BACKGROUND:Surgery for intracranial aneurysm often results in postoperative neurologic deficits. We conducted a randomized trial at 30 centers to determine whether intraoperative cooling during open craniotomy would improve the outcome among patients with acute aneurysmal subarachnoid hemorrhage. METHODS:A total of 1001 patients with a preoperative World Federation of Neurological Surgeons score of I, II, or III ("good-grade patients"), who had had a subarachnoid hemorrhage no more than 14 days before planned surgical aneurysm clipping, were randomly assigned to intraoperative hypothermia (target temperature, 33 degrees C, with the use of surface cooling techniques) or normothermia (target temperature, 36.5 degrees C). Patients were followed closely postoperatively and examined approximately 90 days after surgery, at which time a Glasgow Outcome Score was assigned. RESULTS:There were no significant differences between the group assigned to intraoperative hypothermia and the group assigned to normothermia in the duration of stay in the intensive care unit, the total length of hospitalization, the rates of death at follow-up (6 percent in both groups), or the destination at discharge (home or another hospital, among surviving patients). At the final follow-up, 329 of 499 patients in the hypothermia group had a Glasgow Outcome Score of 1 (good outcome), as compared with 314 of 501 patients in the normothermia group (66 percent vs. 63 percent; odds ratio, 1.14; 95 percent confidence interval, 0.88 to 1.48; P=0.32). Postoperative bacteremia was more common in the hypothermia group than in the normothermia group (5 percent vs. 3 percent, P=0.05). CONCLUSIONS:Intraoperative hypothermia did not improve the neurologic outcome after craniotomy among good-grade patients with aneurysmal subarachnoid hemorrhage.

s: 33rd Annual Meeting of the Society of Neurosurgical Anesthesia and Critical Care: CLINICAL NEUROLOGICAL SCIENCE/PHARMACOLOGY

BACKGROUNDOpioids are known to stimulate surface electroencephalographic activity in patients with temporal lobe epilepsy. The objective of the current study was to compare the electrocorticographic activation effects of the newer short-acting opioid remifentanil with those of alfentanil during epilepsy surgery under general anaesthesia.METHODSThirteen patients undergoing temporal lobe epilepsy surgery under general anaesthesia received alfentanil 30 microg kg(-1) and remifentanil 1 microg kg(-1) as i.v. boluses in sequence. The design was a randomized double-blind cross-over study. After opening the dura, electrocorticogram (ECoG) electrode contact strips were placed over the temporal and supratemporal neocortex and depth electrodes were inserted in the amygdala and hippocampus. Alfentanil 30 microg kg(-1) or remifentanil 1 microg kg(-1) were administered randomly in a blinded fashion. The ECoG was recorded continuously before and after the injection of each drug. The interictal epileptiform activity (spikes and sharp waves) above baseline was analysed.RESULTSBoth drugs increased epileptiform activity especially that recorded from depth electrodes in the temporal limbic structures. No epileptiform activity was recorded from the electrodes overlying the supratemporal neocortex before or after drug administration. The more potent activator was alfentanil, which caused an increase in activation from baseline of 99.8% compared with 67.4% for remifentanil. In addition, alfentanil activated the epileptiform activity in 3 patients in which remifentanil had no effect. There were no changes in heart rate after the opioid boluses. Both remifentanil and alfentanil caused significant reductions in blood pressure at 3 and 5 min after administration.CONCLUSIONWe conclude that at the doses used in this study, alfentanil is the better opioid for intraoperative activation of the ECoG in neurosurgical patients undergoing resection of a temporal lobe epileptic focus. This pharmacological activation of epileptiform activity assists in localizing and confirming the site of surgical excision. Neither alfentanil nor remifentanil activated epileptiform activity in non-epileptic brain tissue.

We investigated the impact of enflurane and halothane (1.1 MAC) on heart rate and blood pressure responses to experimental hypoxaemia (PETo2 6.0 kPa [45 torr]) and small increments in PCO2 (1.3--1.6 KPa [10--12 torr]). The results reaffirm that circulatory signs of mild hypercarbia are vitually abolished by these anaesthetics. The important new observation is that signs of acute moderate hypoxaemia are also markedly depressed. Although potential modifying factors such as surgical stimulation were not evaluated, this study indicates that human subjects anaesthetized with enflurane or halothane lack reliable cardiovascular signs of acute hypoxaemia.

We have assessed the impact of thiopentone on the hypoxic ventilatory reflex, and on the responses to carbon dioxide and doxapram. Thiopentone sedation did not detectably alter any of these aspects of ventilatory control. Thiopentone anaesthesia reduced ventilation and the ventilatory responses to hypoxia, carbon dioxide and doxapram, all approximately in paralle. We conclude that, in contrast to halothane, thiopentone does not selectively reduce the ventilatory response to hypoxia. During light thiopentone anaesthesia, a reasonably brisk hypoxic response is present.