1.Two Cases of Carbon Monoxide Poisoning Showing Low-Density Lesions with Unusual Enhancement on Computed Tomographic Brain Scan.
Il Saing CHOI ; Young Chul CHOI ; Soon Kwan KIM ; Myung Sik LEE
Journal of the Korean Neurological Association 1992;10(3):358-361
No abstract available.
Brain*
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Carbon Monoxide Poisoning*
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Carbon Monoxide*
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Carbon*
2.Chorea as a Clinical Manifestation of Delayed Neurologic Sequelae in Carbon Monoxide Poisoning: Case Report.
Il Saeng CHOI ; Yeon Mi HWANG ; Ki Hwan KIM
Journal of the Korean Neurological Association 1984;2(1):91-93
No abstract available.
Carbon Monoxide Poisoning*
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Carbon Monoxide*
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Carbon*
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Chorea*
3.Acute carbon monoxide poisoning in a Filipino household
Louraine Mae J. Bagares ; Philip Rico P. Mejia ; Rene B. Punsalan ; Marc Conrad C. Molina
Philippine Journal of Neurology 2023;26(2):15-19
There have been multiple reports already regarding acute carbon monoxide/CO poisoning in
the Philippines secondary to misuse of portable generators, especially during the times of
typhoon. We present a case of unintentional carbon monoxide poisoning in a Filipino household
wherein three of its members were found dead and leaving other five unconscious before they
were rushed to the hospital. The index patient had increased serum fraction percentage of
carboxyhemoglobin level and presented with rhabdomyolysis during admission. Neuroimaging
confirmed a hypoxic-ischemic encephalopathy secondary to carbon monoxide intoxication.
Even without hyperbaric oxygen therapy, patient improved with adequate hydration, early
rehabilitation and trauma-focused psychotherapy.
Carbon Monoxide Poisoning
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Carbon Monoxide
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Family Characteristics
4.Epidemiological Studies on the Acute Carbon Monoxide Poisoning.
Soo Hun CHO ; Dork Ro YUN ; In Dal KIM
Korean Journal of Preventive Medicine 1974;7(2):359-366
No abstract available.
Carbon Monoxide Poisoning*
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Carbon Monoxide*
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Carbon*
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Epidemiologic Studies*
5.Carbon Monoxide Poisoning in the Unusual Circumstance: Four Cases Report.
Korean Journal of Legal Medicine 2000;24(1):68-74
Carbon monoxide which is an odorless, colorless, non-irritating gas causes asphyxia by blocking the hemoglobin of the RBC from carrying oxygen to the tissues and from returning carbon dioxide to the lungs. The clinical symptoms of CO poisoning depend on the blood CO saturation level and in a healthy middle-aged individual a blood CO saturation greater than 50% is considered fatal. In forensic science, the investigation of the scene in cases of CO poisoning is imperative to determine the manner of death or the source of CO production, while postmortem diagnosis of CO poisoning is not difficult. The author reported four cases of CO poisoning in the unusual or atypical circumstances, which were not recognized in the scene.
Asphyxia
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Carbon Dioxide
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Carbon Monoxide Poisoning*
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Carbon Monoxide*
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Carbon*
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Diagnosis
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Forensic Sciences
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Lung
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Oxygen
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Poisoning
6.Characteristics of Electrocardiographic Changes in Myocardial Injury with Acute Carbon Monoxide Poisoning.
Journal of the Korean Society of Emergency Medicine 2015;26(4):313-319
PURPOSE: Electrocardiographic findings such as Tp-Te interval, Tp-Te dispersion, and Tp-Te/QT ratio could be used to predict dysrhythmic events regarding any kind of toxic materials. We investigated the prevalence of cardiac toxicity related to acute carbon monoxide (CO) poisoning and the characteristics of electrocardiographic changes corresponding to the severity of intoxication. METHODS: This retrospective observational study was conducted with 113 patients of acute CO poisoning from May, 2013 to July, 2014. Myocardial injury (MI) was determined based on an elevation of serum troponin T within the first 24 hours of the ED visit. The study population was classified according to Acute Neuropsychiatric Status (ANS) scoring: a mild intoxication group (ANS scores 0 and 1) and a severe intoxication group (ANS scores 2 and 3). RESULTS: Prevalence of MI was higher in the severe intoxication group of acute CO poisoning (p<0.001). QTc was significantly prolonged in the MI group (p=0.007). However, no differences in other electrocardiographic parameters were observed between MI group and non-MI group. CONCLUSION: Myocardial injury was combined more frequently with a severe intoxication group of acute CO poisoning compared to a mild intoxication group. A specific feature of eletrocardiogram in myocardial injury with acute CO poisoning was a QTc prolongation.
Carbon Monoxide Poisoning*
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Carbon Monoxide*
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Carbon*
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Electrocardiography*
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Humans
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Observational Study
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Poisoning
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Prevalence
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Retrospective Studies
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Troponin T
7.Clinical significance of QT interval and Cardiac Enzyme in Carbon Monoxide Poisoning.
Mun Ki MIN ; Seung YOO ; Seung Woo HONG ; Jang Yong LEE ; In Soo KIM ; Sung Pil CHUNG ; In Sool YOO
Journal of the Korean Society of Emergency Medicine 2006;17(1):58-64
PURPOSE: This study was performed to investigate the value of corrected QT interval (QTc), corrected QT dispersion (cQTd), cardiac enzyme (Creatinine kinase; CK, CKMB) as a short-term prognosis and severity evaluation in CO poisoning. METHODS: This study reviewed 55 cases of CO poisoning that occurred form January 1, 2000, to June 31, 2005. We have analyzed the admission ECGs of patients with CO poisoning for QTc, QTd (QT dispersion), cQTd and measure CK, CK-MB, too. QTd was defined as the difference between the longest and the least QT intervals in any of the 12 leads. We evaluate short-term outcome with consciousness on discharge from ED and severity with receiving hyperbaric oxygen therapy (HBO). RESULTS: Eighteen of 55 patients received HBO and seven patients received two or more. On admission, cQTd intervals of the intoxicated patients were increased compared to normal (63.2+/-38 ms), but not the QTc, QT, QTd. QTc interval and CK of patients who received HBO were significantly increased compared to patients who not receive(472.0+/-4 7 ms VS 437.2+/-730 ms, p=0.006 158 3.1+/-43174 u/L 138.8+/-2363 u/L p=0.009). Whether or not consciousness on discharge was associated only CK (p= 0.02). CONCLUSION: The QTc interval and CK were prolonged at patients who received HBO. That means that the QTc interval and CK reflected the severity of CO poisoning. CK of Patients who not recover consciousness after HBO were increased significantly. To say, as CK were increase, the short-term prognosis of CO poisoning is the poorer.
Carbon Monoxide Poisoning*
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Carbon Monoxide*
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Carbon*
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Consciousness
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Electrocardiography
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Humans
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Hyperbaric Oxygenation
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Phosphotransferases
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Poisoning
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Prognosis
8.Influence of Acute and Chronic Carbon Monoxide Poisoning on Reproductive Organs of the White Rats: Enzymological Study 2. Lactate Dehydrogenase Activity in the Prostate.
Korean Journal of Urology 1975;16(1):7-9
Influence of acute and chronic carbon monoxide poisoning on the rat prostate has been studied enzymologically and the following results were obtained: 1. An increasing tendency of the total lactate dehydrogenase activity in the prostate tissue was observed is the chronic poisoning groups. 2. The lactate dehydrogenase isoenzyme distribution pattern was not remarkably influenced by chronic poisoning. 3. The lactate dehydrogenase isoenzyme distribution pattern is the prostate tissue was as LDH5> LDH4> LDH3> LDH2> LDH1.
Animals
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Carbon Monoxide Poisoning*
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Carbon Monoxide*
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Carbon*
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L-Lactate Dehydrogenase*
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Lactic Acid*
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Poisoning
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Prostate*
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Rats*
9.Influence of Acute and Chronic Carbon Monoxide Poisoning on Reproductive Organs of the White Rat: Enzymological Study 1. Lactate Dehydrogenase Activity in the Testis.
Korean Journal of Urology 1975;16(1):1-5
Influence of acute and chronic carbon monoxide poisoning on the rat testis has been studied enzymologically and the following results were obtained: Experimental animals were divided as 1) control, C1 (6 animals) 2) acute poisoning with 0.5% carbon monoxide until death, C2 (10 animals) 3) chronic poisoning with 0.05% carbon monoxide for 2 hours daily E1 (5 animals)...3 days/week for 8 weeks E2 (6 animals)...3 days/week for 4 weeks 4) acute poisoning until death with 0.5% carbon monoxide after chronic poisoning with 0.05% carbon monoxide E3 (5 animals)...chronic poisoning for 8 weeks plus acute poisoning E4 (5 animals)...chronic poisoning for 4 weeks plus acute poisoningUsing Neiland's method, the total activities and distribution patterns of lactic dehydrogenase in rat testis were measured. All of the data were analyzed statistically. 1. The total activities of lactic acid dehydrogenase in all experimental groups seemed to increase. In the group E3, the increase was statistically significant.(p<0.05) 2. No significant changes were observed in the lactic acid dehydrogenase isoenzyme distribution pattern of the testis. both is the control and experimental groups. 3. The lactic acid dehydrogenase distribution patterns were as fraction l>2>4>3>5 4. No significant histopathological changes were observed in the rat testis.
Animals
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Carbon Monoxide Poisoning*
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Carbon Monoxide*
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Carbon*
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L-Lactate Dehydrogenase*
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Lactic Acid*
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Oxidoreductases
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Poisoning
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Rats*
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Testis*
10.Effect of Acute Carbon Monoxide Poisoning on Acid Phosphatase Activity of Prostate Gland In Rat: Histochemical Study.
Korean Journal of Urology 1976;17(3):165-169
Effect of acute carbon monoxide poisoning on prostatic acid phosphatase in white rat hag been studied histochemically. The experimental animals were exposed to 0.25% and O. 5% of carbon monoxide from 5 minutes to 4 hours duration. Gomori's modified method was used for acid phosphatase test. Following results are obtained: 1. The acid phosphatase activity increases after 30minutes of exposure in both experimental groups, 0.25% and 0.5% of carbon monoxide, and the changes of acid phosphatase activity become more significant according to the duration of exposure. 2. The changes of acid phosphatase activity are similar in both experimental groups exposed to 0.25% and 0.5% of carbon monoxide. 3. No significant histopathological changes are observed in rat prostate gland.
Acid Phosphatase*
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Animals
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Carbon Monoxide Poisoning*
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Carbon Monoxide*
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Carbon*
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Poisoning
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Prostate*
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Rats*