In neurosurgical patients, opioids are administered to prevent secondary cerebral damage. Complications often related to the administration of opioids are a decrease in blood pressure affording the use of vasopressors and intestinal atonia. One alternative approach to opioids is the application of S(+)-ketamine. However, owing to a suspected elevation of intracranial pressure (ICP), the administration of S(+)-ketamine has questioned for a long time. The aim of the present study was to evaluate ICP, gastrointestinal motility, and catecholamine consumption in neurosurgical patients undergoing 2 different protocols of anesthesia using fentanyl or S(+)-ketamine. Twenty-four patients sustaining traumatic brain injury or aneurysmal subarachnoid hemorrhage received methohexitone plus either fentanyl or S(+)-ketamine to establish a comparable level of sedation. To reach an adequate cerebral perfusion pressure (CPP), the norepinephrine dosage was adapted successively. Enteral nutrition and gastrointestinal stimulation were started directly after admission on the critical care unit. ICP, CPP, and norepinephrine dosage were recorded over 5 days and also the time intervals to full enteral nutrition and first defecation. There was no difference regarding ICP, CPP, and the time period until full enteral nutrition or first defecation between both groups. Patients who underwent analgesia with S(+)-ketamine showed a trend to a lower demand of norepinephrine compared with the fentanyl group. Our results indicate that S(+)-ketamine does not increase ICP and that its use in neurosurgical patients should not be discouraged on the basis of ICP-related concerns.

CSF ubiquitin levels are increased more than four-fold in patients after TBI and nontraumatic subarachnoid hemorrhage. Peak CSF ubiquitin measurements in patients with TBI probably underestimated the actual peak, on the basis of data from the animal model. The progressive rise in CSF ubiquitin in patients with TBI who died suggests that lack of clearance could reflect lethal progression to irreversible brain damage. Erythrolysis is one potential source of CSF ubiquitin.