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CARDIOVASCULAR ANESTHESIA

Somatosensory Evoked Potential Monitoring During Carotid Endarterectomy in Patients with a Stroke

Department of Anesthesia, Toronto Western Hospital, University Health Network, University of Toronto, Toronto, Ontario, Canada

Address correspondence and reprint requests to Dr. Pirjo H. Manninen, Department of Anesthesia, Toronto Western Hospital, 399 Bathurst St., Toronto, Ontario, Canada, M5T 2S8. Address e-mail to Pirjo.Manninen{at}uhn.on.ca

	Abstract

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The aim of our study was to assess the characteristics and feasibility of somatosensory evoked potential (SSEP) monitoring in patients who have had a stroke undergoing carotid endarterectomy. We retrospectively reviewed the medical and SSEP records of 204 patients. The patients were divided into two groups: Stroke (n = 65) and No-Stroke (n = 139). The amplitude and latency of the N20-P25 cortical complex on the ipsilateral side (surgical) were compared with the contralateral side in each group and between groups. Stroke patients showed asymmetry of their cortical waveforms; the ipsilateral N20-P25 baseline amplitude was 1.5 ± 1.0 µv versus 1.9 ± 1.2 µv for the contralateral (P = 0.001), for No-Stroke patients 2.0 ± 1.1 µv versus 2.1 ± 1.1 µv (P = 0.2). Forty-eight percent of Stroke patients had a ratio (ipsilateral/contralateral amplitude) of <1.0 ± 0.2 compared with 26% for No-Stroke patients (P = 0.01). There were no differences in latency measurements, in the incidences of significant SSEP changes (four Stroke, six No-Stroke) and immediate postoperative neurological deficits (two Stroke, six No-Stroke) between the two groups. Nine patients (three Stroke, six No-Stroke) had a decrease in ipsilateral N20-P25 amplitude >50% after cross-clamping, and had a shunt inserted. In conclusion, patients with a history of a stroke before surgery had a decrease in the amplitude of the ipsilateral cortical peak. There were no differences in the incidences of SSEP changes or neurological deficits.

Implications: Patients who have had a preoperative stroke may show asymmetry of theircortical baseline somatosensory evoked potential waveforms; however, this doesnot interfere with the ability to use somatosensory evoked potential as amonitor during surgery.

	Introduction

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Cerebral function is frequently monitored during carotid endarterectomy to detect signs of ischemia, especially during cross-clamping of the carotid artery. Some of the different techniques of monitoring that have been used include an awake patient, electroencephalography (EEG), somatosensory evoked potential (SSEP), measurements of cerebral blood flow and stump pressure, transcranial Doppler, and cerebral oximetry (1,2). SSEP monitoring is used in many institutions as the standard monitor and may be used as the indicator for shunting (3–10). Patients who present for a carotid endarterectomy may be symptomatic or asymptomatic from their carotid stenosis. Symptomatic patients may present with transient ischemic attacks (TIA), amaurosis fugax, a completed or an evolving stroke. Patients who have had a stroke will frequently still have existing neurological deficits before surgery. We examined characteristics of the SSEP waveforms in patients who have had a stroke before surgery. Also, if the SSEP waveform was abnormal, we assessed whether SSEP monitoring was feasible for detection of cerebral ischemia and as an indicator for shunting during the carotid endarterectomy.

	Methods

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With IRB approval, a retrospective review of the medical records of all patients undergoing carotid endarterectomy between 1997 and 2000 was undertaken. The patients’ medical charts were reviewed for demographics and medical history, including preoperative neurological status as well as the indications for surgery. If the patient had a previous stroke, information regarding when the stroke occurred and any evidence of cerebral infarction on computerized tomography (CT) or magnetic resonance imaging (MRI) was noted. All intraoperative events were documented, especially changes with evoked potential monitoring and the insertion of a shunt. The anesthetic and surgical management of the patients was reviewed as well as all intra- and postoperative complications. The neurological status of the patient immediately on awakening was noted.

All evoked potential monitoring was performed by trained evoked potential technicians, by using median nerve SSEP according to standard variables for stimulating and recording. Needle electrodes, inserted after induction of anesthesia, were used for stimulation at both wrists and for recording at Erb’s points and/or cervical spine, and on the scalp. Monitoring was continuously performed throughout the procedure with separate sequential recordings of the ipsilateral and contralateral side of each patient. In our institution, a separate evoked potential chart is made for each patient. The evoked potential data sheets were reviewed by an independent reviewer (RS) documenting the modalities used, the presence and quality of the SSEP waveforms, and all events during monitoring, especially at the time of cross-clamping the carotid artery. The peripheral and cortical waveforms were examined and the N20 and P25 peaks were identified. The amplitude and latency of the N20-P25 complex were measured ipsilateral and contralateral to the side of surgery. For the purposes of this review, measurements taken at baseline (at steady-state anesthesia before cross-clamping), at 5–10 min after cross-clamping, and after cross-clamping during closure were used for analysis. All SSEP changes that were ipsilateral to the side of surgery were noted. A significant evoked potential change was considered to be a >50% decrease in the amplitude of the ipsilateral N20-P25 complex. Our routine practice was to insert a shunt, at the discretion of the surgeon, whenever there was a significant change within 5 min of cross-clamping.

The patients were divided into two groups: history of Stroke before surgery or No-Stroke, which included history of TIA and asymptomatic patients. The two groups were compared with respect to demographics, the incidence of shunting, the occurrence of immediate postoperative neurological deficits, and outcome. The latency and amplitude of the ipsilateral N20-P25 were compared with the contralateral N20-P25 complex at the three points of measurement and between the two groups. The incidence of clinically significant SSEP changes that led to the insertion of a shunt and/or the presence of a postoperative neurological deficit were assessed. Statistical analysis was performed by using t-test, ², and analysis of variance where indicated. A P < 0.05 was considered significant.

	Results

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The medical records for 204 patients were reviewed. Demographics of the patients are shown in Table 1. A history of a recent ipsilateral stroke was present in 65 patients (32%). The interval from the time of the stroke to surgery was 24 ± 34 wk (mean ± SD) (n = 60) with a range of 2 to 156 wk. The time interval was not obtainable for five patients. A TIA was the reason for surgery in 133 patients, and 6 patients were asymptomatic. The severity of the stenosis of the ipsilateral carotid artery was >70% in 93% of Stroke (n = 60) and 92% of No-Stroke patients (n = 124); however, the actual recorded value was greater in Stroke patients (Table 1). Accurate information regarding the presence of contralateral stenosis was available for only 83 patients, and for these, the degree of stenosis was >70% in 20% of Stroke patients and 14% of No-Stroke patients. Previous surgery on the contralateral carotid artery had occurred in 16 patients (1 Stroke, 15 No-Stroke).

All patients were given a general anesthetic. The induction was with IV thiopental or propofol, fentanyl, and a muscle relaxant. Maintenance consisted of nitrous oxide (50%–70%), fentanyl, and isoflurane. Toward the latter part of this review, desflurane was used in place of isoflurane. Standard monitors were used, and an intraarterial catheter was inserted for blood pressure monitoring. Episodes of hypotension were treated by decreasing the concentration of the inhaled anesthetic and/or by the IV administration of vasopressors (ephedrine, phenylephrine). There were no differences in the mean arterial blood pressure, arterial carbon dioxide partial pressure (PaCO₂) or temperature at time of cross-clamp, and the duration of cross-clamp between the two groups (Table 1).

Thirty patients (9 Stroke, 21 No-Stroke) did not have adequate SSEP data for analysis because of inadequate charting (6 Stroke, 15 No-Stroke) and intraoperative technical problems (3 Stroke, 6 No-Stroke). These patients were excluded from the calculation and analysis of latency and amplitude measurements.

The results for the measurements of amplitude are shown in Figure 1. The mean amplitude of the ipsilateral N20-P25 complex was reduced compared with the contralateral N20-P25 peak in patients with a Stroke, as well as from the ipsilateral N20-P25 peak in No-Stroke patients at all three times of measurement. There were no differences in the amplitude measurements between the two groups for the contralateral side. There were no differences in latency measurements at any time in either group, or between the two groups.

View larger version (62K): [in this window] [in a new window]   Figure 1. The mean amplitude of the N20-P25 cortical complex is shown for the ipsilateral and contralateral waveforms for patients with Stroke (n = 56) and No-Stroke (n = 118), before (baseline under anesthesia), during (immediately after cross-clamping), and after (during closure). The ipsilateral amplitude in Stroke patients is reduced when compared with the contralateral amplitude for Stroke patients and from both ipsilateral and contralateral sides for No-Stroke patients at all points of measurement (P < 0.05). Values are mean ± SD.

View larger version (37K): [in this window] [in a new window]   Figure 2. The percentage of patients with a ratio (ipsilateral/contralateral) of the baseline N20-P25 amplitude for each group is shown for three categories. The incidence of a symmetrical waveform (ratio = 1.0 ± 0.2) was not different (P = 0.07), but Stroke patients had an increased incidence of asymmetrical waveforms (ratio <0.8) than No-Stroke patients (P = 0.01).

The mean amplitude of the N20-P25 complex for both the ipsilateral and contralateral sides decreased from the baseline to the cross-clamp measurement (Fig. 1). However, there was no change in the ratio of ipsilateral to the contralateral amplitude. There was a 30%–40% decrease in amplitude of ipsilateral N20-P25 during cross-clamping in five patients (three Stroke, two No-Stroke) that was related to a decrease in blood pressure. The blood pressure was increased, and this resulted in an improvement of the evoked potentials and no deficits. The baseline cortical waveform had been asymmetrical in three patients (two Stroke, one No-Stroke). Other nonsignificant SSEP changes (40% decrease in amplitude), that were not related to blood pressure, occurred in two No-Stroke patients after more than 30 min of cross-clamping and persisted until the clamp was removed. The evoked potentials then fully recovered; however, one patient suffered a transient deficit.

Delayed neurological deficits occurred in three No-Stroke patients 2–3 h after surgery while in the postanesthetic care unit. They were returned to the OR for urgent reoperation for thrombosis of the ipsilateral carotid artery. One patient had had a shunt inserted on the basis of a significant evoked potential change after cross-clamping but the evoked potentials recovered with shunt insertion. The second patient had had no evoked potential changes. Both of these patients had poor outcomes with a prolonged recovery because of major neurological deficits postoperatively. The third patient had had poor baseline evoked potential waveforms and had a good outcome. Delayed neurological complications (seizures with a new stroke) occurred in two No-Stroke patients at 24 h and 4 days postoperatively. The outcome of patients was not different between the two groups (Table 1). At discharge from the hospital, a good outcome occurred in 93% of both the Stroke and No-Stroke groups, a poor outcome occurred in 3% Stroke and 7% No-Stroke, and two Stroke patients died.

	Discussion

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The potential risk for cerebral ischemia during a carotid endarterectomy has promoted the use of cerebral function monitoring to detect ischemia and prevent postoperative neurological deficits (1,2). Many different monitoring techniques have been and are being used. EEG is the most commonly used monitor, as a correlation between EEG changes and cerebral blood flow alterations has been demonstrated (2). Other arguments favoring EEG include the ability to detect functional changes as soon as they occur and use of multiple channels to give a broader field of assessment. The disadvantages of EEG are that it may be too sensitive to many factors such as the level of anesthesia or preexisting brain damage and it is more complex to use and interpret. SSEP is a logical alternative to EEG because it specifically monitors the function of the sensory cortex supplied by the middle cerebral artery, the major territory at risk during cross-clamping of the carotid artery. SSEP appears to have a similar efficacy to EEG in the prediction of postoperative neurological deficits (3,5,6). There is also a threshold relationship between the amplitude of SSEP cortical waveform and cerebral blood flow (11). Other advantages of using SSEP in the OR include the ease of use and interpretation and the fact that it is less affected by anesthesia. Although controversial, the use of evoked potential monitoring has been recommended and is used in many institutions as a monitor for cerebral ischemia and as an indicator for the placement of a shunt during carotid endarterectomy (4–9). The most common evoked potential modality used is the stimulation of the median nerve and analysis of the amplitude and latency of the N20-P25 cortical peak. The criteria used to indicate a significant change are not uniformly agreed upon (3,6,7,12). A commonly used variable is the reduction of the amplitude of N20-P25 by >50%. The best monitor for indicating the need for shunting, as well as the use of a shunt, are also still controversial (4,5,8,9).

There have been several reports questioning whether patients who have had preoperative strokes behave differently during SSEP monitoring. In a review by D’Addato et al. (13) of 920 patients who had a carotid endarterectomy, 29 patients (3.2%) had a history of a preoperative stroke and/or a positive CT scan. Only 72 patients of the total group were monitored with SSEP. Baseline SSEP were similar in all patients, but a pathological SSEP occurred in 53% of the patients who had a positive CT during the first four minutes of cross-clamping. The pathological SSEP was a decrease in the amplitude and increase in latency >15%–20%. These patients received a shunt. In another study, Guérit et al. (14) found that 84% of 205 patients, who had a carotid endarterectomy, had symmetrical preoperative SSEP waveforms. But, the authors noted that there was a relationship between patients who had a stroke before surgery and asymmetry of their preoperative evoked potentials. A >50% asymmetry of the amplitude of the ipsilateral N30-P45 complex occurred in 58% of the 38 patients with a history of a stroke. However, despite the asymmetry of the baseline waveform in these patients, the authors were able to identify the cortical peaks and were able to monitor the patients during surgery. Linstedt et al. (15) reviewed the use of SSEP in 146 patients during carotid endarterectomy. A new postoperative neurological deficit occurred in five patients and four of these patients had had a preoperative stroke but no major intraoperative evoked potential change. One of the conclusions of the authors was that there was an association with preoperative neurological deficits resulting from the stroke, which impeded their ability to use the SSEP as an adequate monitor.

In our study, we found that patients with previous strokes showed asymmetry of their baseline SSEP waveforms. There was a reduction in the amplitude of the N20-P25 complex on the side of the stroke compared with the contralateral side, as well as, to patients with no history of stroke. Some of the asymmetry seen in both groups could be explained by the placement of the recording electrodes. The accuracy of the measurement of the head and placement of electrodes cannot be verified in a retrospective study. Also, the electrodes were placed after the patient was anesthetized, thus we did not have "awake" baseline recordings. The influence of anesthesia cannot be completely eliminated. Although anesthetics should affect both sides equally, that is the ipsilateral and contralateral waveforms, there is the possibility that the anesthetic effect may be increased on the side of a previous stroke. Sedation with IV drugs unmasks or exacerbates focal motor deficits in patients with prior neurological dysfunction (16). We also found that there was an overall decrease in the amplitude of the N20-P25 complex from the baseline measurements over the duration of the procedure. This may reflect the effects of anesthesia or other physiological factors because the effect occurred on both ipsilateral and contralateral sides. However, this did not change the ratio of ipsilateral to contralateral measurements. In our study, we did not see any differences in latency measurements. This may indicate that the amplitude is a more sensitive indicator of ischemia.

Overall, the asymmetry in the amplitude measurements of the N20-P25 complex did not appear to affect our ability to use SSEP as a monitor. There were no differences in the incidence of evoked potential changes, the number of shunts inserted, and the occurrence of new postoperative neurological deficits between the two groups. The correlation of the SSEP findings of asymmetry to CT or MRI evidence of an infarction in the direct area of monitoring was limited by the lack of adequate radiological data for all patients. This needs to be done in a prospective study.

We were unable to directly assess the relationship of an intraoperative evoked potential change to the occurrence of a postoperative neurological deficit. All patients received a shunt whenever there was a significant evoked potential change after cross-clamping, and any changes of less severity were treated by increasing the patient’s blood pressure. This would influence the outcome, as the purpose of the treatment was to prevent a deficit. The occurrence of false-positive and false-negative results is well recognized in evoked potential monitoring, especially when any significant evoked potential change (whether transient or persistent) is used to predict a postoperative neurological deficit (3,4,8). However, comparisons among studies from different centers are complicated by the lack of uniform criteria for a significant SSEP change and for shunting, as well as different practices of shunting, no shunting, or selective shunting. In our review, 10 patients had a SSEP change, but only three had a new deficit. We also do not known the etiology of all the neurological deficits that occurred in our patients after their carotid endarterectomy, or whether they were related to lack of perfusion or embolic in nature. In our study, the incidence of a false-negative finding was 1.2% (two patients with a deficit and no SSEP change), which is similar to other studies. In review of the literature, the incidence of false-negative results ranges from 0% to 3.5% (3,4,6–9,13–15). Wöber et al. (8) performed a meta-analysis of 15 studies and reported that cortical SSEP changes were unreliable predictors of the neurological outcome and not suitable criteria for selective shunting.

The major limitation of this study is that it was retrospective. Some information was not readily available for all patients such as results of CT scans, a thorough neurological examination before surgery, and adequate evoked potential data. This study is also limited by a small sample size.

In summary, patients who have had a stroke before their carotid endarterectomy may have baseline evoked potential waveforms that are asymmetrical. However, SSEP monitoring during surgery is still feasible.

	References

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This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a colleague Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (15) Citing Articles via Google Scholar Google Scholar Articles by Manninen, P. H. Articles by Sarjeant, R. M. Search for Related Content PubMed PubMed Citation Articles by Manninen, P. H. Articles by Sarjeant, R. M. Related Collections Cardiovascular Monitoring (Non-cardiac)