Background: The potential adverse effects of ketamine in neurosurgical anesthesia have been well established and involve increased intracranial pressure (ICP) and cerebral blood flow. However, reexamination of ketamine is warranted because data regarding the effects of ketamine on cerebral hemodynamics are conflicting.
Methods: Eight patients with traumatic brain injury were studied. In all patients, ICP monitoring was instituted before the study. Control of ICP (less than 25 mmHg), hemodynamic values, and blood gas tension (partial pressure of carbon dioxide in arterial blood between 35-38 mmHg) was obtained with propofol infusion (3 mg x kg(-1) x h(-1)) and mechanical ventilation. The effects of three doses of ketamine, 1.5, 3, and 5 mg/kg, respectively, on ICP, cerebral perfusion pressure, jugular vein bulb oxygen saturation, middle cerebral artery blood flow velocity, and electric activity of the brain (EEG) were measured. The three doses were administered intravenously at 6-h intervals over 30 s through a central venous line. Systemic and cerebral hemodynamics and end-tidal carbon dioxide were continuously monitored and recorded at 1-min intervals throughout the 30-min study periods.
Results: Ketamine, in all three doses studied (1.5, 3, and 5 mg/kg) was associated with a significant decrease in ICP (mean +/- SD: 2 +/- 0.5 mmHg [P < 0.05], 4 +/- 1 mmHg [P < 0.05], and 5 +/- 2 mmHg [P < 0.05]) among the study patients regardless of the ketamine dose used. There were no significant differences in cerebral perfusion pressure, jugular vein bulb oxygen saturation, and middle cerebral artery blood flow velocity. Ketamine induced a low-amplitude fast-activity electroencephalogram, with marked depression, such as burst suppression.
Conclusions: These results suggest that ketamine may not adversely alter cerebral hemodynamics of mechanically ventilated head-trauma patients sedated with propofol. These encouraging results should be confirmed in larger groups of similar patients.