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- Anterograde Amnesia after Acute Glufosinate Ammonium Intoxication
- Hyuk-Hoon Kim, Young-Gi Min
- Acute Crit Care. 2018;33(2):110-113. Published online May 31, 2018
- DOI: https://doi.org/10.4266/acc.2016.00444
- 6,217 View
- 137 Download
- 2 Web of Science
- 2 Crossref
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Abstract
PDF - Glufosinate ammonium (GA) intoxication causes several neurologic complications. We report a rare but typical case of GA intoxication associated with anterograde amnesia and bilateral hippocampal involvement. A 53-year-old woman with GA intoxication presented to the emergency department. Initial general and neurologic examinations were unremarkable but, from the day after admission, she exhibited anterograde amnesia. On brain magnetic resonance imaging, the signal intensity in the hippocampus was symmetrically and bilaterally increased. She was discharged with no medical problems, but the anterograde amnesia remained. Eleven days after the onset of amnesia, she returned to the neurology outpatient department with persisting anterograde amnesia but improving symptoms.
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Citations
Citations to this article as recorded by
- Memory impairment with symmetrical hippocampal lesions following acute glufosinate-ammonium intoxication
Daniela Antunes, Daniela Jardim Pereira, Pedro Brás, Joana Jesus-Ribeiro
BMJ Case Reports.2024; 17(1): e259109. CrossRef - Prolonged cognitive dysfunction in patient with splenial lesion of the corpus callosum caused by glufosinate ammonium poisoning
HyunJung Lee, JeongHo Kang
Turkish Journal of Emergency Medicine.2021; 21(2): 82. CrossRef
- Memory impairment with symmetrical hippocampal lesions following acute glufosinate-ammonium intoxication
Original Article
- Pharmacology
- Dexmedetomidine Use in Patients with 33℃ Targeted Temperature Management: Focus on Bradycardia as an Adverse Effect
- Hyo-yeon Seo, Byoung-joon Oh, Eun-jung Park, Young-gi Min, Sang-cheon Choi
- Korean J Crit Care Med. 2015;30(4):272-279. Published online November 30, 2015
- DOI: https://doi.org/10.4266/kjccm.2015.30.4.272
- 5,976 View
- 80 Download
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Abstract
PDF
- Background
This study aimed to investigate bradycardia as an adverse effect after administration of dexmedetomidine during 33℃ target temperature management.
Methods
A retrospective study was conducted on patients who underwent 33℃ target temperature management in the emergency department during a 49-month study period. We collected data including age, sex, weight, diagnosis, bradycardia occurrence, target temperature management duration, sedative drug, and several clinical and laboratory results. We conducted logistic regression for an analysis of factors associated with bradycardia.
Results
A total of 68 patients were selected. Among them, 39 (57.4%) showed bradycardia, and 56 (82.4%) were treated with dexmedetomidine. The odds ratio for bradycardia in the carbon monoxide poisoning group compared to the cardiac arrest group and in patients with higher body weight were 7.448 (95% confidence interval [CI] 1.834-30.244, p = 0.005) and 1.058 (95% CI 1.002-1.123, p = 0.044), respectively. In the bradycardia with dexmedetomidine group, the infusion rate of dexmedetomidine was 0.41 ± 0.15 μg/kg/h. Decisions of charged doctor’s were 1) slowing infusion rate and 2) stopping infusion or administering atropine for bradycardia. No cases required cardiac pacing or worsened to asystole.
Conclusions
Despite the frequent occurrence of bradycardia after administration of dexmedetomidine during 33℃ target temperature management, bradycardia was completely recovered after reducing infusion rate or stopping infusion. However, reducing the infusion rate of dexmedetomidine lower than the standard maintenance dose could be necessary to prevent bradycardia from developing in patients with higher body weight or carbon monoxide poisoning during 33℃ targeted temperature management.
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