• Journal of The Korean Society of Clinical Toxicology
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• v.8 no.1
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• pp.24-29
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• 2010

Purpose: Neonicotinoid insecticides are widely used as they have been proven by experimental studies to have low toxicity to mammals, including humans. As the use of neonicotioids increases, the number of patients with neonicotinoid poisoning has also increased. We conducted a study to investigate the clinical manifestations of neonicotinid poisoning. Methods: We retrospectively analyzed the patients who ingested neonicotinids and who visited the emergency department located in Korea from March 2002 to February 2010. We reviewed the patients' age, gender, the amount of exposure, the elapsed time to presentation, the treatment and the outcome. According to the poisoning severity score, we divided the patients with a Poisoning severity score (PSS) of 0 or 1 into the mild/moderate toxicity group and the patients with a PSS of 2 or 3 into the severe/fatal toxicity group. Results: A total of 24 patients were analyzed. The most common clinical manifestations of neonicotinoid insecticide toxicity were gastrointestinal symptoms (66.7%) such as nausea, vomiting and abdominal pain and the others are respiratory symptoms (16.7%), cardiovascular symptoms (12.5%), metabolic imbalance (12.5%), renal dysfunction (8.3%), CNS symptoms (8.3%), and asymptomatic (29.2%). Twenty patients (83.3%) showed mild/moderate toxicity and 4 patients (16.7%) showed fatal conditions such as shock and mutiorgan failure. The mortality rate was 4.2%. In these fatal cases, the patients developed respiratory failure, hypotension, altered mentality and renal failure at the acute stage and they deteriorated to a more serious condition. This severe toxicity was caused by decreased renal excretion of neonicotinid metabolite, and this was improved after hemodialysis. Conclusion: Most patients with neonicotinoid poisoning and who showed mild toxicity usually improved after symptomatic treatment. However, some patients showed significant toxicity with respiratory failure and renal function deterioration, and intensive care needed, including mechanical ventilation and hemodialysis.

• Journal of The Korean Society of Clinical Toxicology
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• v.9 no.2
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• pp.49-55
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• 2011

Purpose: Acetanilide has been in widespread use as an amide herbicide compound. However, available data regarding acute human poisoning is scarce. The aim of this study was to analyze the clinical characteristics of acetanilide poisoning in order to identify the risk factors associated with severity. Methods: We conducted a retrospective observational study encompassing the period January 2005 to December 2010, including adult ED patients suffering from acetanilide intoxication. Toxicological history, symptoms observed, clinical signs of toxicity, and laboratory test results were collected for each patient. The patients were classified into two groups for analysis, according their poisoning severity score (PSS). Resulting clinical data and prognostic variables were compared between mild-to-moderate poisoning (PSS 1/2 grades), and severe poisonings and fatalities (PSS 3/4 grades). Results: There were a total of 37 patients, including 26 alachlor, 6 s-metolachlor, 4 mefenacet, and 1 butachlor cases. The majority of patients (81.1%) were assigned PSS 1/2 grades. Changes in mental status and observation of adverse neurologic symptoms were more common in the PSS 3/4 group. The median ingested volume of amide herbicide compound was 250 ml (IQR 200-300 ml) in the PSS 3/4 group, and 80 ml (IQR 50-138 ml) in the PSS 1/2 group. Also, the median GCS observed in the PSS 3/4 group was 13 (IQR 10-14), which was markedly low as compared to a median GCS of 15 in the PSS 1/2 group. Overall mortality rate was 5.4%, and profound cardiogenic shock was observed prior to death in all fatalities. Conclusion: When compared to previous reports, acute acetanilide poisoning resulted in relatively moderate severity. The presence of neurologic manifestations, hypotension, lower GCS score, and larger ingested volumes was associated with more serious effects and mortalities.

• Journal of The Korean Society of Clinical Toxicology
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• v.4 no.2
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• pp.166-169
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• 2006

Poisonings caused by 'mad honey' are known to occur in response to grayanotoxins, which bind to sodium channels in the cell membrane, increasing membrane sodium permeability and preventing inactivation. Mild symptoms of mad honey intoxication are dizziness, weakness, hypersalivation, nausea, vomiting, and paresthesia. Severe intoxication, however, leads to serious cardiac manifestations such as atrioventricular block, dose-dependent hypotension, bradycardia, and respiratory depression. Atropine and vasoactive drugs improve symptoms of both bradycardia and respiratory rate depression. We report an unusual case of saliva-type hyperamylasemia in a mad honey poisoning patient who developed clinically significant bradycardia. She recovered fully within 3 days following atropine administration and medical treatment.

• Journal of Medicine and Life Science
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• v.18 no.2
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• pp.31-34
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• 2021

The pharmacokinetic properties of transdermal nicotine patches (TNPs) are different from those of other routes of nicotine administration; further, acute nicotine poisoning by TNPs may present with different clinical features. In the present report, we describe the case of a 23-year-old woman who was admitted to emergency department (ED) at Jeju National University Hospital with loss of consciousness. Five hours before the ED visit, she used multiple TNPs to attempt suicide. Initially, nausea and vomiting occurred, and the symptoms worsened over time. We immediately removed the TNPs, and the application sites were gently washed with sterile water. The patient's level of consciousness gradually improved, and she fully recovered an altered mental status 5 hours later. Her initial urinary cotinine level was 324 ng/mL. Physicians should be aware that acute nicotine poisoning by TNPs can cause various toxic symptoms.

• Plant Resources
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• v.3 no.1
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• pp.100-104
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• 2000

Lampteromyces japonicus is the most popular source of mushroom poisoning in Japan. We isolated poisonous substance, illudin S, 40 years ago, which shower strong anti-tumoric activity. Its analogs are now the most hopeful anti-cancer agent. Clitocybe acromelalgia gives unique poisoning which exhibits symptoms similar to acromelalgia and erythromelalgia. We intended to isolate the toxin causing these poisoning but neuroexciatory compounds, acromelic acids A and B, were isolated. They are now known as the most potent glutamate agonists and good reagents for the study of the glutamate receptor of a neurocell.

• Journal of The Korean Society of Clinical Toxicology
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• v.2 no.2
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• pp.101-105
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• 2004

Purpose: Paraquat is the most commonly used herbicide in Korea. Exposure to paraquat through the skin has resulted in local irritation or inflammation of varying degree, sometimes severe. The purpose of this study was to review the patients with paraquat poisoning by skin absorption. Methods: We analysed retrospectively the clinical and laboratory findings of 45 patients with paraquat poisoning after dermal exposure, who were admitted to Soonchunhyang University Cheonan Hospital from January 1999 to December 2003. Results: Among 870 cases of paraquat poisoning, 45 cases were exposed to paraquat through the skin. The peak incidence was the fifth decade($40\%$). The clinical symptoms were pain, pruritus, nausea, and vomiting. The major skin lesions were generalized vesicobullae and necrotic erosion in face, scrotum, trunk, upper and lower extremities and etc. All patients were survived after skin contact or inhalation of paraquat. Conclusion: This study illustrates the extreme toxicity of paraquat and demonstrates that lethal quantities of paraquat may be absorbed if repeated exposure to it. Stricter precautions, including the mandatory use of protective clothing, should be recommended whenever this material is used.

• Korean Journal of Veterinary Service
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• v.44 no.2
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• pp.113-117
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• 2021

Cocklebur poisoning in livestock can cause sudden death, with clinical signs include depression, inappetite, blindness, reluctance to move, hypersensitivity, ataxia and coma. The cause of cocklebur poisoning is ingestion of cocklebur sprout or seed, which contains carboxyatractyloside. In December 2020, a 47 month-old Hanwoo suddenly developed ataxia, and died after several hours. Hay mixed cocklebur seeds was fed to Hanwoo for 4 days before the symptoms. At autopsy, petechia and ecchymosis were seen on serous membrane of rumen and intestines. Peritoneal cavities contained a yellowish fluid and, hypoglycemia (Glu <20 mg/dL) was measured in blood test result. Microscopic lesions were karyolysis of centriloular hepatocyte and hemorrhage. Based on autopsy, blood and histopathological test, we diagnosed this case as cocklebur poisoning in Hanwoo.

• Journal of The Korean Society of Clinical Toxicology
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• v.5 no.1
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• pp.53-56
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• 2007

Nicotine poisoning arising from the use of nicotine patches is rare. However, because nicotine patches are classified as an OTC drug, the risk of misuse or abuse is increasing. Nicotine poisoning using nicotine patches shows an unusual clinical presentation compared to that from oral ingestion of multiple doses of nicotine. We present a case of misused nicotine patches that cause a nicotine poisoning. A thirty-nine year-old healthy man visited the ER with complaints of an intermittent cramping abdominal pain with nausea and vomiting. Upon physical examination, there were no specific findings except increased bowel sounds, and the patient's initial laboratory findings were also unremarkable except for an increased bilirubin level. CT revealed a mild degree of fatty liver. The patient's symptoms did not improve any further with conservative management. During his ED stay, we meticulously took his history again, and we discovered that he had used nicotine patches for three days, six days before admission, and had misused the nicotine patches as NSAID patches. The patient's diagnosis of nicotine poisoning was confirmed by a urine cotinine level ten times the normal value. After a 12-hour stay in the ED, his symptoms disappeared without any specific management.

• Journal of The Korean Society of Clinical Toxicology
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• v.19 no.1
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• pp.51-54
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• 2021

Chlorfenapyr is a widely used insecticide, that is very lethal if ingested. It exhibits delayed toxicity in which there are few symptoms at first which suddenly worsen after a few days. A 66-year-old female patient ingested about 90 mL of chlorfenapyr liquid hydrating agent (Chlofenapyr 10%) and showed stable vital signs with no specific symptoms and findings other than a mild fever, vomiting, and nausea. From the 3rd day of ingestion, creatine kinase was high, and rhabdomyolysis was suspected. From the 4th day of ingestion, pancreatic enzymes began to gradually increase. A diffusion-weighted image showed a multifocal high signal intensity in the white matter and corpus callosum area. On the 8th day after ingestion, she suffered a high fever and a heart attack and died. Thus, if a patient is suspected of taking chlorfenapyr, he/she needs active treatment and monitoring even if he/she does not exhibit any symptoms.

• Safety and Health at Work
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• v.3 no.1
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• pp.11-16
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• 2012

Lead poisoning is one of the earliest identified and most known occupational disease. Its acute effects have been recognized from antiquity when this condition principally afflicted manual workers and slaves, actually scarcely considered by the medicine of that time. The Industrial Revolution caused an epidemic of metal intoxication, urging scientists and physician of that period to study and identify specific symptoms and organ alterations related to chronic lead poisoning. During the 20th century, the acknowledgment of occupational and environmental toxicity of lead fostered public awareness and legislation to protect health. More recently, the identification of sub-clinical effects have greatly modified the concept of lead poisoning and the approaches of medicine towards this condition. Nowadays, lead poisoning is rarely seen in developed countries, but it still represents a major environmental problem in certain areas. Consequently, it may appear as a paradigm of "occupational and environmental disease," and the history of this condition seems to parallel the historical development of modern "Occupational and Environmental Health" as a more complete medical discipline.