Rajasekar Ramadurai, Srinivasan Swaminathan, Prasanna Udupi Bidkar, Jayanth R Seshan, Sathiaprabhu Anbazhagan, Vivekchandar Chinnarasan
Ketamine as an adjunct to propofol-based TIVA reduced propofol, opioid, and vasopressor requirements. As TIVA was titrated to haemodynamic responses rather than processed EEG, the relative contributions of direct propofol-sparing and ketamine's sympathomimetic effects cannot be determined. No detrimental effects on intracranial pressure, cerebral perfusion pressure, or brain relaxation were detected at the measured intraoperative time points, and no between-group differences in neurological outcomes were detected. Lidocaine demonstrated modest propofol-sparing effects without adverse effects on measured intracranial dynamics.
BACKGROUND: Prevention of secondary brain injury remains a key objective during emergency decompressive craniectomy for traumatic brain injury (TBI). Propofol-based total intravenous anesthesia (TIVA) is widely used in TBI because of its favorable cerebral physiological effects but may cause dose-dependent hypotension and compromise cerebral perfusion. Ketamine and lidocaine have been proposed as adjuncts that may reduce anesthetic requirements while preserving intracranial homeostasis. This study compared the effects of ketamine and lidocaine versus placebo on propofol consumption and perioperative intracranial pressure (ICP), cerebral perfusion pressure (CPP), and brain relaxation during TIVA in patients undergoing emergency decompressive craniectomy for TBI.
METHODS: In this prospective, double-blind, three-arm randomized controlled trial, 150 adults undergoing emergency decompressive craniectomy for traumatic acute subdural hematoma were randomized to receive adjunctive ketamine (0.5 mg/kg/h), lidocaine (2 mg/kg/h), or placebo during propofol-based TIVA. Propofol was administered using target-controlled infusion (TCI) to maintain mean arterial pressure within 20% of baseline. The primary outcome was mean propofol consumption (µg/kg/min). Secondary outcomes included intraoperative opioid consumption, vasopressor requirement, ICP, CPP, brain relaxation, and neurological outcomes.
RESULTS: Mean propofol consumption differed significantly among groups and was lowest with ketamine (100.73 ± 31.72 vs. 115.86 ± 38.11 vs. 131.53 ± 44.54 µg/kg/min for ketamine, lidocaine, and placebo, respectively; p < 0.001). Ketamine was also associated with lower intraoperative fentanyl requirements (63.85 ± 36.23 vs. 83.64 ± 32.27 vs. 153.55 ± 57.28 µg; p < 0.001) and fewer vasopressor boluses (2 [2-3] vs. 3 [2-4] vs. 3 [2-4]; p = 0.031). Intracranial pressure, cerebral perfusion pressure, brain relaxation scores, and Glasgow Outcome Scale-Extended scores were comparable among the groups.
CONCLUSIONS: Ketamine as an adjunct to propofol-based TIVA reduced propofol, opioid, and vasopressor requirements. As TIVA was titrated to haemodynamic responses rather than processed EEG, the relative contributions of direct propofol-sparing and ketamine's sympathomimetic effects cannot be determined. No detrimental effects on intracranial pressure, cerebral perfusion pressure, or brain relaxation were detected at the measured intraoperative time points, and no between-group differences in neurological outcomes were detected. Lidocaine demonstrated modest propofol-sparing effects without adverse effects on measured intracranial dynamics.