1/33. 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.- - - - - - - - - - ranking = 1keywords = consciousness (Clic here for more details about this article) |
2/33. 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.- - - - - - - - - - ranking = 0.125keywords = consciousness (Clic here for more details about this article) |
3/33. 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.- - - - - - - - - - ranking = 0.0037198048226348keywords = state (Clic here for more details about this article) |
4/33. Hyperbaric oxygen for carbon monoxide poisoning-induced delayed neuropsychiatric sequelae.The clinical manifestations of delayed neuropsychiatric sequelae after carbon monoxide (CO) intoxication are variable. In addition, there is no specific therapy for these complications. Fortunately, these complications have occurred less frequently in recent years, probably due to the usage of hyperbaric oxygen (HBO) therapy. We report an 8-year-old boy who developed late psychiatric disturbances 2 days after full recovery of consciousness from initial CO intoxication. His neuropsychiatric symptoms included consciousness disturbance, motor dysfunction, chorea, aphasia and agnosias. He received HBO therapy at 2.0 barr for 60 minutes once a day for 7 consecutive days. Three weeks later, he was functioning normally with no neuropsychiatric symptoms. A literature review concluded that HBO may be effective in treating neuropsychiatric sequelae. Moreover, immediate administration of HBO during acute CO intoxication may prevent these complications.- - - - - - - - - - ranking = 0.25keywords = consciousness (Clic here for more details about this article) |
5/33. Management of the moribund carbon monoxide victim.Carbon monoxide (CO) poisoning is the commonest single cause of fatal poisoning in the U.K. (Broome & Pearson, 1988). The clinical features are numerous and include headache, fatigue, dizziness, confusion, memory loss, paraesthesia, chest pain, abdominal pain, nausea, and diarrhoea as well as coma, convulsions and death. Without adequate treatment many patients develop neuropsychiatric sequelae including headaches, irritability, memory loss, confusion and personality changes. The diagnosis of CO poisoning is often suggested only by circumstances surrounding the victim, and remains a challenge to the A&E department. Hyperbaric oxygen therapy (HBO) is internationally accepted as the most powerful form of treatment in severe cases (Drug & therapeutics Bulletin, 1988; Lowe-Ponsford & Henry, 1989). However, in the U.K. treatment with HBO is often not considered due to lack of hyperbaric facilities (Meredith & Vale, 1988; Anand et al., 1988), and due to inadequate awareness on the part of hospital staff. We report a case of a patient deeply unconscious as a result of CO poisoning, in which serial treatments with HBO over a period of 14 days, produced dramatic results.- - - - - - - - - - ranking = 2.2287634806587keywords = unconscious (Clic here for more details about this article) |
6/33. frontal lobe and cingulate cortical metabolic dysfunction in acquired akinetic mutism: a PET study of the interval form of carbon monoxide poisoning.A middle-aged man suffering from acute carbon monoxide intoxication was clinically assessed to be in an akinetic and mute state. In order to elucidate regional cerebral disturbances, brain metabolism was investigated with fluoro-deoxyglucose positron emission tomography ((18)FDG-PET) 5.5 months after intoxication. Significantly reduced metabolic rates of glucose were revealed in selected brain regions, especially in both the frontal and anterior cingulate cortices, as well as in the subcortical white matter. Frontal and cingulate cortices showed a preserved metabolism of 35-53%, whereas the regional glucose consumption in cerebral white matter was reduced by more than 70%. In contrast, other areas of the brain such as the sensory-motor cortex, parts of the temporal lobes, basal ganglia and brainstem disclosed normal metabolic values. This lesion topography is discussed in relation to the development of akinetic mutism in the present case and in comparison with recent reports on the topic. Considering a plausible pathophysiology, akinetic mutism appears to be based on a different structural neuropathology when compared with the locked-in syndrome and the vegetative state. It is suggested that akinetic mutism is regarded as a specific condition characterized by injury of the frontal neuronal systems which promote executive functions.- - - - - - - - - - ranking = 0.0037198048226348keywords = state (Clic here for more details about this article) |
7/33. Post-interval syndrome after carbon monoxide poisoning.Carbon monoxide (CO) exposure and toxicity is a potentially lethal disorder with immediate and delayed side effects. A 24-y-old driver was admitted to the University-based emergency department with altered mental status. He was found unconscious in the driver's seat of his vehicle in an indoor garage the morning before. An estimated 7 h later, he was comatose and taken to a nearby village clinic. oxygen was administered immediately. Later, he was transferred to the university hospital. At the 12th h after exposure, the glasgow coma scale score was 12/15 (E3, M5, V4). Co-oximetry disclosed a carboxyhemoglobin concentration of 10.5%. Normobaric oxygen was administered. He recovered completely the 3rd d after exposure; however, on the 7th d disorientation and agitation was noted, and the interval form of CO poisoning and leukoencephelopaty were suspected, for which he was readmitted the 10th d after exposure. Analysis of cerebrospinal fluid and blood revealed no abnormalities. magnetic resonance imaging on the 11th d after exposure demonstrated an ischemic area in the posterior temporoparietal area. The patient continued improvement to discharge at 7th d of the second admission. Close follow-up should be scheduled for CO-poisoned patients to rule out the post-interval syndrome for at least 1 mo. This should also include those with apparent clinical and laboratory recovery.- - - - - - - - - - ranking = 2.2287634806587keywords = unconscious (Clic here for more details about this article) |
8/33. Carbon monoxide brain toxicity: clinical, magnetic resonance imaging, magnetic resonance spectroscopy, and neuropsychological effects in 9 people.Carbon monoxide (CO) exposure is a common cause of toxic brain damage, whereby effects range from transient neurological dysfunction to coma and death. A spectrum of severity of magnetic resonance imaging (MRI) findings after CO brain toxicity, including globus pallidus and white matter lesions, is well documented. Reports of MR spectroscopy (MRS) findings re main sparse. This article reports 9 people exposed to CO because of an apartment house's faulty gas heater. Four, with transient loss of consciousness after chronic moderate level CO exposure, suffered intellectual impairment without MRI abnormalities. The MRS of 1 individual demonstrated decreased n-acetyl aspartase in the basal ganglia, bilaterally. Of 5 exposed to high levels for about 12 hours, 1 died prior to clinical and/or MRI evaluation. One who suffered coma recovered but was lost to evaluation. Three, who were unconscious for hours to days, exhibited T2 MRI white matter signal abnormalities. MRS showed decreased basal ganglia n-acetyl aspartase in 2. One of these suffers a Parkinsonian syndrome. All 3 are intellectually impaired. This study demonstrates that although MRI and MRS are useful markers of CO-induced brain damage, they are not always sensitive to resultant intellectual dysfunction.- - - - - - - - - - ranking = 2.3537634806587keywords = unconscious, consciousness (Clic here for more details about this article) |
9/33. Reversible motor and sensory peripheral neuropathy in a patient following acute carbon monoxide intoxication.central nervous system complications following carbon monoxide (CO) poisoning are well reported in the literature but peripheral neuropathy is under-recognized. We report the clinical and electrophysiological studies of the transient peripheral neuropathy developed in a patient following acute CO intoxication. A 27-year-old woman was found unconscious with severe hypoxia and 34.5% serum level of carboxyhemoglobin. She progressed favourably after hyperbaric oxygen therapy. Neurological examination revealed bilateral pyramidal signs. The patient referred weakness and sensory abnormalities in her right foot. An electroencephalogram did not show focal abnormalities and brain magnetic resonance was normal. Needle electromyography of weak right tibialis anterior muscle showed a reduced recruitment pattern but no spontaneous activity. Electroneurographic evaluation revealed findings compatible with a motor and sensory peripheral neuropathy in nerves of both lower limbs. In few months complete clinical recovery was reached, and the electroneurography showed normality a year later Reversible peripheral neuropathy should be considered as a possible neurological complication following acute CO poisoning. The electrophysiological studies were essential for its diagnosis and follow up.- - - - - - - - - - ranking = 2.2287634806587keywords = unconscious (Clic here for more details about this article) |
10/33. An interesting cause of pulmonary emboli: acute carbon monoxide poisoning.carbon monoxide poisoning, a public health problem of considerable significance, is a relatively frequent event today, resulting in thousands of hospitalizations annually. A 70-year-old lady was seen in the emergency department with a provisional diagnosis of carbon monoxide poisoning. The previous night, she slept in a tightly closed room heated with coal ember. She was found unconscious in the morning with poor ventilation. She had a rare presentation of popliteal vein thrombosis, pulmonary emboli, and possible tissue necrosis with carbon monoxide poisoning. oxygen treatment with low-molecular-weight heparin (nadroparine) and warfarin therapy resulted in an improvement in both popliteal and pulmonary circulations. In conclusion, the presence of pulmonary emboli should be sought in patients with carbon monoxide poisoning.- - - - - - - - - - ranking = 2.2287634806587keywords = unconscious (Clic here for more details about this article) |
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