11/269. memory lost and regained following bilateral hippocampal damage. We present a longitudinal neuropsychological study (31 examinations over a period of 18 months) of patient DE DF demonstrated bilateral atrophy of the hippocampal formation and globus pallidus resulting from carbon monoxide poisoning. Eighteen months after the event, the volume of the hippocampal formation was reduced by 42% on the left side and 28% on the right. The patient initially presented with a severe global amnesia. Then, he showed a gradual, yet selective recovery of episodic memory function. Verbal free recall and spatial memory performance remained reduced, whereas immediate word recall and recognition memory, as well as picture learning and memory, improved to levels at the lower range of normal performance. Interestingly, nonspatial associative learning was never much impaired and recovered completely by the end of testing. These data are taken as evidence that the human hippocampal formation does not equally support different forms of episodic memory. ( info) |
| 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. ( info) |
13/269. 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. ( info) |
| 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. ( info) |
| 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. ( info) |
| Carbon monoxide (CO) poisoning is the most common fatal poisoning in the united states. The circumstances often involve an unsuspected increase of CO in an enclosed environment. Victims often are unaware that their activity or environment placed them at risk for CO poisoning. The possibility of open air CO poisonings was first reported in 1987. We present a case of open air CO poisoning resulting in neurologic depression and a markedly elevated carboxyhemoglobin level in a child who had been swimming behind a house boat. Emergency physicians and pediatricians should be aware of the possibility of accidental open air CO poisoning in children and adults who swim around recreational boats. ( info) |
| 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. ( info) |
| 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 ( info) |
19/269. 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. ( info) |
| Unilateral low attenuation areas within the right putamen, globus pallidus and thalamus were observed on CT in a patient after exposure to carbon monoxide. A transient bilateral appearance was found on subsequent CT examinations. Hemorrhagic infarction of the right putamen, and ischemic lesions in both thalami were visualized on MRI 2 weeks later. ( info) |