Journal of The Korean Society of Clinical Toxicology

Original Article

Changes in deoxyhemoglobin and admission duration in carbon monoxide poisoning patients: a retrospective study: Jae Gu Ji, Yang Weon Kim, Chul Ho Park, Yoo Sang Yoon, Yundeok Jang, JI-Hun Kang, Chang Min Park, Sang Hyeon Park; J Korean Soc Clin Toxicol. 2023;21(1):32-38. Published online June 30, 2023; DOI: https://doi.org/10.22537/jksct.2023.00004

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Abstract PDF: Purpose: The purpose of this study was to determine whether deoxyhemoglobin changes were associated with admission duration in carbon monoxide (CO)-poisoned patients.
Methods
This retrospective study included 181 patients who were able to breathe by themselves after CO poisoning. Arterial blood gas analysis was performed to measure their deoxyhemoglobin levels. Their baseline characteristics and clinical outcomes during hospitalization in the emergency department (ED) were collected and compared. To assess changes in deoxyhemoglobin levels, blood samples were taken immediately after patients presented to the ED and then again after 6 hours. For statistical analysis, logistic regression was utilized to determine the effect of deoxyhemoglobin changes on admission duration.
Results
The incidence rates of hypocapnia and hypoxemia at presentation after acute CO poisoning were 28.7% and 43.6%, respectively. Moreover, the magnitude of increasing deoxyhemoglobin levels in patients with hypoxemia (2.1 [1.7–3.1], p<0.001) and changes in deoxyhemoglobin levels appeared to have an impact on the length of hospitalization in the ED (odds ratio, 1.722; 95% confidence interval, 0.547–0.952; p<0.001).
Conclusion
In patients with acute CO poisoning, deoxyhemoglobin levels appeared to increase in those with hypoxemia, which in turn was associated with prolonged hospitalization.

PaCO2 at Early Stage is Associated with Adverse Cardiovascular Events in Acute Carbon Monoxide Poisoning: Keun Mo Yang, Byeong Jo Chun, Jeong Mi Moon, Young Soo Cho; J Korean Soc Clin Toxicol. 2019;17(2):86-93. Published online December 31, 2019; DOI: https://doi.org/10.22537/jksct.2019.17.2.86

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Abstract PDF: Purpose: The objective was to determine the association between PaCO2 and adverse cardiovascular events (ACVEs) in carbon monoxide (CO)-poisoned patients. Methods: This retrospective study included 194 self-breathing patients after CO poisoning with an indication for hyperbaric oxygen therapy and available arterial blood gas analysis at presentation and 6 hours later. The baseline characteristics and clinical course during hospitalization were collected and compared. The mean PaCO2 during the first 6 hours after presentation was calculated. Results: The incidence rates of moderate (30 mmHg< PaCO2 <35 mmHg) or severe (PaCO2 ≤30 mmHg) hypocapnia at presentation after acute CO poisoning were 40.7% and 26.8%, respectively. The mean PaCO2 during the first 6 hours was 33 (31-36.7) mmHg. The incidence of ACVEs during hospitalization was 50.5%. A significant linear trend in the incidence of ACVEs was observed across the total ranges of PaCO2 variables. In multivariate regression analysis, mean PaCO2 was independently associated with ACVEs (OR 0.798 (95% CI 0.641-0.997)). Conclusion: Mean PaCO2 during the first 6 hours was associated with increased ACVEs. Given the high incidence of ACVEs and PaCO2 derangement and the observed association between PaCO2 and ACVEs, this study suggests that 1) PaCO2 should be monitored at the acute stage to predict and/or prevent ACVEs; and 2) further study is needed to validate this result and investigate early manipulation of PaCO2 as treatment.

Acute Respiratory Failure due to Fatal Acute Copper Sulfate Poisoning : A Case Report: Gun Bea Kim; J Korean Soc Clin Toxicol. 2015;13(1):36-39. Published online June 30, 2015

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Abstract PDF: Copper sulfate is a copper compound used widely in the chemical and agriculture industries. Most intoxication occurs in developing countries of Southeast Asia particularly India, but rarely occurs in Western countries. The early symptoms of intoxication are nausea, vomiting, diarrhea, and abdominal cramps, and the most distinguishable clue is bluish vomiting. The clinical signs of copper sulfate intoxication can vary according to the amount ingested. A 75-year old man came to our emergency room because he had taken approximately 250 ml copper sulfate per oral. His Glasgow Coma Scale (GCS) score was 14 and vital signs were blood pressure 173/111 mmHg, pulse rate 24 bpm, respiration rate 24 bpm, and body temperature $36.1^{circ}$ .... Arterial blood gas analysis (ABGa) showed mild hypoxemia and just improved after 2 L/min oxygen supply via nasal cannula. Other laboratory tests and chest CT scan showed no clinical significance. Three hours later, the patient's mental status showed sudden deterioration (GCS 11), and ABGa showed hypercarbia. He was arrested and his spontaneous circulation returned after 8 minutes CPR. However, 22 minutes later, he was arrested again and returned after 3 minutes CPR. The family did not want additional resuscitation, so that he died 5 hours after ED visit. In my knowledge, early deaths are the consequence of shock, while late mortality is related to renal and hepatic failure. However, as this case shows, consideration of early definite airway preservation is reasonable in a case of supposed copper sulfate intoxication, because the patients can show rapid deterioration even when serious clinical manifestation are not presented initially.

A Case of Delayed Administration of Naloxone for Morphine Intoxicated Patient: Gun-Bea Kim, Won-Nyung Park, Hong-Du Gu; J Korean Soc Clin Toxicol. 2012;10(1):33-36. Published online June 30, 2012

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Abstract PDF: Opioids are the one of the most commonly used drugs to control cancer pain all over the world. But, we should not overlook the potential risk of opioid intoxication because they have well-known detrimental side effects. The opioid intoxication can be diagnosed thorough various clinical manifestations. The altered mental status, respiratory depression, and miosis is very representative clinical features although these symptoms don't always appear together. Unfortunately the opioid-toxidrome can be varied. A 42 years old man came to our emergency room after taking about 900 mg morphine sulfate per oral. He was nearly alert and his respiration was normal. Even though his symptoms didn't deteriorated clinically, serial arterial blood gas analysis showed increase in PaCO2. So we decided to use intravenous naloxone. Soon, he was fully awaked and his pupils size was increased. After a continuous infusion of intravenous naloxone for 2 hours, PaCO2 decreased to normal range and his pupil size also returned to normal after 12 hours. Though the levels of serum amylase and lipase increased slightly, his pancreas was normal according to the abdominal computed tomography. He had nausea, vomit, and whole body itching after naloxone continuous infusion, but conservatively treated. We stopped the continuos infusion after 1 day because his laboratory results and physical examinations showed normal. As this case shows, it is very important to prescribe naloxone initially. If you suspect opioid intoxication, we recommend the initial use of naloxone even though a patient has atypical clinical features. In addition, we suggest intranasal administration of naloxone as safe and effective alternative and it's necessary to consider nalmefene that has a longer duration for opioid intoxication.

A Study on Organophosphate Poisoning Patients: Comparison of the Survivor Group and Dead Group: Youn-Gyu Choi, Dong-Hyeon Lee, Woo-Hyung Kim, Gang-Wook Lee, Sun-Pyo Kim, Seong-Jung Kim, Soo-Hyung Cho, Nam-Soo Cho; J Korean Soc Clin Toxicol. 2010;8(1):16-23. Published online June 30, 2010

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Abstract PDF: Purpose: Organophosphate insecticide poisoning is common in Korea, but there is no definitive guideline for determining the severity of the poisoning and the predictive factors. Therefore, we evaluated the organophosphate poisoned patients and we divided them into two groups, the survivors and the dead, and the results might be useful for treating organophosphate poisoning patients. Methods: We performed a retrospective analysis of 68 organophosphate poisoned patients who visited the Chosun University Hospital Emergency Medical Center during a 24-month period from January, 2007 to December, 2008. We made a work sheet of the patients' characteristics and the collected data was analyzed and we compared this data between the survivor group and the dead patient group. Results: There were significant differences between the survivor group and the dead patient group for the mean age, the alcohol intake state and the typically expressed signs. The dead patients had lower blood pressure, tachycardia and a lower Glasgo Coma Score (GCS) score than the survivor group. On the arterial blood gas analysis, the dead patients had more severe acidemia and they had lower saturations. Increased serum amylase levels were found in the dead patients. The survivors'initial and follow up serum pseudocholinesterase activity (after 6~8 days) was significantly higher than that of the dead group. The total amount of atropine injected to patient was less in the survivors than that in the dead patients. Conclusion: Old age and expressing the typical intoxication signs, a lower GCS score and blood pressure, showing acidosis on the gas analysis and low serum cholinesterase activity may be useful as poor prognostic indicators for patients with organophosphate poisoning. We suggest that physicians must pay careful attention to the signs and prognostic factors of organophosphate insecticide poisoned patients.

A Case of Lactic Acidosis after Metformin overdose: Jung-Suk Park, Sung-Pil Chung, Han-Shick Lee, Eui-Chung Kim; J Korean Soc Clin Toxicol. 2007;5(2):126-130. Published online December 31, 2007

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Abstract PDF: Metformin is antihyperglycemic, not hypoglycemic. It causes neither insulin release from the pancreas nor hypo glycemia, even when taken in large doses. But, there are several reports of metformin-associated lactic acidosis (MALT). We present a case report of severe lactic acidosis most probably resulting from high doses of metformin in a patient with no known contraindications for metformin. A 43-year-old female was admitted to the emergency department due to a metformin overdose. She had diabetes for 6 years, well-controlled with metformin and novolet. One hour before admission, she impulsively took 50g metformin (100 mg or 100 tablets). Physical examination for symptoms revealed only irritability, and laboratory evaluation revealed only mild leukocytosis. After one hour the patient was drowsy, and arterial blood gas analysis showed severe lactic acidemia Seven hours after ED arrival, she commenced hemofiltration treatment and was admitted to the intensive care unit. Continuous venovenous hemodiafiltration was initiated. Forty-eight hours later, full clinical recovery was observed, with return to a normal serum lactate level. The patient was discharged from the intensive care unit on the third day. A progressive recovery was observed and she was discharged from the general word on the thirteenth day.

A Fatal Case of Dicamba Intoxication: Dae-Young Hong, Wook-Hyun Um, Kyoung-Mi Lee, Ji-Hye Kim, Seung-Baik Han, Joo-Hyun Suh, Jun-Sig Kim, Hyung-Keun Roh; J Korean Soc Clin Toxicol. 2006;4(1):69-72. Published online June 30, 2006

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Abstract PDF: Dicamba is a benzoic acid and classified as a chemically related chlorophenoxy herbicide which is widely used for the control of broad-leaved weeds. While the chlorophenoxy herbicide poisoning is known to be uncommon, its ingestion can result in serious or sometimes fatal outcome. A 65-year-old man ingested about 300 ml of dicamba in a suicidal attempt and three hours later he was admitted hospital, complaining abdominal pain, nausea and vomiting. On admission his vital signs were normal and laboratory findings were not remarkable except metabolic acidosis in arterial blood gas analysis. Shortly after the admission endotracheal tube was inserted due to altered mental state and activated charcoal was given after performing gastric lavage. However, his vital signs became unstable 6hrs after the ingestion and mechanical ventilation was started with administration of inotropic agents. In spite of urine alkalization for rapid elimination of the absorbed dicamba, the metabolic acidosis was aggravated with concomitant rhabdomyolysis and acute renal failure, and he died 24 hrs after the ingestion.

Reactive Airways Dysfunction Syndrome (RADS) from Chlorine Gas Releasing Cleaning Agents: Kwang-Hyun Cho, Seung-Hwan Kim, Young-Soon Cho, Hahn-Shick Lee, Joon-Seok Park; J Korean Soc Clin Toxicol. 2005;3(1):60-62. Published online June 30, 2005

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Abstract PDF: A previously healthy 57-year-old woman with dyspnea and wheezing presented to the emergency department a few minutes after exposure to unknown gas from mixing bleach (sodium hypochlorite) and cleaning agent (hydrochloric acid) at work place. Initial physical examination revealed severe wheezing on both whole lung fields, but the chest radiograph was normal. Arterial blood gas analysis showed only moderate hypoxemia. The patient was treated with oxygen, $eta$adrenergic bronchodilators, antihistamines and corticosteroids, after then symptoms were improved. And the patient discharged against medical advice. We report a rare case of reactive airways dysfuntion syndrome from chlorine gas exposure.

Hydrogen Sulfide Poisoning: Young-Hee Choi, Byung-Kuk Nam, Hyo-Kyung Kim, Ji-Kang Park, Eun-Seog Hong, Yang-Ho Kim; J Korean Soc Clin Toxicol. 2004;2(1):31-36. Published online June 30, 2004

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Abstract PDF: Three workers, field operators in lubricating oil processing of petroleum refinery industry were found unconscious by other worker. One of them who were exposed to an high concentration of H2S was presented with Glasgow Coma Score of 5, severe hypoxemia on arterial blood gas analysis, normal chest radiography, and normal blood pressure. On hospital day 7, his mental state became clear, and neurologic examination showed quadriparesis, profound spasticity, increased tendon reflexes, abnormal Babinski response, and bradykinesia. He was also found to have decreased memory, attention deficits and blunted affect which suggest general cognitive dysfunction, which improved soon. MRI scan showed abnormal signals in both basal ganglia and motor cortex, compatible with clinical findings of motor dysfunction. Neuropsychologic testing showed deficits of cognitive functions. SPECT showed markedly decreased cortical perfusion in frontotemporoparietal area with deep white matter. Another case was recovered completely, but the other expired the next day.

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