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Journal Article
Randomized Controlled Trial
Ketofol as an Anesthetic Agent in Patients With Isolated Moderate to Severe Traumatic Brain Injury: A Prospective, Randomized Double-blind Controlled Trial.
Journal of Neurosurgical Anesthesiology 2023 January 2
BACKGROUND: The effects of ketofol (propofol and ketamine admixture) on systemic hemodynamics and outcomes in patients undergoing emergency decompressive craniectomy for traumatic brain injury (TBI) are unknown and explored in this study.
METHODS: Fifty patients with moderate/severe TBI were randomized to receive ketofol (n=25) or propofol (n=25) for induction and maintenance of anesthesia during TBI surgery. Intraoperative hemodynamic stability was assessed by continuous measurement of mean arterial pressure (MAP) and need for rescue interventions to maintain MAP within 20% of baseline. Brain relaxation scores, serum biomarker-glial fibrillary acidic protein levels, and extended Glasgow Outcome Scale (GOSE) at 30 and 90 days after discharge were also explored.
RESULTS: MAP was lower and hemodynamic fluctuations more frequent in patients receiving propofol compared with those receiving ketofol (P<0.05). MAP fell >20% below baseline in 22 (88%) patients receiving propofol and in 10 (40%) receiving ketofol (P=0.001), with a greater requirement for vasopressors (80% vs. 24%, respectively; P=0.02). Intraoperative brain relaxation scores and GOSE at 30 and 90 day were similar between groups. Glial fibrillary acidic protein was lower in the ketofol group (3.31±0.43 ng/mL) as compared with the propofol (3.41±0.17 ng/mL; P=0.01) group on the third postoperative day.
CONCLUSION: Compared with propofol, ketofol for induction and maintenance of anesthesia during decompressive surgery in patients with moderate/severe TBI was associated with improved hemodynamic stability, lower vasopressor requirement, and similar brain relaxation.
METHODS: Fifty patients with moderate/severe TBI were randomized to receive ketofol (n=25) or propofol (n=25) for induction and maintenance of anesthesia during TBI surgery. Intraoperative hemodynamic stability was assessed by continuous measurement of mean arterial pressure (MAP) and need for rescue interventions to maintain MAP within 20% of baseline. Brain relaxation scores, serum biomarker-glial fibrillary acidic protein levels, and extended Glasgow Outcome Scale (GOSE) at 30 and 90 days after discharge were also explored.
RESULTS: MAP was lower and hemodynamic fluctuations more frequent in patients receiving propofol compared with those receiving ketofol (P<0.05). MAP fell >20% below baseline in 22 (88%) patients receiving propofol and in 10 (40%) receiving ketofol (P=0.001), with a greater requirement for vasopressors (80% vs. 24%, respectively; P=0.02). Intraoperative brain relaxation scores and GOSE at 30 and 90 day were similar between groups. Glial fibrillary acidic protein was lower in the ketofol group (3.31±0.43 ng/mL) as compared with the propofol (3.41±0.17 ng/mL; P=0.01) group on the third postoperative day.
CONCLUSION: Compared with propofol, ketofol for induction and maintenance of anesthesia during decompressive surgery in patients with moderate/severe TBI was associated with improved hemodynamic stability, lower vasopressor requirement, and similar brain relaxation.
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