• Journal of Physiology & Pathology in Korean Medicine
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• v.19 no.1
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• pp.279-283
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• 2005

After initial recovery from acute carbon monoxide(CO) intoxication, some patients occasionally undergo severe neuropsychiatric deterioration, which is called postanomic delayed encephalopathy(sequelae). This is the clinical study about one patient, a 53-year-old woman, diagnosed with delayed encephalopathy after acute CO intoxication. The patient's symptoms were mental dysfunction including memory impairment and disorientation, aphasia, atrophy and weakness throughtout the body. She had completely recovered after an anomic episode, but the neurological symptoms that developed were preceded by an interval of apparent nomality.(the 'lucid interval'). She was characterized as suffering deficiency syndrome of the heart(心虛) and was prescribed for her an Ansinschungnoi-tang(安神淸腦湯), and thereafter her symptoms improved remarkably. For the evaluation of clinical improvement, we use the Modified Barthel Index(MBI).

• Journal of The Korean Society of Clinical Toxicology
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• v.4 no.2
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• pp.122-127
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• 2006

Purpose: It is not easy to detect carbon monoxide (CO) leakage, and CO-intoxicated patients do not show a specific set of symptoms. The aims of this study are to clinically evaluate patients with CO gas intoxication from a CO leak at an underground shopping center, and to discuss the establishment of a disaster prevention plan. Methods: A total of 51 patients intoxicated by CO gas exposure in a gas disaster at a underground shopping center in Seoul on September 8, 2006 were enrolled in this study, and the patients' medical records were retrospectively reviewed. Results: The mean patient age was $29.4{\pm}6.3$. The initial mean COHb level was $14.98{\pm}6.97%$. The number of patients with COHb greater than 25% was three, and six patients experienced a syncopal attack. Only one patient-was treated with hyperbaric oxygen therapy. However, none of the patients complained of severe neurologic or cardiovascular symptoms. Conclusion: The symptoms of CO intoxication are non-specific and difficult to define, and the detection of CO leak-age is difficult. Thus, workplaces should be equipped with leakage sensors and automatic alarm systems and should have develop disaster prevention plans.

• Proceedings of the KOR-BRONCHOESO Conference
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• 1977.06a
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• pp.3.2-3
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• 1977

Deafness has been considered in recent publications a transient feature in the neurological complications of carbon monoxide poisoning. The inner ear is a sensitive as central nervous system to anoxia. It is well known a similar vulnerability to the toxic action of carbon monoxide for the two neurosensory epithelia of the organ of Corti. There is geographical character in the carbon monoxide poisoning and more frequently experienced in Korea. 10 cases of hearing loss due to carbon monoxide intoxication were reported with the literature review.

• Journal of The Korean Society of Clinical Toxicology
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• v.17 no.2
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• pp.66-78
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• 2019

Purpose: Thallium (TI+) autometallography is often used for the imaging of neuronal metabolic activity in the rodent brain under various pathophysiologic conditions. The purpose of this study was to apply a thallium autometallographic technique to observe changes in neuronal activity in the forebrain of rats following acute carbon monoxide (CO) intoxication. Methods: In order to induce acute CO intoxication, adult Sprague-Dawley rats were exposed to 1100 ppm of CO for 40 minutes, followed by 3000 ppm of CO for 20 minutes. Animals were sacrificed at 30 minutes and 5 days after induction of acute CO intoxication for thallium autometallography. Immunohistochemical staining and toluidine blue staining were performed to observe cellular damage in the forebrain following intoxication. Results: Acute CO intoxication resulted in significant reduction of TI+ uptake in major forebrain structures, including the cortex, hippocampus, thalamus, and striatum. In the cortex and hippocampal CA1 area, marked reduction of TI+ uptake was observed in the cell bodies and dendrites of pyramidal neurons at 30 minutes following acute CO intoxication. There was also strong uptake of TI+ in astrocytes in the hippocampal CA3 area following acute CO intoxication. However, there were no significant histological findings of cell death and no reduction of NeuN (+) neuronal populations in the cortex and hippocampus at 5 days after acute CO intoxication. Conclusion: The results of this study suggest that thallium autometallography can be a new and useful technique for imaging functional changes in neural activity of the forebrain structure following mild to moderate CO intoxication.

• YAKHAK HOEJI
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• v.36 no.3
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• pp.269-277
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• 1992

The effects of ginseng saponins on the distribution of nerve cells in cerebral cortex of carbon monoxide (CO)-intoxicated mice were studied in the young ($5{\sim}8$ weeks) and aged ($43{\sim}52$ weeks) mice. Mice were exposed to 5000 ppm of CO for 40 minutes (72% HbCO). After that, nerve cells in motor(area 4), somatosensory(area 3) and visual(area 17) area of cerebral cortex was observed. In young mice, the number of nerve cells in each area was significantly decreased on 1st, 7th and 14th day after CO intoxication. In aged mice, that was also decreased after CO intoxication. Especially the number of the nerve cells in motor and somatosensory area was significantly decreased on 1st and 7th day, while that in visual area was decreased only on 1st day. The number of nerve cells in young mice pretreated with ginseng saponins were significantly decreased less on 7th and 14th day than that of untreated mice. The number of nerve cells in each area of normal aged mice was larger than that of normal young mice. The results suggest that CO exposure causes local degeneration or disturbance of nerve cells and delayed neurologic sequelae, while ginseng saponins might play a role of protective action on the nerve cells which were damaged by CO.

• Journal of The Korean Society of Clinical Toxicology
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• v.11 no.1
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• pp.41-45
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• 2013

Following are brief statements about the delayed encephalopathy of a patient who recovered without disturbance of consciousness after acute carbon monoxide poisoning. A 72-year-old male was found without consciousness at home and then visited the ER center. Later we learned that the patient was using briquettes as a household heating source. Blood carbon monoxide hemoglobin level was 17.5%. As carbon monoxide poisoning was uncertain after the first interview with the patient, hyperbaric oxygen therapy was not administered at the early stage. After supplying 100% oxygen, the patient recovered consciousness, however, the strength of the lower limb muscle had decreased to class II. The patient showed continued weakening of the lower limb muscle and an increase of CPK; therefore, he was diagnosed as carbon monoxide intoxication and rhabdomyolysis and then admitted to the intensive care unit (ICU) for conservative treatment. During the hospitalization period, continued weakening of the lower limb muscle was observed and he was diagnosed as myopathy after EMG/MCV. However, he suddenly showed altered mentality on the 20th day of hospitalization, and underwent brain MRI. T2 weighted MRI showed typically high signal intensity of both globus pallidus and periventricular white matter; therefore, he was diagnosed as delayed carbon monoxide encephalopathy. This case showed delayed encephalopathy accompanied by rhabdomyolysis and myopathy of a patient who recovered without disturbance of consciousness.

• Journal of The Korean Society of Clinical Toxicology
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• v.9 no.2
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• pp.88-94
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• 2011

Purpose: Delayed neuropsychological sequelae (DNS) commonly occurs after recovery from acute carbon monoxide poisoning. The aim of this article is to identify the factors associated with DNS development. Methods: We retrospectively evaluated patients, admitted to the medical center emergency department from June 2005 to March 2011, who were suffering from acute carbon monoxide (CO) poisoning. We categorized the patients into two groups - those with DNS, and those without DNS. Multiple regression analysis was performed to identify the factors related to manifestation of DNS. Results: Of the total one hundred fifty seven patients (157) recruited for the study, twenty two (22) developed DNS. Longer CO exposure times and lower GCS scores were positively associated with development of DNS symptoms. Conclusion: Our study identified two potential factors which are predictive of DNS development in CO intoxication, however, more studies are needed. Adequate follow-up after hospital discharge to monitor for and accurately identify manifestation of DNS, is also important.

• Journal of Yeungnam Medical Science
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• v.8 no.1
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• pp.86-97
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• 1991

To obtain the basic data of prognosis of acute carbon monoxide(CO) intoxication, one hundred and sixteen cases of CO intoxication defined by carboxyhemoglobin(COHb) and admitted via emergency room of Yeungnam University Hospital from Oct. '85 to April' 89 have been clinically analyzed and evaluated, including delayed postanoxic encephalopathy(DPE) and the following results were obtained. 1. The ratio of male to female was 1:1.5 and mental state was drowsy mostly(26.2% of 116 cases) 2. The more disturbed the mental state, the more decreased was the arterial pH and $PaCO_2$, which may be the result of metabolic acidosis. 3. The early laboratory findings in patients of CO intoxication were as follows : leukocytosis-65.5%, increase of hematocrit-23.3%, hyperglycemia-19.8%, increase of GPT-19.8% increase of creatinine-0.9%, and glucosuria-12.1%. 4. The early findings of EKG were abnormal in 35.3% : change of rhythm-25.0%, abnormal ST segment-15.5% (change of rhythm and abonormal ST segment-5.2%) but the conduction disorder was not present. 5. The abnormal EEG above mild degree was 93.1%, of which moderate was most frequent(80.2%). 6. The incidence of DPE was 7.8% among all admitted CO patients. DPE cases had long duration of exposure time(8 hours), severe leukocytosis(20,000) and an abnormal EEG(MA).

• Proceedings of the Korea Institute of Fire Science and Engineering Conference
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• 2010.04a
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• pp.174-178
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• 2010

원문이미지 참조

• YAKHAK HOEJI
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• v.36 no.1
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• pp.56-65
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• 1992

The present study examined the effects of carbon monoxide (CO) intoxication and aging on learning and memory deficit in young($5{\sim}8$ weeks) and aged($52{\sim}66$ weeks) mice, using the step down and step through passive avoidance failure techniques. We also investigated the effects of ginseng saponins on memory deficit. Significant decrease in memory registration, retention and retrieval function in young mice and decrease in memory registration and retention function in aged mice were observed. Normal young mice were apt to perform to a great degree of passive avoidance response than normal aged mice, but there was no difference between both groups by CO exposure. Administration of ginseng saponins showed an improvement on passive avoidance failure induced by CO exposure.