Antoun Koht

Surgical and Electrophysiological Observations during Clipping of 134 Aneurysms with Evoked Potential Monitoring

Somatosensory evoked potentials (SEPs) were monitored during 113 operations for the clipping of 134 cerebral aneurysms. Changes in peak latency and amplitude of early cortical SEP as well as central conduction time were evaluated. In 58 cases surgical occlusion of arterial vessels or other events occurred, and in 17 of these cases such events were associated with SEP changes or loss. Arterial occlusions resulted from temporary clipping of a feeding blood vessel (22), accidental clipping of a vessel (12), and intentional permanent vessel occlusion (8). A total SEP loss was seen in 2 cases of accidental vessel occlusion and in 6 cases of temporary vessel clipping. Significant SEP changes were found in 6 patients with temporary clipping, and once each with retraction of the cerebellum, retraction of the middle cerebral artery, and after intentional permanent vessel occlusion. Response to these changes included reapplication of aneurysm clips, repositioning of retractors, or removal of temporary clips. Stable SEP signals during 13 cases allowed the surgeon to proceed with the surgical course. Despite the limitations of SEP monitoring in certain anatomical locations, it has been found to be helpful in the operative management of some cases such as multilobed aneurysms of the middle cerebral artery, giant aneurysms, trapping procedures, and procedures requiring temporary vessel occlusion.

Effects of Etomidate, Midazolam, and Thiopental on Median Nerve Somatosensory Evoked Potentials and the Additive Effects of Fentanyl and Nitrous Oxide

In 30 patients undergoing spinal disc operations, the effects of bolus injections followed by intravenous infusions of thiopental, etomidate, and midazolam on median nerve Somatosensory-evoked potentials (SSEPs) were studied. Possible additive effects of fentanyl and nitrous oxide were also evaluated. Serial SSEP measurements were made before and for 25 minutes after the start of anesthesia. After induction with one of the three intravenous agents, fentanyl (10 μg/kg) was administered and SSEPs were again measured 1 and 5 minutes after administration. Sixty-five% nitrous oxide in 35% oxygen was administered after tracheal intubation and was followed by final SSEP measurements. The three intravenous agents affected SSEP signals differently. Etomidate increased both amplitude and latency. Thiopental decreased amplitude and increased latency. Midazolam had no effect on amplitude but increased latency. The addition of fentanyl and nitrous oxide had different effects in response to the three intravenous induction agents. This study emphasizes the differences in SSEP responses not only to different intravenous induction agents but also to the addition of fentanyl and nitrous oxide.

Serum potassium levels during prolonged hypothermia

Hypokalemia (mean serum potassium 2.3±0.4 mEq/l) was observed in six hypothermic patients (30°–32°C) with head injuries or brain hypoxia. In the first three patients, potassium was administered to maintain serum levels above 3.5 mEq/l and on rewarming after 48 h of hypothermia hyperkalemia (peak serum potassium=7.1±0.5 mEq/l) associated with cardiac arrhythmias developed. The remaining three patients received sufficient potassium to approximately replace measured losses during the hypothermic period. These patients did not become hyperkalemic on rewarming. Clinically insignificant sinus bradycardia, premature arrial contractions and junctional rhythms were seen during hypothermia with hypokalemia. We conclude that hypothermia produces hypokalemia by a shift of potassium from the extracellular to intracellular or extra vascular spaces. Potassium therapy during controlled hypothermia in the range 30°–32°C should only replace measured losses.

Improvement of Intraoperative Somatosensory Evoked Potentials by Etomidate

Use of somatosensory evoked potentials (SSEPs) for monitoring of the nervous system during corrective surgery on the spine has stimulated interest in the effect of anesthetics on SSEPs. Inhalation anesthetics have generally demonstrated a dose-dependent depression of amplitude and increase in latency, with intravenous agents generally showing lesser depression of amplitude and latency. This suggested to many that a narcotic-based anesthetic technique may be superior when monitoring patients with lowamplitude evoked responses. A particular monitoring challenge occurs in patients in whom preexisting neural abnormalities may make monitoring difficult. These patients may be at greater risk for neural complications, making monitoring most important at a time when it is also most difficult (1). As with the following case, the intraoperative evoked responses may be too poor to be reliably monitored. An anesthetic that would increase the amplitude of evoked responses might make the response usable for monitoring. Etomidate may be such an agent. As shown in several studies ( 2 4 , etomidate increases the amplitude of cortically derived median nerve SSEPs. We now report a case in which the introduction of etomidate during a narcotic anesthetic improved SSEPs responses from posterior tibial nerve stimulation and allowed the patients neural function to be monitored when it would otherwise have been considered unreliable.

Adenosine-Induced Flow Arrest to Facilitate Intracranial Aneurysm Clip Ligation: Dose-Response Data and Safety Profile

BACKGROUND: Adenosine-induced transient flow arrest has been used to facilitate clip ligation of intracranial aneurysms. However, the starting dose that is most likely to produce an adequate duration of profound hypotension remains unclear. We reviewed our experience to determine the dose-response relationship and apparent perioperative safety profile of adenosine in intracranial aneurysm patients. METHODS: This case series describes 24 aneurysm clip ligation procedures performed under an anesthetic consisting of remifentanil, low-dose volatile anesthetic, and propofol in which adenosine was used. The report focuses on the doses administered; duration of systolic blood pressure <60 mm Hg (SBP<60 mm Hg); and any cardiovascular, neurologic, or pulmonary complications observed in the perioperative period. RESULTS: A median dose of 0.34 mg/kg ideal body weight (range: 0.29–0.44 mg/kg) resulted in a SBP<60 mm Hg for a median of 57 seconds (range: 26–105 seconds). There was a linear relationship between the log-transformed dose of adenosine and the duration of a SBP<60 mm Hg (R2 = 0.38). Two patients developed transient, hemodynamically stable atrial fibrillation, 2 had postoperative troponin levels >0.03 ng/mL without any evidence of cardiac dysfunction, and 3 had postoperative neurologic changes. CONCLUSIONS: For intracranial aneurysms in which temporary occlusion is impractical or difficult, adenosine is capable of providing brief periods of profound systemic hypotension with low perioperative morbidity. On the basis of these data, a dose of 0.3 to 0.4 mg/kg ideal body weight may be the recommended starting dose to achieve approximately 45 seconds of profound systemic hypotension during a remifentanil/low-dose volatile anesthetic with propofol induced burst suppression.

Does midazolam cause retrograde amnesia, and can flumazenil reverse that amnesia?

M idazolam is a benzodiazepine agonist that has a rapid onset and fast distribution and that causes few cardiovascular or respiratory effects (1). Midazolam is water soluble and has a low incidence of venous irritation after intravenous (IV) injection (2). These properties make midazolam a good choice for conscious sedation and for induction and maintenance of anesthesia. Although midazolam causes anterograde amnesia (l), retrograde amnesia has not been demonstrated (3). We report an incidence of profound amnesia, anterograde and retrograde, in a patient after a laparoscopic cholecystectomy. The patient’s memory was restored after IV injections of the benzodiazepine antagonist flumazenil.

Anesthesia and evoked potentials: overview.

SummaryEvoked potentials are increasingly used for intraoperative monitoring. Their use is based on their ability to detect early changes caused by surgical maneuvers which may result in post operative deficits. However, not all changes are surgically related and any decrease in the non surgical causes of evoked potential changes increases the yield of intraoperative monitoring. In this review I will discuss the anesthetic effects on evoked potentials; these include a general description of the anesthetic effects on evoked potentials followed by the effects of premedication, induction, and maintenance agents. Also, described are the effects of adjunct anesthetic agents and techniques. Changes related to anesthesia are not similar and the knowledge of such differences is essential for the planing of anesthesia during the use of evoked potentials. An out line of the anesthetic techniques are described at the end of this review.

Intraoperative Deterioration of Evoked Potentials During Spinal Surgery

Successful intraoperative monitoring using cortical SSEP was achieved in 381 out of 395 patients undergoing corrective surgery for pathology of the spinal cord or spinal column. SSEP deterioration due to physical, anesthetic and technical factors in 36 cases was not associated with neurological deterioration. Likewise in 14 cases reversible SSEP changes due to surgical factors had no neurological sequelae, but 8 patients in whom SSEP deterioration could not be reversed had postoperative neurological deficits.

Reversible loss of somatosensory evoked potentials during anterior cervical spinal fusion

Occlusion of the carotid artery has been reported as a complication of retractor placement for anterior cervical spine surgery (1). Failure to detect this occlusion can possibly cause cerebral ischemia and consequent cortical damage. Palpation of the temporal artery pulse has been used as a means of detecting vascular occlusion, but anatomical variations and inability to locate the pulse intraoperatively can make this technique unreliable for monitoring during surgery. Somatosensory evoked potentials (SSEP) have been used during surgery on the spinal column as a means of continuously assessing cord function. For surgical procedures in the cervical region, SSEP from median or posterior tibial nerve stimulation may be used for the monitoring of operations in the high or low cervical spine, respectively. Somatosensory evoked potentials have also been used for the detection of central or brainstem ischemia (2,3). In addition, median nerve evoked responses have been used as a method of monitoring adequate cerebral perfusion during carotid endarterectomy (6). We present three case reports of patients undergoing operations for anterior cervical spinal fusion, in which changes in the SSEP signal occurred concurrently with retractor placement and returned to baseline after the retractor was repositioned.

Trigeminocardiac reflex in the Postanesthesia care unit.

Bradycardia caused by the oculocardiac reflex is an anticipated occurrence during certain surgeries. The afferent pathway involves the trigeminal nerves ophthalmic division. Reflex bradycardia from the trigeminocardiac reflex, via stimulation of maxillary or mandibular divisions of cranial nerve V, although less well known, has also been reported intraoperatively. Unstable bradycardia associated with stimulation of the mandibular division of cranial nerve V during trigeminal neuralgia pain episodes in the Postanesthesia Care Unit is presented.