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Case Report
Pulmonary thromboembolism following organophosphate intoxication: a case report
Ji Ho Lee
J Korean Soc Clin Toxicol. 2023;21(1):64-67.   Published online June 30, 2023
DOI: https://doi.org/10.22537/jksct.2023.00002
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AbstractAbstract PDF
Various symptoms manifest after organophosphate intoxication due to muscarinic, nicotinic, and central nervous system effects. Complications are common, and morbidity occurs due to respiratory center depression, cardiovascular complications, aspiration pneumonia, general weakness, and neurological symptoms. Some studies have reported a statistically significant association between organophosphate intoxication and deep vein thrombosis. However, cases of pulmonary thromboembolism (PTE) resulting from organophosphate poisoning are very rare. A 45-year-old male patient was transferred to our hospital after ingesting an unknown amount of an insecticide and receiving 6 L of gastric lavage at a local hospital. Other than nausea, no symptoms (e.g., dyspnea) were present, but a hemodynamic test showed an elevated lactic acid level, and metabolic acidosis worsened over time. Accordingly, we conducted initial treatment including continuous renal replacement therapy. After 7 hours, the poisoning analysis result was confirmed, and lambda-cyhalothrin and chlorpyrifos (0.441 µg/mL and 0.401 µg/mL, respectively) were detected. We introduced pralidoxime. Although no increase in pseudocholinesterase was found during hospitalization, continuous renal replacement therapy and pralidoxime were discontinued because the patient did not show symptoms of intermediate syndrome, including dyspnea and altered consciousness. The patient complained of abdominal pain on hospital day 8. Abdominal computed tomography was performed to evaluate the possibility of a corrosive injury to the stomach or esophagus, and we confirmed PTE. The D-dimer level was 1.96 mg/L (normal range, 0–0.55 mg/dL). A radiologic examination showed a PTE in the main pulmonary artery leading to the segmental pulmonary artery. After heparinization, the patient was discharged after being prescribed a vitamin K-independent oral anticoagulant. Through this case, we would like to emphasize the need for a thorough evaluation of clinical symptoms because atypical symptoms can occur after poisoning with organophosphate pesticides.
Two Cases of Neurotoxin Tetramine Poisoning Following Ingestion of Buccinum Striatissinum
So Eun Kim, Jae Baek Lee, Young Ho Jin, Jae Chol Yoon, Si On Jo, Jeong Moon Lee, Tae Oh Jeong
J Korean Soc Clin Toxicol. 2016;14(1):66-69.   Published online June 30, 2016
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Some carnivorous gastropods have heat stable tetramine toxins in their salivary glands. This toxin is an autonomic ganglionic blocking agent that enables them to catch the prey easily by paralyzing their targets. Acute tetramine toxin poisoning in humans from eating whelks has been well described based on numerous cases, but is rare in Korea. Symptoms of tetramine poisoning include eyeball pain, blurred vision, headache, dizziness, muscular twitching, tingling of hands and feet, weakness, paralysis and sometimes collapse. Gastrointestinal symptoms, such as abdominal pain, nausea, and vomiting can also occur. However, intoxication is self-limiting and patients will usually recover in about 24 hours. Herein, we report 2 cases of tetramine poisoning after ingestion of Buccinum striatissinum as meat and soup.
A Case of Podostroma Cornu-Damae Intoxication Induced Pancytopenia and Skin Desquamation: Successful Treatment with Granulocyte Colony Stimulation Factor (G-CFS)
Jung Seok Kim, Gyu Won Kim, Jae Il Chung, Myoung Ki Sim, Ki Chul Yoon, Yong Hoon Choi, Ha Ram Yi, In Zoo Choi, Chan Sup Shim, Joung Ho Han
J Korean Soc Clin Toxicol. 2015;13(1):50-54.   Published online June 30, 2015
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Podostroma cornu-damae is a rare species of fungus belonging to the Hyocreaceae family. Its fruit body is highly toxic, as it contains trichothecene mycotoxins. The morphology is similar to that of immature Ganoderma lucidum, making identification difficult for non-experts. We experienced such a case of a 56- year-old male who picked and consumed podostroma cornu-damae, and consumed. Later that day, he developed digestive system symptoms, including nausea, vomiting, and abdominal pain. He presented to the emergency room (ER), there were no abnormal physical findings, symptoms improved after gastric lavage, and the patient voluntarily discharged himself on the same day. The following day, as the symptoms gradually deteriorated, he was admitted via the ER. He was presented with severe pancytopenia, alopecia, desquamation of skin, and acute renal failure. He recovered without any complications after conservative care, antibiotics therapy, and granulocyte colony stimulating factor administration. The most commonly reported complications of podostroma cornu-damae intoxication were reported pancytopenia, infection, disseminated intravascular coagulation, acute renal failure, etc. since Prevention is especially important because its toxicity can be lethal and there is no particular treatment to date, prevention is especially important. Promotion and education for the public are needed.
Two Cases of Alocasia Intoxication
Dae Han Wi
J Korean Soc Clin Toxicol. 2012;10(2):122-125.   Published online December 31, 2012
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AbstractAbstract PDF
Alocasia was originally distributed throughout subtropical and tropical areas. Recently, in Korea, it has been used in air cleaners and in control of humidity. Despite easy access in Korea, there are few reports on Alocasia toxicity. We report on two cases of Alocasia intoxication. One patient was a 16-month-old male, who was admitted with a complaint of irritability after biting leaves of Alocasia. Four hours later, he was discharged without any symptoms. Another patient, a 52-year-old female, complained of oral pain, numbness on the perioral area, dysphonia, swallowing difficulty, and chest and abdominal pain after eating root stuck of alocasia odora. She underwent gastrointestinal fibroscopy (GIF) due to lasting chest and abdominal pain. Finding on GIF showed erythema and swelling in the aryepiglottic fold and larynx. Her symptoms lasted 13 days; she was then discharged without any complications or sequelae.
Clinical Features of Pokeweed Intoxication Experienced in a University Hospital
Dong Kil Jeong, Hyung Jun Moon, Jung Won Lee, Sae Hoon Park, Hyung Jung Lee, Seung Whan Seol, Ah Reum Kim, Jae Hyung Choi, Jae Woo Kim
J Korean Soc Clin Toxicol. 2012;10(2):86-90.   Published online December 31, 2012
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AbstractAbstract PDF
Purpose: Although Pokeweed intoxication is relatively less severe, there is little data on the clinical presentation of Pokeweed intoxication in Korea. This study examined the clinical aspects to provide basic data for evaluating Pokeweed intoxication. Methods: A retrospective study by a chart review was performed on 19 patients who ingested Pokeweed and presented to an academic emergency department with an annual census of 40,000 between March 2012 and May 2012. Results: Nineteen patients were identified. All patients were intoxicated unintentionally. The most common symptoms were vomiting with diarrhea and abdominal pain. The onset time varied, but occurs 30 minutes to 5 hours post ingestion of Pokeweed. All patients were discharged without fatal complications. Conclusion: Compared to previous reports, most pokeweed poisoning patients complain of gastrointestinal symptoms. Supportive care is the mainstay of the management of pokeweed intoxication. All symptoms were resolved over a 24 to 48 hour period.
Three Cases of Cardiac Toxicity after Intake of Symplocarpus Renifolius
Tae-Hoon Kim, Hyun Kim, Oh-Hyun Kim, Yong-Sung Cha, Kyoung-Chul Cha, Kang-Hyun Lee, Sung-Oh Hwang
J Korean Soc Clin Toxicol. 2012;10(1):41-45.   Published online June 30, 2012
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AbstractAbstract PDF
Recently, some patients have visited the emergency department for treatment of different symptoms of acute poisoning after intake of unidentified herbs, which can be mistaken for wild edible greens, because wild edible greens are good for health and contain vitamins, enzymes, minerals, fibers, and anticancer materials. Winter or early spring, is extremely high, with rapid onset of severe symptoms of poisoning. There have been no reports of poisoning by SymplocarpusRenifolius in Korea, however, we report on three severe cases involving patients who experienced cardiogenic shock with nausea, vomiting, abdominal pain, chest discomfort, dizziness, numbness, and general weakness.
Corrosive Injury Due to Edible Vinegar
Do-Hyoun Kim, Sung-Woo Lee, In NamGung, Jong-Hak Park, Su-Jin Kim, Yun-Sik Hong
J Korean Soc Clin Toxicol. 2011;9(1):34-38.   Published online June 30, 2011
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AbstractAbstract PDF
Vinegar is a very popular ingredient used in many cuisines. It is also known for its beneficial health, beauty and possible weight-loss properties. The authors report on a patient who presented to the emergency department with unstable vital signs complaining of generalized abdominal pain after ingestion of 450 ml of apple cider vinegar. We documented a case of corrosive gastrointestinal injury with persistent metabolic acidosis occurring after ingesting apple cider vinegar with an acetic acid concentration of 12~14%. Toxic damage to the liver and kidney were also observed, peaking on post-ingestion day 3. The patient received supportive care and hemoperfusion for three days without much clinical improvement and died in the seventh day of intensive care due to disseminated intravascular coagulation and multi organ failure. Edible vinegar, when taken in large amounts, is capable of inducing corrosive injuries of the GI tract as well as severe systemic toxicities, such as metabolic acidosis. Safety precautions regarding vinegar deserve more public attention and clinicians also should be astute enough to recognize the potential damage accompanying vinegar ingestion.
Clinical Characteristics of Patients with Neonicotinoid Insecticide Poisoning
Jin-Chul Kim, Byung-Hak So, Han-Joon Kim, Hyung-Min Kim, Jung-Ho Park, Se-Min Choi, Kyu-Nam Park, Kyoung-Ho Choi
J Korean Soc Clin Toxicol. 2010;8(1):24-29.   Published online June 30, 2010
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AbstractAbstract PDF
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.
Two Cases of Phytolacca Americana Intoxication with Confusion and Abdominal Cramping
Yang-Weon Kim, Yoo-Sang Yoon, Mi-Ran Kim, Sang-Hoon Park, Jun-Cheol Choi
J Korean Soc Clin Toxicol. 2008;6(2):146-148.   Published online December 31, 2008
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AbstractAbstract PDF
Phytolacca americana poisoning is a benign plant intoxication that causes gastrointestinal symptoms, including abdominal cramps, vomiting, diarrhea, and gastrointestinal bleeding. Other signs and symptoms include diaphoresis, salivation, visual disturbance, and seizures or mental changes. We report two cases of patients who experienced confusion and abdominal pain, vomiting, and hematemesis after oral ingestion of pokeweed. A 60-year-old female with confusion and a 67-year-old female with abdominal pain, vomiting, and diarrhea were admitted to the emergency department after pokeweed poisoning. After supportive treatment of hydration and gastrointestinal medication, the two patients showed full recovery within 24 h and were discharged from the hospital.
Nicotine Poisoning Using Nicotine Patches
You-Dong Sohn, Jae-Sung Lee, Gu-Hyun Kang, Jung-Tae Choi, Moo-Eob Ahn, Jeong-Youl Seo, Hee-Cheol Ahn
J Korean Soc Clin Toxicol. 2007;5(1):53-56.   Published online June 30, 2007
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AbstractAbstract PDF
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.
Neurotoxic Shellfish Poisoning after Ingesting Whelk
Young-Gil Ko, Ji-Young Ahn, Seok-Yong Ryu, Sang-Lae Lee, Suk-Jin Cho, Mi-Ran Kim
J Korean Soc Clin Toxicol. 2006;4(2):147-150.   Published online December 31, 2006
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AbstractAbstract PDF
Neurotoxic shellfish poisoning (NSP) can result from eating filter-feeding shellfish carrying brevetoxins produced by the marine dinoflagellate Krenia brevis (formally Gymnodinium breve). Brevetoxins enhance sodium entry into cells via voltage-sensitive sodium channels and have an excitatory effect. The incubation period is three hours (range 15 minutes-18 hours). NSP is characterized by gastroenteritis combined with neurologic symptoms. Gastrointestinal (GI) symptoms include abdominal pain, nausea, diarrhea and burning pain in the rectum. Neurologic symptoms are paresthesia, reversal of hot and cold temperature sensation, myalgia, headache, vertigo, and ataxia. Other symptoms may include malaise, tremor, dysphagia, bradycardia, decreased reflexes, dilated pupils, seizure, and coma. The health problem caused by K. breviscan be associated with a red tide bloom. We encountered 3 cases of neurotoxic shellfish poisoning. They all presented with GI and neurologic symptoms andrecovered after conservative treatment.
Ventricular Arrhythmia Following Aconitine-Ingestion - 2 Case Reports -
Mi-Ran Kim
J Korean Soc Clin Toxicol. 2006;4(2):180-186.   Published online December 31, 2006
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The various species of aconitum contain diterpene (C-20) and norditerpene (C-19) forms of the natural alkaloid aconitine that cause neurologic, gastrointestinal, cardiovascular symptoms. In chinese medicine, these plants has been used as drugs to treat pain, dyspepsia, cerebrovascular disease, and so on. Because the therapeutic window is narrow, poisoning may occur from unintentional exposure, with a variety of toxic effects such as arrhythmia, hypotension, paresthesia, paralysis, nausea, vomiting, and abdominal pain. Aconitine-containing folk remedies are widely used in Korea. We encountered two cases of ventricular arrhythmia in patients who ingested tablets, known as 'Wha-Pung-Dan' made with aconitine extracts and were subsequently admitted to the ED. A 42 year-old man who took 35 tablets presented with ventricualr tarchycardia, and 40 year-old woman who took 40 tablets showed premature ventricular contractions. Both patients were discharged normally without any complications after three days.
2 Cases of Toad Venom Intoxication
Cheong-Hoon Kwon, Woo-Chan Jun, Yoon-Suk Jung, Jung-Hwan Ahn
J Korean Soc Clin Toxicol. 2006;4(1):58-60.   Published online June 30, 2006
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AbstractAbstract PDF
The venom gland of Toad contains large quantities of cardiac glycosides, and toad venom poisoning is similar to digitalis toxicity and carries a high mortality. Sometimes after ingestion of aphrodisiac pills which contain dried toad, a patient develops gastrointestinal symptoms and bradycardia, psychoneurologic symptoms. We have experienced 2 cases of toad venom intoxication, who ingested asian toads. Patients were presented to our ED with nausea, vomiting, and abdominal pain. The patients were peformed monitoring and conservative treatment and were fully recovered. Toad venom intoxication should be considered in patients with clinical manifestation of gastrointestinal irritation, cardiac arrhythmias, hyperkalemia, and detectable serum digoxin level without current medication of digoxin.
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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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.
Severe Liver Toxicity Caused by Amatoxin (Case Series)
Joo-Hyun Suh, Sung-Jin Kim, Young-Kuk Chung, Woong-Gil Choi, Young-Se Kwon, Hyung-Keun Roh
J Korean Soc Clin Toxicol. 2006;4(1):73-77.   Published online June 30, 2006
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Poisoning with mushroom containing amatoxin may be a real medical emergency and is characterized by long incubation time lag, gastrointestinal symptoms, hepatotoxic phase and sometimes death. We report a family of parents and two children who ingested wild mushroom and recovered from varying degrees of hepatotoxicity. After eating cooked wild mushroom and its soup, they all developed abdominal pain, vomiting and diarrhea 11 hours later, Their liver enzymes reached peak level between 48 and 72 hours after the ingestion. Among the family members, 5-year-old girl showed the most severe hepatic toxicity of AST/ALT 14,099/13,176 IU/L. They were all treated with supportive measures including repeated activated charcoal and penicillin G and recovered from the hepatotoxicity between 7 and 28 days after the ingestion. Being based on the shape and a typical course of the amatoxin poisoning, we presume that this wild mushroom belongs to Amanita virosa.

JKSCT : Journal of The Korean Society of Clinical Toxicology