High-Frequency Analysis of the Cerebral Physiological Impact of Ketamine in Acute Traumatic Neural Injury
Acute traumatic neural injury, also known as traumatic brain injury (TBI), is a leading cause of death. TBI treatment focuses on the use of sedatives, vasopressors, and invasive intracranial pressure (ICP) monitoring to mitigate ICP elevations and maintain cerebral perfusion pressure (CPP). While co...
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Mary Ann Liebert
2025-01-01
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| Series: | Neurotrauma Reports |
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| Online Access: | https://www.liebertpub.com/doi/10.1089/neur.2024.0146 |
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| author | Davis McClarty Logan Froese Tobias Bergmann Kevin Y. Stein Amanjyot S. Sainbhi Abrar Islam Nuray Vakitbilir Noah Silvaggio Izabella Marquez Alwyn Gomez Frederick A. Zeiler |
| author_facet | Davis McClarty Logan Froese Tobias Bergmann Kevin Y. Stein Amanjyot S. Sainbhi Abrar Islam Nuray Vakitbilir Noah Silvaggio Izabella Marquez Alwyn Gomez Frederick A. Zeiler |
| author_sort | Davis McClarty |
| collection | DOAJ |
| description | Acute traumatic neural injury, also known as traumatic brain injury (TBI), is a leading cause of death. TBI treatment focuses on the use of sedatives, vasopressors, and invasive intracranial pressure (ICP) monitoring to mitigate ICP elevations and maintain cerebral perfusion pressure (CPP). While common sedatives such as propofol and fentanyl have significant side effects, ketamine is an attractive alternative due to its rapid onset and cardiovascular stability. Despite these benefits, ketamine’s use remains controversial due to historical concerns about increasing ICP. Using high-frequency monitoring, this retrospective study compared cerebral pressure-flow dynamics in patients with moderate/severe TBI who received ketamine with those who did not. Statistical analysis included descriptive statistics, comparisons within and between patients receiving ketamine, and evaluation of physiological response around incremental dose changes in ketamine. Various cerebral physiological indices were analyzed, including ICP, CPP, regional cerebral oxygen delivery, intracranial compliance, and cardiovascular reactivity metrics. A total of 122 patients were studied, with 17 receiving ketamine (median age: 37 years) and 105 not receiving ketamine (median age: 42 years). Results indicated higher median ICP in the ketamine group compared with the no ketamine group (9.05 mmHg and 14.00 mmHg, respectively, p = 0.00017); however, this is likely due to differences in patient characteristics and injury severity between the groups. No significant differences were observed in any other index of cerebral pressure-flow dynamics or between any incremental dose change condition. These findings suggest that ketamine does not significantly impact cerebral pressure-flow dynamics, challenging historical concerns about its use in patients with TBI. |
| format | Article |
| id | doaj-art-b2c8fd3e6cfb475c8d5d2e40959774d5 |
| institution | Kabale University |
| issn | 2689-288X |
| language | English |
| publishDate | 2025-01-01 |
| publisher | Mary Ann Liebert |
| record_format | Article |
| series | Neurotrauma Reports |
| spelling | doaj-art-b2c8fd3e6cfb475c8d5d2e40959774d52025-08-20T03:49:37ZengMary Ann LiebertNeurotrauma Reports2689-288X2025-01-016123224110.1089/neur.2024.0146High-Frequency Analysis of the Cerebral Physiological Impact of Ketamine in Acute Traumatic Neural InjuryDavis McClarty0Logan Froese1Tobias Bergmann2Kevin Y. Stein3Amanjyot S. Sainbhi4Abrar Islam5Nuray Vakitbilir6Noah Silvaggio7Izabella Marquez8Alwyn Gomez9Frederick A. Zeiler10Undergraduate Medicine, College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Manitoba, Canada.Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.Department of Biomedical Engineering, Price Faculty of Engineering, University of Manitoba, Winnipeg, Manitoba, Canada.Department of Biomedical Engineering, Price Faculty of Engineering, University of Manitoba, Winnipeg, Manitoba, Canada.Department of Biomedical Engineering, Price Faculty of Engineering, University of Manitoba, Winnipeg, Manitoba, Canada.Department of Biomedical Engineering, Price Faculty of Engineering, University of Manitoba, Winnipeg, Manitoba, Canada.Department of Biomedical Engineering, Price Faculty of Engineering, University of Manitoba, Winnipeg, Manitoba, Canada.Department of Human Anatomy and Cell Science, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Manitoba, Canada.Undergraduate Biosystems Engineering, Price Faculty of Engineering, University of Manitoba, Winnipeg, Manitoba, Canada.Department of Human Anatomy and Cell Science, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Manitoba, Canada.Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.Acute traumatic neural injury, also known as traumatic brain injury (TBI), is a leading cause of death. TBI treatment focuses on the use of sedatives, vasopressors, and invasive intracranial pressure (ICP) monitoring to mitigate ICP elevations and maintain cerebral perfusion pressure (CPP). While common sedatives such as propofol and fentanyl have significant side effects, ketamine is an attractive alternative due to its rapid onset and cardiovascular stability. Despite these benefits, ketamine’s use remains controversial due to historical concerns about increasing ICP. Using high-frequency monitoring, this retrospective study compared cerebral pressure-flow dynamics in patients with moderate/severe TBI who received ketamine with those who did not. Statistical analysis included descriptive statistics, comparisons within and between patients receiving ketamine, and evaluation of physiological response around incremental dose changes in ketamine. Various cerebral physiological indices were analyzed, including ICP, CPP, regional cerebral oxygen delivery, intracranial compliance, and cardiovascular reactivity metrics. A total of 122 patients were studied, with 17 receiving ketamine (median age: 37 years) and 105 not receiving ketamine (median age: 42 years). Results indicated higher median ICP in the ketamine group compared with the no ketamine group (9.05 mmHg and 14.00 mmHg, respectively, p = 0.00017); however, this is likely due to differences in patient characteristics and injury severity between the groups. No significant differences were observed in any other index of cerebral pressure-flow dynamics or between any incremental dose change condition. These findings suggest that ketamine does not significantly impact cerebral pressure-flow dynamics, challenging historical concerns about its use in patients with TBI.https://www.liebertpub.com/doi/10.1089/neur.2024.0146acute brain injuriesketaminesedationtraumatic brain injury |
| spellingShingle | Davis McClarty Logan Froese Tobias Bergmann Kevin Y. Stein Amanjyot S. Sainbhi Abrar Islam Nuray Vakitbilir Noah Silvaggio Izabella Marquez Alwyn Gomez Frederick A. Zeiler High-Frequency Analysis of the Cerebral Physiological Impact of Ketamine in Acute Traumatic Neural Injury Neurotrauma Reports acute brain injuries ketamine sedation traumatic brain injury |
| title | High-Frequency Analysis of the Cerebral Physiological Impact of Ketamine in Acute Traumatic Neural Injury |
| title_full | High-Frequency Analysis of the Cerebral Physiological Impact of Ketamine in Acute Traumatic Neural Injury |
| title_fullStr | High-Frequency Analysis of the Cerebral Physiological Impact of Ketamine in Acute Traumatic Neural Injury |
| title_full_unstemmed | High-Frequency Analysis of the Cerebral Physiological Impact of Ketamine in Acute Traumatic Neural Injury |
| title_short | High-Frequency Analysis of the Cerebral Physiological Impact of Ketamine in Acute Traumatic Neural Injury |
| title_sort | high frequency analysis of the cerebral physiological impact of ketamine in acute traumatic neural injury |
| topic | acute brain injuries ketamine sedation traumatic brain injury |
| url | https://www.liebertpub.com/doi/10.1089/neur.2024.0146 |
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