No abstract available.
Brain* ; Carbon Monoxide Poisoning* ; Carbon Monoxide* ; Carbon*

No abstract available.
Carbon Monoxide Poisoning* ; Carbon Monoxide* ; Carbon* ; Chorea*

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 ; Carbon Monoxide ; Family Characteristics

No abstract available.
Carbon Monoxide Poisoning* ; Carbon Monoxide* ; Carbon* ; Epidemiologic Studies*

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 ; Carbon Dioxide ; Carbon Monoxide Poisoning* ; Carbon Monoxide* ; Carbon* ; Diagnosis ; Forensic Sciences ; Lung ; Oxygen ; Poisoning

Pathophysiology of acute carbon monoxide poisoning is not clear. It is generally accepted that hypoxic and/or anoxic insult is very significant role in the pathophysiology of acute acrbon monoxide poisoning, but many arguments are documented especially focal hypoxia or metabalic acidosis within brain parenchyme. In sofar such a focal change seems to be largely depend upon focal change of neuroendocrine substances including B-endorphin. Also B-endorphin is known to be responsble to the pathogenesis of cerebral ischemia. Though the possible relationship between the alteration of level of B-endorphin and hypoxia, it is seldom to pay attention to the role of B-endorphin in carbon monoxide intoxication. We measured plasma B-endorphin in acute carbon monoxide intoxication and compared with the value of control group. There was no difference between control group and acute carbon monoxide poisoning group, the possible role of B-endorphin in acute carbon monoxide poisoning should not be excluded. We suggest the more comprehensive and newly programmed study seems to need for clarifying the possible role of B-endorphin in acute carbon monoxide poisoning.
Acidosis ; Anoxia ; Brain ; Brain Ischemia ; Carbon Monoxide Poisoning* ; Carbon Monoxide* ; Carbon* ; Plasma* ; Poisoning

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* ; Animals ; Carbon Monoxide Poisoning* ; Carbon Monoxide* ; Carbon* ; Poisoning ; Prostate* ; Rats*

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 ; Carbon Monoxide Poisoning* ; Carbon Monoxide* ; Carbon* ; L-Lactate Dehydrogenase* ; Lactic Acid* ; Poisoning ; Prostate* ; Rats*

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 ; Carbon Monoxide Poisoning* ; Carbon Monoxide* ; Carbon* ; L-Lactate Dehydrogenase* ; Lactic Acid* ; Oxidoreductases ; Poisoning ; Rats* ; Testis*

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* ; Carbon Monoxide* ; Carbon* ; Consciousness ; Electrocardiography ; Humans ; Hyperbaric Oxygenation ; Phosphotransferases ; Poisoning ; Prognosis