High-Frequency Analysis of the Cerebral Physiological Impact of Ketamine in Acute Traumatic Neural Injury.

Ketamine does not significantly impair cerebral pressure-flow dynamics in patients with moderate to severe traumatic brain injury (TBI), challenging historical concerns that it might raise intracranial pressure (ICP). A retrospective study of 122 patients (17 who received ketamine, 105 who did not) found higher median ICP in the ketamine group (14.00 mmHg vs. 9.05 mmHg), but this difference likely reflects greater injury severity rather than a drug effect. No other measures of cerebral physiology—including cerebral perfusion pressure, oxygen delivery, intracranial compliance, or cardiovascular reactivity—differed between groups or changed with incremental ketamine doses. Ketamine remains a viable sedative option for TBI.

Study at a glance

Abstract

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.