• 동의생리병리학회지
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• 제19권1호
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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).

• 대한임상독성학회지
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• 제4권2호
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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.

• 대한기관식도과학회:학술대회논문집
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• 대한기관식도과학회 1977년도 제11차 학술대회연제 순서 및 초록
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• pp.3.2-3
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• 1977

우리나라에서는 우리들의 현실생활에서 겨울철의 주연료가 되고있는 연탄과 무연탄으로 인한 일산화탄소 중독환자를 많이 보아봤으며, 우리나라 가구의 약 90%가 연탄등을 주연료로 사용하고 있는 현실에서 볼 때 CO중독에 따른 잇달은 사고는 사회적으로도 중요한 문제가 될 뿐아니라 이런 CO 중독의 후유증으로서 유발되는 청력손실 또한 큰 문제가 아닐 수 없다. CO 중독성난청은 혼수상태의 기간 및 고압산소기의 사용유무등에 따라서 크게 영향을 받으며 대부분 전정기의 장애를 동반한 감음신경성난청의 형태로 나타나는 경우가 많다. Lumio (1948)는 만성 CO 중독환자 700례중에서 73.3%의 감음신경성난청을 보고한바 있으며, Strzelczyk (1964)는 CO 중독성난청의 대부분이 만성중독에 의한 것임을 밝히는 한편 이들의 60%가 와우신경절후 병변임을 증명하였다. 난청만을 유발한 급성 CO 중독 증례는 그의 발생환경에서 고찰해 볼 때에도 외국에서는 매우 드물 례라고 하겠으나 특히 우리나라에서는 이때까지 이와 같은 증례를 보게되는 경우가 많았으며, 금번 저자들은 난청을 동반한 CO 중독환자 10명을 경험하여 청각학적 고찰을 실시한바 있기에 이에 보고하는 바이다.

• 대한임상독성학회지
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• 제17권2호
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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.

• 약학회지
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• 제36권3호
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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.

• 대한임상독성학회지
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• 제11권1호
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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.

• 대한임상독성학회지
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• 제9권2호
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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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• 제8권1호
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• pp.86-97
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• 1991

급성 일산화탄소중독환자의 예후를 예측하는 기초자료를 얻고자 1985년 10월부터 1989년 4월까지 급성 일산화탄소중독으로 영남대학병원 응급실을 통해 COHb검사로 확진되어 입원치료한 116명의 환자를 대상으로 입상소견 및 검사 소견을 비교, 분석하고 이들 소견과 지연성 후유증과의 관련성을 조사하여 다음과 같은 성적을 얻었다. 1. 입원환자 116례의 내원시 의식상태는 기면상태의 군이 36.2%로 가장 많았으며, 남녀의 비는 1:1.5로 여자가 많았다. 2. 내원시 의식장애가 심할수록 동맥혈의 pH 및 $PaCO_2$는 감소하는 경향을 보였는데, 이는 대사성산증에 의한 소견으로 보인다. 3. 일산화탄소중독으로 인한 초기 검사소견중 백혈구증다증은 65.5%. 헤마토크리트의 상승은 23.3%, 고혈당은 19.8%, GPT의 상승은 19.8%, creatinine의 상승은 0.9%, 뇨당검출은 12.1%였다. 4. 심전도 검사에서는 35.5%에서 이상소견을 보였는데 25.0%가 rhythm의 변화를, 15.5%가 ST, T절의 이상을 보였고, 이중 5.2%는 rhythm의 변화와 ST, T절의 이 상과 함께 나타났으나 전도장애의 이상은 없었다. 5. 뇌파검사에서는 경도이상의 이상소견을 보인 환자가 93.1%였으며, 이중 중등도의 이상소견을 보인 환자가 80.2%로 가장 많았다. 6. 입원환자중 지연성 후유증의 발생빈도는 7.8%였으며, 이들은 노출시간이 길고(>8시간), 백혈구증다증(>20,000) 및 뇌파이상(>중등도)이 심하였다.

• 한국화재소방학회:학술대회논문집
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• 한국화재소방학회 2010년도 춘계학술논문발표회 논문집
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• pp.174-178
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• 2010

원문이미지 참조

• 약학회지
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• 제36권1호
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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.