Journal of The Korean Society of Clinical Toxicology

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.

Evaluation of Cardiac Function by Transthoracic Echocardiography in Patients with Myocardial Injury Secondary to Organophosphate Poisoning: Yoonsuk Lee, Oh Hyun Kim, Hyung Il Kim, Kyoung Chul Cha, Hyun Kim, Kang Hyun Lee, Sung Oh Hwang, Yong Sung Cha; J Korean Soc Clin Toxicol. 2015;13(2):62-70. Published online December 31, 2015

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Abstract PDF: Purpose: Cardiac complications may occur in cases of organophosphate (OP) poisoning. However, a few studies regarding patterns of cardiac toxicity as determined by transthoracic echocardiography (TTE) after exposure to OP have been reported. In the current study, the authors examined cardiac functions using TTE in patients with myocardial injury caused by exposure to OP. Methods: A retrospective review was conducted on 16 consecutive cases of OP poisoning with myocardial injury (defined as elevated troponin I within 48 hours of arrival at the regional emergency center in South Korea and diagnosed and treated at the center from January 2012 to November 2014. Results: TTE was performed in 11 (69%) of the 16 patients with an elevated troponin I (TnI) level within 48 hours. Of these 11 patients, 5 patients (45.5%) exhibited reduced ejection fraction (EF), and 3 exhibited regional wall motion abnormality (RWMA). Two patients (18.2%) had both reduced systolic function and RWMA. Two of the 5 patients with reduced EF returned to normal systolic function, however two patients did not regain normal systolic function after admission. One patient expired due to multiple organ failure, and 4 patients were transferred with a moribund status. Twelve of 15 patients who survived to discharge (at 4 to 35 months) were followed. Five of these patients died during follow-up and 7 survived without further complications. Conclusion: OP can cause reversible cardiac dysfunction including reduced systolic function and RWMA. Serum TnI may be useful for initial assessment of cardiac function during the workup of patients suffering from OP poisoning. After the initial assessment of cardiac enzyme, further evaluation with TTE in patients with abnormal cardiac enzyme will be necessary to understand the cardiac toxicity.

Cardiovascular Manifestations and Clinical Course after Acute Carbon Monoxide Poisoning: In Soo Lee, Yoon Seok Jung, Young Gi Min, Gi Woon Kim, Sang Cheon Choi; J Korean Soc Clin Toxicol. 2012;10(2):103-110. Published online December 31, 2012

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Abstract PDF: Purpose: The aim of this study was to evaluate the cardiovascular manifestations and clinical course in patients with acute carbon monoxide poisoning. Methods: A retrospective study was conducted over a 36 month period on consecutive patients who visited an emergency medical center and were diagnosed with acute carbon monoxide poisoning. A standardized data extraction protocol was performed on the selected patients. Results: A total of 293 patients were selected during the study period. Cardiac manifestations were observed in 35.2% (n=103) of the patients: hypotension in 11 patients (3.8%), ECG abnormalities in 44 patients (15.0%) and cardiac enzyme abnormalities in 103 patients (35.2%). Echo cardiography was performed on 56 patients with cardiac toxicity: 12 patients had abnormal results (5 patients with global hypokinesia and 7 patients with regional wall akinesia). Five patients died within 3 hours after ED admission, and the remaining patients were discharged alive. At 3 months after discharge, none of these patients had died.The SOFA scores in the severe cardiac toxicity group and non-severe cardiac toxicity group at the time of arrival were $2.53{pm}2.29$ and $2.19{pm}2.12$, respectively (p=0.860). Conclusion: Cardiovascular manifestations occur after acute CO poisoning at arateof 35.2%. Even those with severe cardiovascular toxicity recovered well within 10 days after admission. Therefore, the importance of cardiac toxicity after acute CO poisoning is not significant in itself in the clinical course, and the short-term prognosis of cardiac toxicity is unlikely to be unfavorable in acute CO poisoning.

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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Abstract 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.

Cardiac Toxicity Following a Diphenhydramine Overdose: Sung-Jun Park, Jong-Hak Park, In-Kyung Um, Kyung-Ae Park, Do-Hyoun Kim, Su-Jin Kim, Sung-Woo Lee, Yun-Sik Hong; J Korean Soc Clin Toxicol. 2011;9(1):20-25. Published online June 30, 2011

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Abstract PDF: Purpose: This study was designed to analyze the contributing factors, as well as the incidence and nature of the cardiac toxicity, in patients presenting with diphenhydramine overdose. Methods: We retrospectively reviewed the medical records of the intoxicated patients who presented to the ED of Korea University Anam Hospital from January 2008 to December 2010. Those patients who visited due to a diphenhydramine overdose were selected and the following features were recorded for analysis: the general characteristics, vital signs, the amount of ingested diphenhydramine, the time interval from ingestion to presentation, the coingested drugs (if any), the toxicities and the ECG findings. Cardiac toxicity, while defined mainly in terms of the temporary ECG changes such as QTc prolongation, right axis deviation, QRS widening, high degree AV block and ischemic changes, also encompassed cardiogenic shock, which is a clinical finding. Results: A total of eighteen patients were enrolled. Of the eighteen patients, eight had ingested diphenhydramine only, while ten had ingested other drugs in addition to diphenhydramine. The most commonly observed toxicity following diphenhydramine overdose included cardiac toxicity (78%). Cardiac toxicity was observed in all the patients who presented to the emergency department 2 hours after ingestion. The patients with QTc prolongation turned out to have ingested significantly larger amounts of diphenhydramine. Conclusion: QTc prolongation and right axis deviation were common findings for the patients with a diphenhydramine overdose. QTc prolongation was more likely to occur with ingesting larger amounts of diphenhydramine. Close monitoring is mandatory for patients who have ingested large amounts of diphenhydramine to prevent such potentially lethal cardiac toxicity.

Cardiac Toxicity in Patients with Antidepressant Intoxication: Jung-Taek Park, Se-Min Choi, Young-Min Oh, Joo-Suk Oh, Yeon-Young Kyoung, Hang-Joo Cho, Kyoung-Ho Choi; J Korean Soc Clin Toxicol. 2010;8(2):97-105. Published online December 31, 2010

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Abstract PDF: Purpose: Although cardiac toxicity is a key parameter of significant toxicity, in antidepressant intoxication, there are few studies on the cardiac toxicity of serotonin reuptake inhibitor and the intoxication with the new generation of antidepressants. The aim of this study is to investigate the relative cardiac toxicity of serotonin reuptake inhibitor and intoxication with the new generation of antidepressants as compared with that of tricyclic antidepressant intoxication. Methods: We retrospectively reviewed the medical records of 109 antidepressant intoxicated patients who visited the Emergency Department from January, 2005 to December, 2009 to collect and analyze the demographic and clinical data. Sixteen patients were excluded. The enrolled seventy eight patients were classified into three groups: the tricyclic antidepressant group (TCA) (n=32), the selective serotonin reuptake inhibitor subgroup (SSRI) (n=28) and the new generation antidepressant subgroup (NGA) (n=18). Results: The demographic and clinical data of the SSRI and NGA groups were not significantly different from that of the TCA group. The QRS duration of the SSRI subgroup ($86.4{pm}12.0$ msec) and the NGA subgroup ($91.8{pm}11.9$ msec) was not significantly different from that of the TCA group ($90.0{pm}13.5msec$) (p=0.598). The QTc interval of the SSRI group ($444.5{pm}33.5msec$) and the NGA group ($434.9{pm}35.9msec$) (p=0.260) were not significantly different from that of the TCA group ($431.2{pm}44.1msec$) (p=0.287). Conclusion: Intoxication with SSRI and the new generation antidepressants seemed to show significant cardiac toxicity, like what is seen in tricyclic antidepressant intoxication. Clinicians must pay attention to SSRI and new generation antidepressant intoxication.

Acute Coronary Syndrome In Acute Carbamate Ingestion: Dai-Hai Choi; J Korean Soc Clin Toxicol. 2007;5(1):74-78. Published online June 30, 2007

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Abstract PDF: The carbamates are a group of insecticides derived from carbamic acid, with a broad spectrum of uses as agricultural and household garden insecticides. Carbamate insecticides are reversible cholinesterase inhibitors. Their inhibitory action is mediated by reversible carbamylation of acetylcholine, as with the organophosphate insecticides. Carbamates are absorbed by the body through multiple routes, including inhalation, ingestion, and dermal absorption. Although poisoning can result from occupational exposure or accidental ingestion, in most cases there is suicidal intent. This is particularly true in developing countries, where the highest incidence of morbidity and mortality from this cause occurs. Cardiac complications often accompany poisoning by carbamate compounds, which may be serious and often fatal. The extent, frequency, and pathogenesis of cardiac toxicity from carbamate compounds has not been clearly defined. Possible mechanismsinclude sympathetic and parasymphatetic overactivity, hypoxemia, acidosis, electrolyte derangements, and a direct toxic effect of the compounds on the myocardium. Patients with carbamate poisoning should immediately be transferred to an intensive or coronary care unit where appropriate monitoring and resuscitative facilities are available. We here report a case of acute coronary syndrome resulting from acute carbamate ingestionthat resulted in a healthy discharge.

Transient Change of Electrocardiogram in Two Young Women With Salicylate Intoxication - Two Cases Report -: Je-Sung You, Jong-Woo Park, Young-Hwan Choi, Young-Soon Cho, Kwang-Hyun Cho, Jun-Seok Park, Sung-Pil Chung, Hahn-Shick Lee; J Korean Soc Clin Toxicol. 2006;4(1):44-47. Published online June 30, 2006

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Abstract PDF: Symptoms of aspirin overdose may vary from acid-base disturbance, electrolyte abnormality, non-cardiogenic pulmonary edema, chemical hepatitis, seizure to cardiac toxicity. Cardiac adverse effects from aspirin are uncommon but there are reports of arrhythmia, cardiopulmonary arrest, and myocardial infarction. We report 2 cases of young women with aspirin overdose who exhibited ischemic changes on their ECGs a few hours after the ingestion with spontaneous recovery in a few days. First case, a 29 year old woman, presented to the emergency department 6 hours after ingesting 250 tablets of aspirin (325 mg/T). On examination, the temperature was $36.3^{circ}C$: blood pressure, 105/72mmHg; Pulse, 111/min and respiratory rate, 24/min. Second case, a 27 year old woman, an hour after ingesting 60 tablets (325mg/T). On examination, the temperature was $36.0^{circ}C$: blood pressure, 102/72 mmHg; pulse, 89/min and respiratory rate, 25/min. In both cases, ECG after 6 hours of ingestion had sinus tachycardia and developed T wave inversion on the anterior leads in the following ECGs. Their initial serum salicylate levels after 6 hours of ingestion were 71.2 mg/dL and 28.4 mg/dL respectively. These salicylate levels were resolving when these ECGs were observed. The ECG changes resolved in the following days and they were discharged without any further symptoms. Further studies are needed, but for the time being, when dealing with salicylate overdose, transient cardiac depression should be kept in mind to avoid adverse ischemic cardiac events.

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