• Journal of The Korean Society of Clinical Toxicology
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• v.17 no.2
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• pp.118-125
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• 2019

Purpose: Non-benzodiazepine hypnotic drugs (including zolpidem) are associated with an increased risk of suicide and suicidal ideation. Considering the wide usage of zolpidem, this drug should be considered a possible etiology for stupor or coma in any patient exposed to this drug. However, there are no reports on zolpidem blood levels in emergency department patients in Korea. We therefore reviewed the analyzed data of a toxicology laboratory at one university affiliated hospital. Methods: The sex, age, chief symptoms, suspiciousness of poisoning, and presumption of poison were analyzed from January 2018 to June 2019. The detection frequency and level of zolpidem in the patient blood were compared to the mental changes presented, which is the main consequence of zolpidem. Results: A total of 229 toxicological analyses, requested to a toxicological laboratory at one university affiliated hospital, were reviewed. Among 229 patients, the mean age was 54.3±20.7 years old with 113 women and 116 men. 8.7% of patients have psychiatric illness and 39.7% were poisoned intentionally. The chief symptoms detected were: mental change 55.0%, gastrointestinal 14.4%, cardiovascular 10.5%, focal neurological 7.4%, respiratory 3.5%, none 8.7%, and unknown 0.4%. A request for detailed reports revealed that causative poisons were specified only in 20.1% cases. Zolpidem was detected in 22.3% cases (51/229), with median blood level 1.26 mg/L (interquartile 0.1, 5.06 mg/L) and urine 0.90 mg/L (interquartile 0.11, 5.6 mg/L). Furthermore, zolpidem was more frequently detected in toxicology analysis of patients where mental change was the primary symptom, as compared to other symptoms (32.5% vs. 9.7%, p<0.01). Conclusion: This study reported the blood level of zolpidem in suspected poisoning patients admitted to the emergency department.

• Journal of The Korean Society of Emergency Medicine
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• v.29 no.5
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• pp.509-518
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• 2018

Objective: The evidence that hyperbaric oxygen (HBO) therapy is more effective for improving the acute neuropsychological status (ANS) of carbon monoxide poisoning than normobaric oxygen (NBO) therapy is not convincing. This is because the levels of carboxyhemoglobin (COHb) do not correlate with the clinical severity of carbon monoxide poisoning and there is no universally accepted severity scale of carbon monoxide poisoning. This paper suggests a new scale for the clinical and neurological severity of carbon monoxide poisoning, called the ANS, and assesses the effect of HBO therapy for each level of ANS compared to NBO therapy. Methods: A total of 217 patients who had been hospitalized because of carbon monoxide poisoning from January 2009 to July 2013 were studied. ANS was suggested as a new severity scale of carbon monoxide poisoning considered in the Glasgow Coma Scale, acute neuro-psychologic signs and symptoms, or cardiac ischemia on the initial medical contact. HBO therapy is indicated in those who have a loss of consciousness, seizure, coma, abnormal findings on a neurological examination, pregnancy, persistent cardiac ischemia, level of COHb >25%, or severe metabolic acidosis (pH <7.2). The end point is the day of discharge, and recovery is defined as a normal neuro-psychological status without any sequelae. Results: The levels of troponin T and creatinine increased significantly with increasing ANS score. In the moderate to severe group (ANS 2 and 3), the recovery rate was significantly higher when treated with HBO therapy than with NBO therapy (P=0.030). On the other hand, the development of delayed neuro-psychological sequelae (DNS) did not correlate with any level of ANS, type of oxygen therapy, or recovery on discharge. Conclusion: In the moderate to severe poisoned group, HBO therapy is more effective for improving the ANS from carbon monoxide poisoning than NBO therapy. On the other hand, the development of DNS of HBO therapy is no more preventable than with NBO therapy. Although the level of ANS is low, the patient needs to be provided with sufficient information and a follow-up visit is recommended for any abnormal symptoms because the ANS does not correlate with the development and degree of DNS.

• The Korean Journal of Physiology
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• v.1 no.2
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• pp.185-191
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• 1967

In order to evaluate the elimination of CO through the lung comparing with the decrease of CO content in the blood, authors had induced acute CO poisoning on 9 dogs. Arterial CO-Hb saturation, CO concentration, %, in expired gas and eliminated CO amount through the lung were measured at 1,5,10,30,60, and 120 minutes after acute CO poisoning in 6 dogs breathing room air and 3 dogs breathing room air and oxygen alternately. Results obtained are summarized as follows. In room air breathing group, arterial CO-Hb saturation averaged 50.8% , and 53.67 ml of CO was blew off through the lung during 120 minutes and in alternately air and oBygen breathing group, the arterial CO-Hb saturation averaged 65.6% and 95.6 ml of CO was blew off through the lung. The amount of CO eliminated in expired gas for 120 minute was much less than the amount of decreased CO in arterial blood which was calculated with the decreased CO-Hb content in the estimated circulating blood volume. Such difference between the amount of eliminated CO in expired gas and the decreased CO in blood might be attributed to the oxidation of CO to $CO_2$ in the tissues. Concentration of CO in expired gas was markedly increased and the rate of decrease in arterial CO-Hb saturation is enhanced by oxygen breathing. In early period of recovery from acute CO poisoning, neither the CO concentration in expired gas, nor, the rate of CO elimination (unlit 2 minutes after CO poisoning) showed close correlation with the blood CO-Hb saturation level. The reason seemed to be due to irregularly depressed or unevenly stimulated respiration which were induced by acute CO poisoning.

• Journal of Advanced Marine Engineering and Technology
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• v.37 no.8
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• pp.855-861
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• 2013

Small-pore Cu-chabazite SCR catalysts with high NOx conversion at low temperatures are of interest for marine diesel engines with exhaust temperatures in the range of 150 to $300^{\circ}C$. Unfortunately, fuels for marine diesel engines can contain a high level of sulfur of up to 1.5% by volume, which corresponds to a $SO_2$ level of 500 ppm in the exhaust gases for an engine operating with an A/F ratio of 50:1. This high level of $SO_2$ in the exhaust may have detrimental effects on the NOx performance of the Cu-chabazite SCR catalysts. In the present study, a bench-flow reactor is used to investigate the effects of sulfur poisoning on the NOx performance of Cu-chabazite SCR catalysts. The SCR catalysts were exposed to simulated diesel exhaust gas stream consisted of 500 ppm $SO_2$, 5% $CO_2$, 14% $O_2$, 5% $H_2O$ with $N_2$ as the balance gas at 150, 200, 250 and $300^{\circ}C$ for 2 hours at a GHSV of 30,000 $h^{-1}$. After sulfur poisoning the low-temperature NOx performance of the SCR catalyst is evaluated over a temperature range of 150-$300^{\circ}C$ to determine the extent of the catalyst deactivation. Desulfation is also carried out at 600 and $700^{\circ}C$ for 30 minutes to determine whether it is possible to recover the NOx performance of the sulfur-poisoned SCR Catalysts.

• Journal of The Korean Society of Clinical Toxicology
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• v.16 no.2
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• pp.86-92
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• 2018

Purpose: Cardiovascular or respiratory complications of acute intoxication are the most common causes of mortality. Advanced cardiac life support (ACLS) or specific antidotes help manage these cardiac or respiratory complications in acute intoxication. On the other hand, some cases do not respond to ACLS or antidotes and they require some special treatment, such as extracorporeal life support (ECLS). ECLS will provide the chance of recovery from acute intoxication. This study examined the optimal timing of ECLS in acute intoxication cases. Methods: This paper is a brief report of a case series about ECLS in acute poisoning. The cases of ECLS were reviewed and the effects of ECLS on the blood pressure and serum lactate level of the patients were analyzed. Results: A total of four cases were reviewed; three of them were antihypertensive agent-induced shock, and one was respiratory failure after the inhalation of acid. The time range of ECLS application was 4.8-23.5 hours after toxic exposure. The causes of ECLS implementation were one for recurrent cardiac arrest, two for shock that did not respond to ACLS, and one for respiratory failure that did not respond to mechanical ventilator support. Three patients showed an improvement in blood pressure and serum lactate level and were discharged alive. In case 1, ECLS was stared at 23.5 hours post toxic exposure; the patient died due to refractory shock and multiple organ failure. Conclusion: The specific management of ECLS should be considered when a patient with acute intoxication does not recovery from shock or respiratory failure despite ACLS, antidote therapies, or mechanical ventilator support. ECLS improved the hemodynamic and ventilator condition in complicated poisoned patients. The early application of ECLS may improve the tissue perfusion state and outcomes of these patients before the toxic damage becomes irreversible.

• Korean Journal of Animal Reproduction
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• v.25 no.1
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• pp.35-42
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• 2001

This study was performed to elucidate the patho-physiology of copper-poisoned rats after consecutive oral administrations of the copper sulfate. The changes in feed and water intake, gains of body weight, blood pictures and mineral compositions of several organs were observed to measure the effects of copper poisoning. 1. Compared with control group, every experimental group of which 1,000, 2,000, or 4,000 ppm/kg of copper sulfate was administered displayed a gradual decrease in feed intake in dose-dependent manners. 2. After 1,000, 2,000 or 4,000 ppm/kg of copper sulfate administration, water intake seemed to decrease in every experimental group in dose-dependent manners, but there was little statistical significance. 3. After 1,000, 2,000 or 4,000 ppm/kg of copper sulfate administration, body weight decreased in every experimental group in dose-dependent manners. 4. After 1000, 2,000 or 4,000 ppm/kg of copper sulfate administration, the PLT values and numbers of RBC and WBC significantly increased after copper sulfate administration, but the values of Hb and PCV were lower than those of control group's. 5. After 2,000 or 4,000 ppm/kg of copper sulfate administration, the levels of Cu, Mn, Fe, Pb and Zn in the liver were lowered, but the levels of Mn, Fe, Pb and Zn in the kidneys increased except Cu levels.

• Journal of Nutrition and Health
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• v.24 no.6
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• pp.526-533
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• 1991

The effect of dietary selenium on the activity of $\delta$-aminolevulinic acid dehydratase (ALAD) inhibited by the administration of lead were investigated in rats. The levels of dietary lead in the acetate form were 0(contro)200, 1, 000, 2, 000 and 5, 000ppm. Except control group four-level of lead diet groups were again subdivided into two depending on with and without 0.5ppm selenium supplementation. Sixty-three 40-day-old male Sprague-Dawley rats weighing 141$\pm$5g were distributed into total of nine diet groups according to RCB design and fed ad libidum for 4 weeks. Lead dietary groups did not show any significnat difference in food intake from the control group. Food efficiency and weight gain were lower in 2.000ppm and 5, 000ppm lead groups but not found in selenium supplemented ones. Hemoglobin contents hematocrit values ALAD activities in blood were significantly decreased and urinary aminolevulinic acid(ALA) excretion increa-sed with increasing dietary lead levels but partly restored by selenium supplementation. however only in 200, 1, 000 and 2, 000ppm dietary lead groups. On the other hand the hepatic ALAD activites of all four lead groups were recovered 19-30% from suppression by selenium supplementation. It was concluded that selenium administration alleviated lead toxicity in rats.

• Korean Journal of Animal Reproduction
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• v.25 no.2
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• pp.139-145
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• 2001

This study was performed to elucidate the patho-physiology of lead acetate-poisoned rats after consecutive oral administrations of the lead. The changes in feed and water intake, gains of body weight, blood pictures and mineral compositions of several organs were observed to measure the effects of lead acetate-poisoning. 1. Compared with control group, every experimental group of which 1,000, 2,000, or 4,000 ppm/kg of lead acetate was administered displayed a gradual decrease in feed intake in dose-dependent manners. 2. After 1,000, 2,000 or 4,000 ppm/kg of lead acetate administration, water intake seemed to decrease in every experimental group in dose-dependent manners. 3. After 1,000, 2,000 or 4,000 ppm/kg of lead acetate administration, body weight decreased in every experimental group in dose-dependent manners. 4. After 1000, 2,000 or 4,000 ppm/kg of lead acetate administration, the PLT values and numbers of RBC and WBC significantly increased after lead acetate administration, but the values of Hb and PCV were lower than those of control group's. 5. After 2,000 or 4,000 ppm/kg of lead acetate administration, the levels of Pb, Mn, Fe, Pb and Zn in the livers were lowered, but the levels of Pb, Mn, Fe, Pb and Zn in the kidneys.