. When oxygenation and ventilation cannot be achieved via maximal ventilatory management, extracorporeal support may prevent death if initiated rapidly.
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5/32. Management of carbon monoxide poisoning using oxygen therapy.

    The management of carbon monoxide poisoning requires an accurate assessment of the extent of blood oxygenation. Measuring the fractional oxyhaemoglobin content by using co-oximetry gives a true picture of the oxygen-carrying capacity of blood in the presence of carboxyhaemoglobin. The use of readings from pulse oximetry or a standard blood gas analyser is insufficient and can be misleading. We report on a case of carbon monoxide poisoning to illustrate this potential pitfall.
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6/32. Apoptotic and necrotic brain lesions in a fatal case of carbon monoxide poisoning.

    A 41-year-old man was accidentally exposed to carbon monoxide (CO) gas and found in a state of cardiopulmonary arrest while he took bath. After admission, he was resuscitated and underwent artificial ventilation in a comatose state and died about 19h later. Computed tomography (CT) examination disclosed bilateral low density area in the basal ganglia and the thalamus, a well-known finding in the CO intoxication. Necropsy, histological examination, dna ladder assay gave the first line of evidence for the presence of apoptosis as well as necrosis in the human case of CO intoxication. TdT-mediated dUTP-biotin nick-end labeling (TUNEL) positive apoptotic cells were more predominant in the CA2 area than in CA1 area. There is general co-relation between the ratio of TUNEL-positive cells and the dna laddering on the agarose gel. basal ganglia and thalamus, which showed bilateral low density area in CT, were revealed to be severe edema. The two types of cell death occurred in the cortex, basal ganglia, hippocampus, thalamus, and cerebellum. Hypoxia caused by CO-hemoglobin formation alone cannot explain the phenomena.
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7/32. Unique case of fatal carbon monoxide poisoning in the absence of a combustible fossil fuel.

    A 37-year-old man died as a result of exposure to carbon monoxide within an apartment. An investigation of the apartment showed no gas appliances or gas supply to the apartment and no evidence of any combustion event to any part of the apartment or roof space. inhalation of dichloromethane was excluded. heating to the apartment was found to be via an electrical storage heater, the examination of which revealed that the cast-iron core and insulating material showed evidence of heat damage with significant areas devoid of carbon. This electric storage heater is hypothesized to be the source of carbon for the fatal production of carbon monoxide within the apartment.
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8/32. Asphyxial deaths caused by automobile exhaust inhalation not attributable to carbon monoxide toxicity: study of 2 cases.

    The authors report two suicides that resulted from the intentional inhalation of automobile exhaust gases in which death occurred without the formation of physiologically significant amounts of carboxyhemoglobin. These circumstances are correlated with measurements of the involved vehicles' exhaust gases, which showed reduced concentrations of carbon monoxide present, reflecting improvements in automobile engine technology. In the absence of carbon monoxide toxicity, the authors attribute death in these cases to asphyxia caused by carbon dioxide intoxication and diminished atmospheric oxygen concentrations.
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9/32. Carbon-monoxide poisoning resulting from exposure to ski-boat exhaust--georgia, June 2002.

    Carbon monoxide (CO) is an odorless, colorless gas produced from the incomplete combustion of carbon-based fuels such as gasoline or wood. In the united states, CO poisoning causes approximately 500 unintentional deaths each year. Although CO poisonings often have been reported to occur in enclosed and semi-enclosed environments, they can also occur in open-air environments. This report describes two related cases of CO poisoning that occurred in children who were participating in recreational activities on a ski boat. Recreational boaters should be aware of the dangers of open-air CO poisoning, and engineering solutions are needed to reduce the amount of CO in boat exhaust.
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10/32. MRI and neuropsychological correlates of carbon monoxide exposure: a case report.

    A 45-year-old woman experienced long-term, chronic exposure to carbon monoxide in the restaurant kitchen where she was employed as a cook. After returning to the restaurant after 5 days off work, she noticed that her symptoms returned immediately; she then aired out the room and called the gas company. Approximately 6 hr after a leak was detected, the patient went to the hospital, where her carboxyhemoglobin was found to be within normal limits and results of a neurologic examination were described as normal. Based on her symptoms, the patient believed she had been exposed to CO for at least 1 year before the leak was discovered. Initially, she experienced flu-like symptoms, which eventually resolved. At the time of her first neuropsychological evaluation (17 months after the exposure was identified), her persisting complaints included difficulties in reading, writing, speaking and word retrieval. The test results were consistent with secondary frontal lobe dysfunction associated with subcortical disorders such as those seen after CO exposure. Results of a subsequent neuropsychological examination (29 months postexposure) showed slight improvement in performance, but her performance was still consistent with mild frontal/subcortical dysfunction. Although the initial screening of a brain magnetic resonance image (MRI) performed 15 months after the exposure was interpreted as being within normal limits, two subsequent blind reviews of the same scans identified multiple bilateral lesions in the basal ganglia, which were consistent with chronic CO exposure. We present this case as an example of the utility of MRI and neuropsychological examinations in detecting central nervous system dysfunction secondary to CO exposure.
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