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Toxicology

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Intravenous lipid emulsion therapy for cardiac arrest and refractory ventricular tachycardia due to multiple herb intoxication
Clin Exp Emerg Med. 2019;6(4):366-369.   Published online December 31, 2019
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Intravenous lipid emulsion therapy for cardiac arrest and refractory ventricular tachycardia due to multiple herb intoxication
Clin Exp Emerg Med. 2019;6(4):366-369.   Published online December 31, 2019
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Herbal products have been used for therapeutic purposes for a long time. However, many herbs can be toxic and even life-threatening. If refractory ventricular tachycardia (VT) is caused by herbal products and shows no response to conventional therapy, intravenous lipid emulsion (ILE) therapy can be considered. We report a case of herbal intoxication leading to refractory VT, which was successfully treated with ILE therapy. A 36-year-old woman with aplastic anemia presented with mental changes. She had taken an unknown herbal decoction three days before visiting the hospital. Soon after coming to the hospital, she went into cardiac arrest. Cardiopulmonary resuscitation was performed, and return of spontaneous circulation with VT was achieved. Synchronized cardioversion was then performed and amiodarone was administered. However, VT with pulse continued, so ILE therapy was attempted, which led to the resolution of VT.

Citations

Citations to this article as recorded by  Crossref logo
  • The possible therapeutic role of intravenous lipid emulsion in acute aluminium phosphide poisoning: a randomized controlled clinical trial
    Hafsa Salah Gheat, Manar M Fayed, Fatma M Elgazzar, Eman I Draz, Rabab S El-Kelany
    Toxicology Research.2024;[Epub]     CrossRef
  • Evaluation of extraction methods for pharmacologically active compounds from anticonvulsant traditional Chinese medicines: Gou Teng, Tian Ma, Jiang Can using DART-TOF-MS
    Kimberly N. Karin, Justin L. Poklis, Michelle R. Peace
    Analytical Methods.2021; 13(7): 884.     CrossRef
  • Lipid Emulsion Treatment of Nonlocal Anesthetic Drug Toxicity
    Seong-Ho Ok, Miyeong Park, Ju-Tae Sohn
    American Journal of Therapeutics.2021; 28(6): e742.     CrossRef
  • Amiodarone

    Reactions Weekly.2020; 1789(1): 24.     CrossRef
  • Lipid emulsion treatment for ventricular tachycardia induced by the toxicity of multiple herbs
    Ju-Tae Sohn
    Clinical and Experimental Emergency Medicine.2020; 7(2): 139.     CrossRef
  • 8,493 View
  • 127 Download
  • 4 Web of Science
  • 5 Crossref

Original Article

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Serum markers and development of delayed neuropsychological sequelae after acute carbon monoxide poisoning: anion gap, lactate, osmolarity, S100B protein, and interleukin-6
Clin Exp Emerg Med. 2018;5(3):185-191.   Published online September 30, 2018
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Serum markers and development of delayed neuropsychological sequelae after acute carbon monoxide poisoning: anion gap, lactate, osmolarity, S100B protein, and interleukin-6
Clin Exp Emerg Med. 2018;5(3):185-191.   Published online September 30, 2018
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Objective
Reliable biomarkers of delayed neuropsychological sequelae (DNS) after acute carbon monoxide (CO) poisoning are lacking. This study investigated the associations between potential serum markers and the development of DNS after acute CO poisoning.
Methods
Retrospective chart reviews were conducted for patients diagnosed with acute CO poisoning during a 28-month period. The patients were divided into two groups according to the presence or absence of having developed DNS. Multivariate analysis was performed to identify predictors of DNS after CO poisoning.
Results
Of a total of 102 patients, 10 (9.8%) developed DNS. The levels of serum osmolarity, S100B protein, and serum lactate, as well as serum anion gap, were statistically significant in univariate analysis. Multiple logistic regression analysis showed that anion gap (adjusted odds ratio [AOR], 1.36; 95% confidence interval [CI], 1.11 to 1.88), serum lactate level (AOR, 1.74; 95% CI, 1.26 to 2.75), and serum S100B protein level ([AOR, 7.02×105; 95% CI, 4.56×102 to 9.00×1010] in model 1, [AOR, 3.69×105; 95% CI, 2.49×102 to 2.71×1011] in model 2) were independently associated with DNS development.
Conclusion
Based on our preliminary results, serum lactate level, serum anion gap, and serum S100B protein level in the emergency department could be informative predictors of DNS development in patients with acute CO poisoning. These markers might have the potential to improve early recognition of DNS in patients with acute CO poisoning.

Citations

Citations to this article as recorded by  Crossref logo
  • Clinical characteristics and the risk factors analysis in patients with delayed encephalopathy after acute carbon monoxide poisoning
    Ziang Han, Sumeng Shi, Yan Zhang, Ding Yuan, Zhigao Xu, Yanxia Gao
    Human & Experimental Toxicology.2025;[Epub]     CrossRef
  • Optic nerve sheath diameter measurements to predict delayed neurological sequelae after carbon monoxide poisoning
    Yusuf Kenan Tekin
    Clinical Toxicology.2024; 62(2): 88.     CrossRef
  • Effectiveness of Initial Troponin I and Brain Natriuretic Peptide Levels as Biomarkers for Predicting Delayed Neuropsychiatric Sequelae in Patients with CO Poisoning: A Retrospective Multicenter Observational Study
    Myung Hyun Jung, Juncheol Lee, Jaehoon Oh, Byuk Sung Ko, Tae Ho Lim, Hyunggoo Kang, Yongil Cho, Kyung Hun Yoo, Sang Hwan Lee, Chang Hwan Sohn, Won Young Kim
    Journal of Personalized Medicine.2023; 13(6): 921.     CrossRef
  • Predicting scale of delayed neuropsychiatric sequelae in patients with acute carbon monoxide poisoning: A retrospective study
    Shijun Yang, Huichun Liu, Qifeng Peng, Jinlan Li, Qunhui Liu
    The American Journal of Emergency Medicine.2022; 52: 114.     CrossRef
  • Prognostic value of the myeloperoxidase index for early prediction of neurologic outcome in acute carbon monoxide poisoning
    Joong Seok Moon, Sung Hwa Kim, Yong Sung Cha
    Clinical and Experimental Emergency Medicine.2022; 9(3): 230.     CrossRef
  • Serum phosphate is not an early predictor of neurocognitive outcomes in acute carbon monoxide poisoning patients
    Yuseon Lee, Sung Hwa Kim, Yong Sung Cha
    Clinical and Experimental Emergency Medicine.2022; 10(1): 74.     CrossRef
  • Assessment of serum glucose/potassium ratio as a predictor for delayed neuropsychiatric syndrome of carbon monoxide poisoning
    E Demirtaş, İ Korkmaz, YK Tekin, Es Demirtaş, İ Çaltekin
    Human & Experimental Toxicology.2021; 40(2): 207.     CrossRef
  • Risk factors for delayed encephalopathy following carbon monoxide poisoning: Importance of the period of inability to walk in the acute stage
    Yasuhiro Suzuki, Benito Soto-Blanco
    PLOS ONE.2021; 16(3): e0249395.     CrossRef
  • Serum NSE and S100B protein levels for evaluating the impaired consciousness in patients with acute carbon monoxide poisoning
    Litao Zhang, Jing Zhao, Qingqing Hao, Xin Xu, Hu Han, Jianguo Li
    Medicine.2021; 100(25): e26458.     CrossRef
  • Use of hyperbaric oxygen therapy for preventing delayed neurological sequelae in patients with carbon monoxide poisoning: A multicenter, prospective, observational study in Japan
    Motoki Fujita, Masaki Todani, Kotaro Kaneda, Shinya Suzuki, Shinjiro Wakai, Shota Kikuta, Satomi Sasaki, Noriyuki Hattori, Kazuyoshi Yagishita, Koji Kuwata, Ryosuke Tsuruta, Tai-Heng Chen
    PLOS ONE.2021; 16(6): e0253602.     CrossRef
  • Incidence patterns of nervous system diseases after carbon monoxide poisoning: a retrospective longitudinal study in South Korea from 2012 to 2018
    Bangshill Rhee, Hyuk-Hoon Kim, Sangchun Choi, Young Gi Min
    Clinical and Experimental Emergency Medicine.2021; 8(2): 111.     CrossRef
  • Prediction of delayed neuropsychiatric sequelae after carbon monoxide poisoning via serial determination of serum neuron-specific enolase levels
    Sangun Nah, Sungwoo Choi, Gi Woon Kim, Ji Eun Moon, Young Hwan Lee, Sangsoo Han
    Human & Experimental Toxicology.2021; 40(12_suppl): S339.     CrossRef
  • Does alcohol play the role of confounder or neuroprotective agent in acute carbon monoxide poisoning?
    Jeong Mi Moon, Byeong Jo Chun, Yong Soo Cho, Jong Goo Mun
    Clinical Toxicology.2020; 58(3): 161.     CrossRef
  • S-100β in predicting the need of hyperbaric oxygen in CO-induced delayed neurological sequels
    Amal SAF Hafez, Ghada N El-Sarnagawy
    Human & Experimental Toxicology.2020; 39(5): 614.     CrossRef
  • Clinical and Magnetic Resonance Imaging Findings of Patients with Acute Carbon Monoxide Poisoning
    Nezih KAVAK, Burcu DOĞAN, Hasan SULTANOĞLU, Rasime Pelin KAVAK, Meltem ÖZDEMİR
    Konuralp Tıp Dergisi.2020; 12(3): 443.     CrossRef
  • Observation on promoting resuscitation in the patients with coma of acute carbon monoxide poisoning by acupuncture combined with hyperbaric oxygen
    Mao-li LUO, Hui-jie LI, Liang-ce MA, Yuan JIANG
    World Journal of Acupuncture - Moxibustion.2019; 29(2): 103.     CrossRef
  • 8,980 View
  • 131 Download
  • 21 Web of Science
  • 16 Crossref
Case Report

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Metoprolol treatment of dual cocaine and bupropion cardiovascular and central nervous system toxicity
Clin Exp Emerg Med. 2019;6(1):84-88.   Published online January 31, 2018
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Metoprolol treatment of dual cocaine and bupropion cardiovascular and central nervous system toxicity
Clin Exp Emerg Med. 2019;6(1):84-88.   Published online January 31, 2018
Close
Cardiovascular and central nervous system (CNS) toxicity, including tachydysrhythmia, agitation, and seizures, may arise from cocaine or bupropion use. We report acute toxicity from the concomitant use of cocaine and bupropion in a 25-year-old female. She arrived agitated and uncooperative, with a history of possible antecedent cocaine use. Her electrocardiogram demonstrated tachycardia at 130 beats/min, with a corrected QT interval of 579 ms. Two doses of 5 mg intravenous metoprolol were administered, which resolved the agitation, tachydysrhythmia, and corrected QT interval prolongation. Her comprehensive toxicology screen returned positive for both cocaine and bupropion. We believe clinicians should be aware of the potential for synergistic cardiovascular and CNS toxicity from concomitant cocaine and bupropion use. Metoprolol may represent an effective initial treatment. Unlike benzodiazepines, metoprolol directly counters the pharmacologic effects of stimulants without respiratory depression, sedation, or paradoxical agitation. A lipophilic beta-blocker, metoprolol has good penetration of the CNS and can counter stimulant-induced agitation.

Citations

Citations to this article as recorded by  Crossref logo
  • Unopposed alpha-1 constriction: a critical review of beta blocker use in cocaine-associated cardiovascular events
    Jeremy Jong, Clipper F. Young, Jennifer M. Abueg, Christina Kinnevey Greig
    Journal of Osteopathic Medicine.2026;[Epub]     CrossRef
  • Pediatric Bupropion Ingestions in Adolescents vs. Younger Children—a Tale of Two Populations
    Steve Offerman, Michael Levine, Jasmin Gosen, Stephen H. Thomas
    Journal of Medical Toxicology.2020; 16(1): 6.     CrossRef
  • Sympathomimetic amine compounds and hepatotoxicity: Not all are alike—Key distinctions noted in a short review
    Cyril Willson
    Toxicology Reports.2019; 6: 26.     CrossRef
  • The clinical toxicology of caffeine: A review and case study
    Cyril Willson
    Toxicology Reports.2018; 5: 1140.     CrossRef
  • 54,661 View
  • 240 Download
  • 4 Web of Science
  • 4 Crossref