Journal of The Korean Society of Clinical Toxicology

Use of succimer as an alternative antidote in copper sulfate poisoning: A case report: Sang Kyoon Han, Sung Wook Park, Young Mo Cho, Il Jae Wang, Byung Kwan Bae, Seok Ran Yeom, Soon Chang Park; J Korean Soc Clin Toxicol. 2021;19(1):59-63. Published online June 30, 2021; DOI: https://doi.org/10.22537/jksct.2021.19.1.59

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Copper sulfate is widely used as a fungicide and pesticide. Acute copper sulfate poisoning is rare but potentially lethal in severe cases. Copper sulfate can lead to cellular damage of red blood cells, hepatocytes, and myocytes. Toxic effects include intravascular hemolysis, acute tubular necrosis and, rhabdomyolysis. A 76-year-old man presented with vomiting and epigastric pain. He had ingested a copper-containing fungicide (about 13.5 g of copper sulfate) while attempting suicide 2 hours prior to presentation. From day 3 at the hospital, laboratory findings suggesting intravascular hemolysis were noted with increased serum creatinine level. He was treated with a chelating agent, dimercaptosuccinic acid (succimer). His anemia and acute kidney injury gradually resolved with a 19-day regimen of succimer. Our case suggests that succimer can be used for copper sulfate poisoning when other chelating agents are not available.

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Acute poisoning of copper sulfate: a case report and review literature
Samaneh Hajimohammadi, Somayeh Gharibi, Vahid Pourbarkhordar, Seyed Reza Mousavi, Hanieh Salmani Izadi
The Egyptian Journal of Internal Medicine.2022;[Epub] CrossRef

A Fatal Case of Methylene Blue Threatment Failure in Methemoglobinemia: Ji-Yae Shim, Yun-Seok Seo, Jong-Oh Yang, Eun-Young Lee, Sae-Yong Hong, Hyo-Wook Gil; J Korean Soc Clin Toxicol. 2006;4(2):151-154. Published online December 31, 2006

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Abstract PDF: Acute toxic methemoglobinemia is an infrequent complication of the use of various drugs. Severe methemoglobinemia is very often fatal. Methylene blue is an effective drug in the treatment of methemoglobinemia patients. However, failure to respond to methylene blue has been described in patients with sulfhemoglobinemia, chlorate poisoning, and glucose-6-phosphate dehydrogenase deficiency. It is even possible that hemolysis may occur due to methylene blue treatment itself. We encountered a case of a 71-year-old woman who developed methemoglobinemia caused by alprazolam intoxication. She presented with hemolytic anemia and did not respond to methylene blue. In spite of concerted N-acetylcysteine therapy, the hemolytic anemia became aggravated and the patient died eleven days after intoxication.

Arsenic Poisoning: Yang Ho Kim, Ji Ho Lee, Chang Sun Sim, Kyoung Sook Jeong; J Korean Soc Clin Toxicol. 2004;2(2):67-71. Published online December 31, 2004

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Abstract PDF: Arsenic poisoning has three types of poisoning. First, acute arsenic poisoning is usually caused by oral intake of large amount of arsenic compound with purpose of homicide or suicide. Second, chronic arsenic poisoning is caused by inhalation of arsenic in the occupational setting or by long-term oral intake of arsenic-contaminated well water. Third, arsine poisoning occurs acutely when impurities of arsenic in non-ferrous metal react with acid. Clinical manifestation of acute arsenic poisoning is mainly gastrointestinal symptoms and cardiovascular collapse. Those of chronic poisoning are skin disorder and cancer. Arsine poisoning shows massive intravascular hemolysis and hemoglobinuria with acute renal failure. Exposure evaluation is done by analysis of arsenic in urine, blood, hair and nail. Species analysis of arsenic is very important to evaluate inorganic arsenic acid and mono methyl arsenic acid (MMA) separated from dimethyl arsenic acid (DMA) and trimethyl arsenic acid (TMA) which originate from sea weed and sea food. Treatment with dimercaprol (BAL) is effective in acute arsenic poisoning only.

A Case Report of Glacial Acetic Acid Ingestion Complicated with Hepatic Necrosis: Yeon Young Kyong, Mi Jin Lee, Seung Pil Choi, Kyu Nam Park, Won Jae Lee, Se Kyung Kim; J Korean Soc Clin Toxicol. 2004;2(1):23-26. Published online June 30, 2004

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Abstract PDF: Caustic ingestion can produce a progressive and fatal injuries to esophagus, stomach and other organs. Reported exposure to acetic acid results injuries to gastrointestinal tract, hemolysis and disseminated intravascular coagulation is general, but causing hepatic necrosis by direct injuries are rare. A 47-year-old man visited our emergency medical center complaining odynophagia and abdominal pain after ingesting glacial acetic acid ($99\%$) with suicidal ideation. At the time of arrival, the patient complained mild abdominal pain but a few hours later the patient complained severe abdominal pain with markedly elevated liver enzymes. The Abdominal Computerized Tomography showed diffuse gastric wall edema and density of wedge shaped hypodense area in right hepatic dome showing focal hepatic necrosis without significant inflammation. This seems likely to be a direct effect of the noxious agent on hepatocyte involving the portal circulation.

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