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Meeting Abstracts  |   July 1997
Society of Neurosurgical Anesthesia and Critical Care 
Author Notes
  • Associate Professor, Department of Anesthesiology, University of Florida, Gainesville, Florida 32610–0254.
Article Information
Meeting Abstracts   |   July 1997
Society of Neurosurgical Anesthesia and Critical Care 
Anesthesiology 7 1997, Vol.87, 188-190. doi:
Anesthesiology 7 1997, Vol.87, 188-190. doi:
James C. Eisenach, M.D., Editor.
Society of Neurosurgical Anesthesia and Critical Care. New Orleans, Louisiana, October 18, 1996.
The 24th annual meeting of the Society of Neurosurgical Anesthesia and Critical Care was held at the Hilton Hotel Riverside in New Orleans, Louisiana, on October 18, 1996. Lectures and panel discussions addressed the effects of nitric oxide on the central nervous system, the results of recent clinical therapeutic trials in head injury and subarachnoid hemorrhage, and the current status of available techniques for intraoperative cerebral protection. Oral and poster presentations addressed techniques to monitor the central nervous system, effects of drugs on cerebral circulation, techniques of cerebral protection, and innovations in clinical neuroanesthesiology.
Richard J. Traystman, Ph.D., from the Department of Anesthesiology, John Hopkins, and Verna L. Baughman, M.D., of the Department of Anesthesiology, University of Illinois, discussed laboratory and clinical research into the effects of nitric oxide on cerebral circulation and ischemia. Dr. Traystman cited results of laboratory investigations of the role of nitric oxide. He reviewed animal research showing that nitric oxide synthase inhibition leads to decreases in cerebral blood flow (CBF) and increases in cerebrovascular resistance without causing changes in cerebral metabolic rate. In reviewing the role of nitric oxide in cerebral ischemia, he noted that the effects of nitric oxide vary among the regions of the brain and that it may play a role in both focal and global cerebral ischemia. He discussed the controversy regarding the role of nitric oxide in the cerebrovascular response to changes in carbon dioxide. Dr. Traystman concluded that nitric oxide does not play a major role in mediating the cerebrovascular response to changes in the partial pressure of carbon dioxide. Similarly, he reviewed data suggesting that nitric oxide is not involved in CBF responses to hypoxia. He stated that an issue important to the anesthesiologists regarding nitric oxide was that nitric oxide synthase inhibition decreases the minimum alveolar concentration.
Dr. Baughman discussed the clinical relevance of nitric oxide. She emphasized the effects of nitric oxide on organ systems other than the central nervous system and how that would affect the clinical utility of therapeutic manipulation of nitric oxide pathways. She compared the cardiovascular and central nervous system with regard to nitric oxide, noting that nitric oxide has beneficial effects for the cardiopulmonary system, whereas nitric oxide synthase inhibition has more beneficial effects for the central nervous system.
A discussion providing an update on clinical trials of therapies for cerebral injury was presented. The panelists noted that a better understanding of the mechanism of brain injury would greatly facilitate researchers' ability to design clinical trials of potential therapeutic agents. Steven J. Allen, M.D. (USA) reviewed clinical trials of induced hypothermia after head trauma. He described two trials conducted at the universities of Texas and Pittsburgh. Both trials showed improvement in outcome with induced hypothermia after severe head injury. Hypothermia induced for 48 h proved more beneficial than that for 24 h. Results from a multicenter study revealed improvement in outcomes with hypothermia for 48 h after head injury. In addition, the researchers conducting these trials identified the time between injury and achieving induced hypothermia as an important determinant of efficacy. If the time between injury and hypothermia exceeded 8 h, the benefit of hypothermia was greatly decreased.
E. Clarke Haley, M.D. (USA) reviewed use of trilizad in patients suffering head injury and subarachnoid hemorrhage. The European and Asian experience with patients with subarachnoid hemorrhage treated using trilizad has shown a decrease in the number of deaths, a trend toward decreased symptomatic cerebral vasospasm, an increase in the incidence of good neurologic function outcomes, but an equal incidence of cerebral vasospasm by angiographic criteria, with greater benefits in men. However, the American trial has not revealed any significant benefit with use of trilizad after subarachnoid hemorrhage. Ongoing trials are examining larger doses, especially in women. Head injury trials with trilizad are ongoing, with no conclusive results available yet.
M. Ross Bullock, M.D. (USA) reviewed use of N-methyl-D-aspartate antagonists with brain injuries. He first reviewed mechanisms of brain injury and the role of glutamate. In clinical studies of head injury, elevated glutamate levels were found in areas of contusion or severe secondary injury, whereas in patients with uncomplicated extracerebral hematomas, no elevation in brain glutamate was found. Despite these results, which suggest glutamate-mediated worsening of brain injury, N-methyl-D-aspartate antagonist trials have shown little therapeutic benefit. In addition, the disadvantages of N-methyl-D-aspartate antagonists such as psychotropic effects and hypotension were noted.
Whether the ability to provide intraoperative cerebral protection is a current clinical option was debated. Christopher Thompson, M.D., presented the argument in support of currently available cerebral protective techniques. He reviewed data regarding current use of thiopental for cerebral protection. Michael M. Todd, M.D., (USA) presented the opposite viewpoint that intraoperative cerebral protection is not yet a proven option. He based his argument on lack of any systematic studies showing cerebral protection in a clinical model. The limitation of many available laboratory studies, according to Dr. Todd, is that measurement of physiologic variables such as CBF or metabolic state is not enough to demonstrate protection, and neurologic outcome must be measured instead. Dr. Todd agreed that there data are available that suggest that thiopental and hypothermia may provide cerebral protection during operation.
Cerebral Injury and Protection 
D. J. Cole and colleagues (USA) presented data regarding the role of nitric oxide in etomidate-induced worsening of neurologic injury after focal cerebral ischemia. Using a rat model of middle cerebral artery occlusion, they showed that etomidate treatment after suppression of nitric oxide synthase with L-NAME resulted in no further worsening of neurologic injury. The addition of L-arginine to increase nitric oxide lessened neurologic injury. These results suggest that etomidate worsens cerebral injury by a nitric oxide-mediated mechanism. C. Werner and W. Reeker and colleagues (Germany) presented studies of the neuroprotective effects of desflurane, isoflurane, and ketamine using a rat model of focal cerebral ischemia induced with hemorrhagic hypotension and unilateral carotid occlusion. Improved neurologic outcome was seen with 1 MAC isoflurane, 1 and 1.5 MAC desflurane, and ketamine (0.25, 1 mg [center dot] kg sup -1 [center dot] min sup -1) compared with nitrous oxide and fentanyl controls 3 days after injury. Depressed catecholamine levels were seen in all treatment groups, which may play a role in cerebral protection.
D. S. DeWitt and colleagues (USA) presented data investigating the effect of superoxide dismutase after traumatic brain injury in a rat model. Their results show that superoxide dismutase preserves cerebral autoregulation in the injured brain. J. C. Drummond and colleagues (USA) investigated the effect of decreased colloid oncotic pressure on cerebral edema after fluid percussion injury in a rat model of resuscitation with isotonic or hypotonic crystalloid, whole blood, or hetastarch. They confirmed that decreases in osmotic pressure cause an increase in cerebral edema, but they also showed that decreases in oncotic pressure worsened cerebral edema. Y. Shapira and colleagues (Israel) studied the effect of magnesium administered after head injury in a rat model. Six hundred milligrams per kilogram given 1 h after injury decreased brain edema and improved neurologic scores.
P. de Haan and colleagues (The Netherlands) investigated the protective effects of U-74389G (a 21-aminosteroid) and hypothermia on spinal cord injury after spinal cord ischemia from aortic occlusion. They showed that mild hypothermia (34–35 [degree sign] Celsius) with and without U-74389G lessened spinal cord injury, but that U-74389G alone did not decrease the paraplegia rate.
Cerebral Blood Flow and Physiology 
K. Z. Baker and colleagues (USA) compared the effects of remifentanil and fentanyl on CBF responsiveness to changes in the partial pressure of carbon dioxide in patients undergoing craniotomy. The results indicate that the effects of remifentanil on CBF response to changes in carbon dioxide tension are similar to fentanyl. G. P. Lu (USA) studied the effects of sevoflurane and isoflurane on CBF in a rat model with normal and elevated intracranial pressure. Both drugs caused significant systemic hypotension. In the absence of intracranial hypertension, sevoflurane had a lesser effect on CBF; however, with elevated intracranial pressure, sevoflurane resulted in more significant decreases in CBF. From these results, they suggested that isoflurane would be the preferred agent when CBF is critical in patients with mass lesions. A. D. J. Watts and colleagues (Canada) in a rabbit model of elevated intracranial pressure studied the combined effects of propofol and hyperventilation on intracranial pressure. Their results showed an additive effect in decreasing intracranial pressure regardless of the order of administration. A. B. Hudetz and coworkers (USA) presented the results from a study of the effect of neuronal nitric oxide synthase inhibition on cerebral capillary flow response to isovolemic hemodilution. Nitric oxide synthase inhibition blocked increases in capillary flow to moderate hemodilution, but not severe hemodilution in this rat model. C. T. Wass and colleagues (USA) studied brain-to-core (esophageal) temperature gradients in dogs anesthetized with halothane or pentobarbital during cooling to 28 [degree sign] Celsius via cardiopulmonary bypass and during rewarming. In halothane-anesthetized animals, the brain-to-core temperature gradient was < 1 [degree sign] Celsius at all times. However, in the pentobarbital group, during cooling the brain temperature was consistently higher than core temperature, but during rewarming, the brain temperature was consistently lower than the core temperature. The authors attributed this uncoupling of brain and core temperatures to the cerebral vasoconstrictive effects of barbiturates.
Monitoring 
D. D. Doblar and colleagues (USA) reported results from patients undergoing carotid endarterectomy with transcranial Doppler monitoring of blood flow velocity. They compared collateral flow determined by preoperative angiography and changes in flow velocity during carotid artery cross clamping. They found that patients with collateral flow via the anterior communicating artery had higher flow velocities during cross clamping and a lower incidence of cross-clamp-related ischemia than did patients without collateral flow via the anterior communicating artery. Also using transcranial Doppler monitoring, E. Visco and colleagues (USA) assessed cerebral autoregulation in patients with mild to moderate head injury without focal lesions. They found that the autoregulatory response was intact in some patients, shifted rightward in some, and was absent in others. W. M. Coplin and coworkers (USA) evaluated the accuracy of continuous jugular bulb oximetry in the intensive care unit. They found that jugular venous oxygenation saturation measured by oximetry was less accurate than previously reported in the operating room setting. Although the trend of using continuous jugular venous oxygenation saturation is helpful, desaturation should be confirmed by measuring blood gas before instituting treatment.
T. B. Sloan and J. N. Rogers (USA) reported results of propofol, etomidate, and isoflurane on multipulse electrical transcranial motor evoked potentials. Only low doses of etomidate (0.1 mg/kg) enhanced transcranial motor evoked potentials. Higher doses of etomidate, all doses of propofol, and isoflurane depressed transcranial motor evoked potentials. For multipulse stimulation, propofol and etomidate did not alter the optimal interstimulus interval, whereas isoflurane altered the optimal interstimulus interval in a dose-dependent manner. W. S. Jellish and colleagues (USA) reported their results of improved preservation of vocal cord function during infratentorial tumor resection using intraoperative vagal nerve monitoring. The vagal nerve was monitored by placing a hook-wire electrode into the ipsilateral vocalis muscle through the cricothyroid membrane and performing electromyographic monitoring during operation.
Clinical Neurosciences 
The Young Investigator Award was presented to Guy J. Hindman of Duke University for his research project in which he compared remifentanil and fentanyl in patients having supratentorial craniotomy. He reported similar hemodynamics with induction and similar emergence times with the two narcotics. However, more naloxone was needed in the fentanyl group, whereas more antihypertensive and postoperative analgesic agents were needed in the patients receiving remifentanil. In addition, there were fewer patients in the fentanyl group with normal recovery scores 30 min after operation.
M. M. Todd (USA) reported the results of a pilot trial of mild induced hypothermia during intracranial aneurysm clipping. No significant differences were found between the normothermic and hypothermic groups except that hypothermic patients were more likely to be intubated immediately after operation and were less likely to be intubated at 24–72 h. This trial showed the feasibility of a large multicenter trial in this patient population.
Two presentations addressed the incidence and prevention of nausea and vomiting after craniotomy. J. M. Fabling and colleagues (USA) found that the incidence of nausea and vomiting was independent of anesthetic technique (general vs. MAC) and fentanyl dose but was higher with infratentorial procedures and in women. E. T. Holak and colleagues (USA) pretreated patients having cerebellopontine angle tumor resection with ondansetron. However, there was no decrease in the rate of postoperative nausea and vomiting. Tumor size was associated with a risk for nausea and vomiting.
M. R. Weglinski (USA) reported the use of desflurane during carotid endarterectomy. Desflurane 0.5 MAC in nitrous oxide was compatible with electroencephalographic monitoring, and the critical CBF for this type of evidence of ischemia during carotid cross clamping was found to be < 10 ml/100 g. W. J. Perkins and colleagues (USA) reported on electroencephalographic changes and CBF during carotid endartectomy from a retrospective review. Cerebral blood flow < 10 ml [center dot] 100 g sup -1 [center dot] min sup -1 and electroencephalographic changes of ischemia during carotid cross clamping were found to be predictive of stroke. Although most strokes occurred after operation, the authors believe that these intraoperative findings identify a group of patients at high risk for postoperative neurologic complications.
In two clinical studies of patients with head injuries by D. K. Menon, A. D. Fole, and colleagues (United Kingdom) adhesion molecule expression was found to be increased at 24 h, with maximal increases 48–72 h after head injury. These results suggest that leukocyte-mediated injury may be maximal later after head injury than in some animal models. Findings such as these may influence clinical trials aimed at blocking leukocyte adhesion-mediated secondary cerebral injury.
The abstracts for the meeting have been published in 1996, in volume 8, number 4, of the Journal of Neurosurgical Anesthesiology. The next meeting of the Society of Neurosurgical Anesthesia and Critical Care will be October 17, 1997.
Susan Black, M.D.
Associate Professor; Department of Anesthesiology; University of Florida; Gainesville, Florida 32610–0254