Journal of The Korean Society of Clinical Toxicology

Original Article

Poisoning patients’ clinical features according to the blood level of propranolol: Sungheon Kim, Byung Hak So, Hyung Min Kim, Kyeong Man Cha, Hwan Song, Won Jung Jeong; J Korean Soc Clin Toxicol. 2023;21(1):56-63. Published online June 30, 2023; DOI: https://doi.org/10.22537/jksct.2023.00010

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Abstract PDF: Purpose: Propranolol is widely prescribed to psychiatric patients to control adrenergic symptoms. However, propranolol poisoning can be fatal due to cardiovascular complications. We analyzed associations between blood levels of propranolol and patients’ clinical features, with the aim of predicting progression to severe complications.
Methods
Data were collected from patients aged 18 years or older who presented to the emergency department with propranolol poisoning between January 2016 and May 2022. We retrospectively analyzed their medical records and compared blood levels of propranolol between those who had cardiovascular complications and those who did not.
Results
Two hundred patients were included in this study. The blood levels of propranolol were significantly higher in patients with hypotension, bradycardia, and prolonged QT intervals, with median values of 247.0 ng/mL (interquartile range [IQR], 56.5–333.8 ng/mL), 275.8 ng/mL (IQR, 154.3–486.4 ng/mL), and 159.0 ng/mL (IQR, 33.9–310.8 ng/mL), respectively. In the predictive analysis of cardiovascular complications using a receiver operating characteristic curve, the area under the curve was 0.729 with a cut-off value of 72.40 ng/mL (sensitivity, 0.667; specificity, 0.819). In addition, the correlation coefficient between blood levels and the amount of drug described during the history-taking at the time of presentation was 0.634, which was found to have a significantly higher relationship.
Conclusion
Because blood levels of propranolol can be used as predictors of exacerbation in patients with propranolol poisoning, patients with blood levels above 72.40 ng/dL require careful treatment and observation from their initial presentation at the emergency department.

A case of various clinical aspects associated with cardiotoxicity after glufosinate poisoning: Seon Tae Kim; J Korean Soc Clin Toxicol. 2021;19(2):133-138. Published online December 31, 2021; DOI: https://doi.org/10.22537/jksct.2021.19.2.133

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Abstract PDF: Glufosinate-containing herbicides is a non-selective herbicide commonly used worldwide. As the use of them increased gradually since paraquat was banned in 2012, the number of suicides by their ingestion is also increasing continuously. Complications of glufosinate-containing herbicide poisoning include various central nervous system (CNS) toxicities such as convulsions, loss of consciousness, memory impairment, and respiratory depression, which may be accompanied by hemodynamic changes such as bradycardia and hypotension. However, it is very rare that arrhythmias other than bradycardia occurred and Takotsubo cardiomyopathy was combined due to cardiotoxicity. A 71-year-old female patient was transferred to our hospital after ingesting 500 mL of glufosinate-containing herbicide and receiving 5 L of gastric lavage at a local hospital. A few hours later, she presented stuporous mentality, respiratory depression, and convulsions, and was accompanied by hypotension and bradycardia. On the second day of admission, electrocardiogram (ECG) showed bradycardia and QTc prolongation with hemodynamic Instability. Accordingly, we conducted the early treatment with continuous renal replacement therapy (CRRT) and the application of temporary cardiac pacemaker. An echocardiogram demonstrated decreased ejection fraction (EF) and Takotsubo cardiomyopathy on the third day of admission. Then, she was discharged safely with conservative treatment. At the follow-up after 1 year, Takotsubo cardiomyopathy, EF and QTc prolongation were recovered on echocardiogram and ECG. Because cardiac toxicity after glufosinate-containing herbicide poisoning may cause life-threatening consequences, caution is required while treating the patient. Therefore, if electrocardiogram changes are seen in the elderly with a large amount of glufosinate herbicide ingestion, additional cardiac function test through echocardiography should be concerned, and early treatment through CRRT or artificial cardiac pacing should be considered.

Clinical and Epidemiological Characteristics of Severe Poisoning Patients and Analysis of Prognostic Factors: Young Yun Jung, Chul Min Ha, Sung Tae Jung, Hyoung Ju Lee; J Korean Soc Clin Toxicol. 2020;18(2):94-101. Published online December 31, 2020; DOI: https://doi.org/10.22537/jksct.2020.18.2.94

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Abstract PDF: Purpose: This study examined the clinical and epidemiological characteristics of intensive care unit (ICU) patients admitted or died in the emergency medical center with acute-poisoning to investigate the variables related to the prognosis. Methods: The data were collected from poisoning patients admitted or died in the emergency medical center of a general hospital located in Seoul, from January 2014 to February 2020. The subjects of this study were 190 patients. The medical records were screened retrospectively, and the clinical and epidemiological characteristics of the patients in the emergency room (ER) and ICU were examined to investigate the contributing factors that influence the poor prognosis. Results: The study analyzed 182 patients who survived after being admitted to the intensive care unit (ICU). The results are as follows. The mental change (87.4%) was the most common symptom. Sedative poisoning (49.5%) was the commonest cause. For most patients, pneumonia (26.9%) was the most common complication. Hypotension (23.7%), tachycardia (42.1%), fever (15.8%), seizures (10.5%), dyspnea (2.6%), high poisoning severity score (PSS), type of toxic material, mechanical ventilator application (39.5%), inotropes application (39.5%), and pneumonia (55.3%) were correlated the LOS over 5 days in the ICU. 8 patients died. In the case of death pesticides and carbon monoxide were the main toxic materials; tachycardia, bradycardia, and hypotension were the main symptoms, and a mechanical ventilator and inotropes were applied. Conclusion: Patients with unstable vital signs, high PSS, and non-pharmaceutical poisoning had a prolonged LOS in the ICU and a poor prognosis.

Treatments of Calcium Channel Blocker Overdose: Sung Woo Lee; J Korean Soc Clin Toxicol. 2020;18(1):1-10. Published online June 30, 2020; DOI: https://doi.org/10.22537/jksct.2020.18.1.1

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Abstract PDF: Pharmaceutical agents are the most common causes of poisoning in Korea. Calcium channel blockers (CCBs) are commonly used in Korea for the management of hypertension and other cardiovascular diseases, but are associated with a risk of mortality due to overdose. Due to the frequent fatalities associated with CCB overdose, it is essential that the emergency physician is capable of identifying CCB intoxication, and has the knowledge to manage CCB overdose. This article reviews the existing clinical guidelines, retrospective studies, and systematic reviews on the emergency management of CCB overdose. The following are the varied treatments of CCB overdose currently administered. 1) For asymptomatic patients: observation with enough time and decontamination, if indicated. 2) For symptomatic patients: infusion of calcium salt, high dose insulin therapy, and vasopressor (norepinephrine) or atropine for bradycardia. 3) For patients refractory to the first line therapy or with refractory shock or impending arrest: lipid emulsion therapy and extracorporeal membrane oxygenation. 4) As adjunct therapy: phosphodiesterase inhibitors, glucagon, methylene blue, pacemaker for AV block. Small CCB ingestion is known to be fatal for pediatric patients. Hence, close observation for sufficient time is required.

A Case Report of Acute Nicotine Poisoning from Subcutaneous Injection of Nicotine Solution for Electronic Cigarette: Jiun Choi, Dong Ryul Ko, Je Sung You, Sung Phil Chung; J Korean Soc Clin Toxicol. 2017;15(1):60-64. Published online June 30, 2017; DOI: https://doi.org/10.22537/jksct.2017.15.1.60

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Abstract PDF: Nicotine-poisoning related to the electronic cigarettes (e-cigarette) is increasing worldwide. Moreover, the American Association of Poison Control Centers has advised the public to use caution with e-cigarette devices and highly concentrated liquid nicotine after a surge in related poisonings. We report here the first case of nicotine poisoning from self-injected e-cigarette fluid in Korea. A 17-year-old male patient subcutaneously injected himself with 0.5 ml of nicotine solution for an electronic cigarette via the dorsum of his hand, after which he complained of nausea, vomiting, dizziness and dyspnea. His vital signs were within the normal range, but his mental status was drowsy. He was admitted for observation and the symptoms disappeared the following day. Sinus bradycardia with a rate of 45/min was observed on the third hospital day, but improved after 6 hours. He was discharged without complications.

Clinical Analysis of Patients with Cardiotoxicity Caused by Himalayan Mad Honey: Sung Ho Kim, Dong Woo Seo, Seung Mok Ryoo, Won Young Kim, Bum Jin Oh, Kyoung Soo Lim, Chang Hwan Sohn; J Korean Soc Clin Toxicol. 2013;11(2):119-126. Published online December 31, 2013

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Abstract PDF: Purpose: The aim of this study was to evaluate the clinical characteristics and outcome of patients who presented to the emergency department (ED) with cardiotoxicity caused by ingestion of Himalayan mad honey. Methods: Medical records of 12 patients who presented to the ED from January 1, 2005 to December 31, 2012 with cardiotoxicity caused by ingestion of Himalayan mad honey were retrospectively reviewed. Results: The mean age of patients was 54.5 years and 58.3% were men. The median amount of mad honey ingested was 30.0 cc, and the mean time from ingestion to onset of symptoms was 39.4 minutes. All patients had hypotension and bradycardia upon arrival in the ED. The initial electrocardiogram showed sinus bradycardia in seven patients, junctional bradycardia in four patients, and atrial fibrillation with slow ventricular response in one patient. Four patients were treated with intravenous normal saline solution only. Eight patients were treated with intravenous normal saline solution and atropine sulfate in a dose ranging from 0.5 to 2.0 mg. Blood pressure and pulse rate returned to normal limits within 24 hours in all patients. Conclusion: Our study showed that all patients with cardiotoxicity caused by ingestion of Himalayan mad honey had severe hypotension, bradycardia, and bradyarrythmias, including sinus bradycardia and junctional bradycardia and all patients responded well to conservative treatment, including intravenous normal saline solution and intravenous atropine sulfate.

A Case of Mental Change in a Patient Who Received a Zoletil Injection: Yeong Ki Lee, In Gu Kang, Cheol Sang Park, Seok Jin Heo, Youn Seok Chai, Seong Soo Park, Jae Kwang Lee, Hyun Jin Kim, Won Joon Jeong; J Korean Soc Clin Toxicol. 2013;11(1):23-27. Published online June 30, 2013

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Abstract PDF: Zoletil is a non-opioid, non-barbiturate animal anesthetic and proprietary combination of two drugs, a dissociative anesthetic drug, tiletamine, with the benzodiazepine anxiolytic drug, zolazepam. Zoletil has greater potency than ketamine. Zoletil is abused for recreational purposes, especially by people with easy access to medicine. However, in Korea, it is available over-the-counter. Here we report on a case of an 83-year-old woman who received injection of seven vials of "Zoletil 50" by her daughter and presented with an altered mental change. Her mental state was stupor and vital sign was hypotension, bradycardia. Her blood tests indicated metabolic and respiratory acidosis and hyperkalemia. She was treated with intravenous naloxone and flumazenil but was not responsive. She was admitted to the ICU and treated with supportive therapy. Her mental state showed transient recovery, however, her clinical manifestation worsened and she expired.

Grayanotoxin Poisoning from Honey - A Case Report: Gi-Hun Choi, Ki-Cheol You, Soon-Joo Wang, Tae-Jin Park; J Korean Soc Clin Toxicol. 2012;10(1):37-40. Published online June 30, 2012

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Abstract PDF: Honey is produced by bees from nectar collected from nearby flowers. Sometimes, honey produced from the Rhododendron species is contaminated by Grayanotoxin (GTX) in Nepal and other countries. There have been reports of GTX intoxication, also known as 'mad honey disease', from honey produced in countries other than Korea. The importation of wild honey has been prohibited by the Korean Food and Drug Administration since 2005, yet it is still distributed within Korea by the occasional tourist. We report a case of GTX intoxication from contaminated honey which included the symptoms of nausea, vomiting, general weakness, dizziness, blurred vision, hypotension and sinus bradycardia. By means of infusion with normal saline and atropine sulfate, the patient's condition fully recovered within 8 hours of hospital admission, and she was discharged without any complications.

A case of Systemic Toxicity that Occurred in an Adult Who Intentionally Ingested Rhododendron Sclippenbashii: Sang-Min Jeong, Seung-Han Lee, Jeong-Soo Lim, Sang-Yeol Yoon, Seung Ryu, Jin-Woong Lee, Seung-Whan Kim, In-Sool Yoo, Yeon-Ho You; J Korean Soc Clin Toxicol. 2009;7(2):180-182. Published online December 31, 2009

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Abstract PDF: It is well known that Rhododendron sclippenbashii contains the toxic material grayanotoxin. So, Koreans do not eat it, but they do eat azalea although it contains grayanotoxin. That is why there have been no reports about Rhododendron sclippenbashii intoxication after ingesting it intentionally, not accidentally. In this case, the patient was admitted to the emergency room with several toxic symptoms after intentionally consuming 50 blossoms of Rhododendron sclippenbashii to get rid of thirst. Treatment with saline infusion and atropine was successful and the outcome was favorable enough in this case to produce a complete cure without any sequelae at discharge. But toxic symptoms were seen for 24 hours, although the symptoms usually fade in 9 hours. Therefore, we should carefully treat and observe, for over 24 hours, the patient who intentionally ingests about 50 blossoms of Rhododendron sclippenbashii.

A Case of Fatal Arrhythmia after Propafenone Overdose: Yeon-Young Kyong, Kyoung-Ho Choi; J Korean Soc Clin Toxicol. 2008;6(2):123-129. Published online December 31, 2008

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Abstract PDF: A 36-year-old female was transferred to our emergency medical center with decreased mental status after a 6.0 g propafenone overdose because of domestic disturbance. She had no previous history of epilepsy, diabetes mellitus, hypertension or psychiatric illness. Before presenting to our center, gastrointestinal decontamination, charcoal administration, and endotracheal intubation due to bradycardia and generalized seizure had been performed. Soon after hospital arrival, at 5 h after ingestion, she collapsed into shock and fatal arrhythmia. We successfully resuscitated the patient with amiodarone, sodium bicarbonate, a large volume of normal saline, calcium, and ventilator care. At 23 h after ingestion, she was fully recovered and had no subjective signs or symptoms. To our knowledge, this is the first case report of intentional propafenone overdose in Korea, which we report with reviews of the previous literature.

A Case of a Patient with Stuporous Mentality and Hypotension after Amitraz Ingestion: Si-Young Jung, Jin-Hee Jung, Eun-Kyung Eo; J Korean Soc Clin Toxicol. 2007;5(2):123-125. Published online December 31, 2007

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Abstract PDF: Amitraz is a formamidine-derived insecticide and acaricide which is commonly used throughout the world. Amitraz intoxication is mediated through ${alpha}_2$ adrenergic receptor agonist effects, similar to those of the ${alpha}_2$ agonist clonidine. We report a case of a patient who experienced coma and hypotension after amitraz ingestion. A 37-year-old woman visited the ER with symptoms of vomiting and altered mental state. She had ingested a mouthful of liquid amitraz concentrate (12.5%), which rapidly led to vomiting, hypotension, bradycardia, hyperglycemia, and mental stupor. Supportive treatment, including mechanical ventilation and administration of inotropics, resulted in full recovery within four days.

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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Abstract 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.

A Case Report of Saliva-type Hyperamylasemia in Mad Honey Poisoning: Kun-Woo Lee, Kyu-Nam Park, Mi-Jin Lee; J Korean Soc Clin Toxicol. 2006;4(2):166-169. Published online December 31, 2006

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Abstract PDF: 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.

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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Abstract 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.

Two Cases of Mad-Honey Poisoning with Cardiovascular Symptom: Young-Gil Ko, Kyung-Hwan Kim, Ah-Jin Kim, Dong-Wun Shin, Jun-Soek Park, Jun-Young Roh, Ji-Young Ahn; J Korean Soc Clin Toxicol. 2006;4(1):78-81. Published online June 30, 2006

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Abstract PDF: Mad-honey poisoning is mainly brought about by the honey imported from Napal, Turkey, Brazil and other parts of Europe. This mad honey is extracted from Ericaceae plants of Rhododendron species and contains grayanotoxins that causes poisoning. These toxic compounds exert a specific stimulatory action on membrane permeability to Na+ions in various excitable tissues and cause depolarization of cell membranes. The toxic effects of grayanotoxins contained honey are mainly cardiovascular disturbances with bradycardia, cardiac arrhythmia, hypotension. There are Other symptoms like nausea, vomiting, salivation, dizziness, weakness and loss of consciousness. The precise amount for a toxic dose is not known. In general the severity of the honey poisoning depends on the amount ingested. Two cases of mad-honey poisoning are described here. Both patients showed bradycardia and arterial hypotension after ingestion of honey which was brought from Nepal. They were recovered fully within 24 hours after administration of fluids and atropine sulphate.

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