The Pruitt-Inahara shunt maintains mean middle cerebral artery velocities within 10% of preoperative values during carotid endarterectomy

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The Pruitt-Inahara shunt maintains mean middle cerebral artery velocities within 10% of preoperative values during carotid endarterectomy P. D. Hayes, FRCS(Ed), Tryphon Vainas, BSc, S. Hartley, BSc, M. M. Thompson, MD, FRCS, N. J. M. London, MD, FRCS, P. R. F. Bell, MD, FRCS, and A. R. Naylor MD, FRCS(Ed), Leicester, United Kingdom Objective: The purpose of this study was to assess the ability of the Pruitt-Inahara shunt to maintain adequate middle cerebral artery velocities during carotid endarterectomy. Study design: Prospectively collected data recorded during 548 carotid endarterectomies performed at a single university hospital were analyzed to look at changes in cerebral blood flow velocities at different stages during the procedure. Parallel data relating to blood pressure and end-tidal carbon dioxide were also examined. Results: During the first carotid artery cross clamp, middle cerebral artery velocity fell by 42%. A total of 169 patients (31%) had velocities that fell below 15 cm/s (electrical activity in the brain becomes altered below this level). After shunt insertion, only 2% of patients had middle cerebral artery velocities less than 15 cm/s. In only one patient was the velocity less than 10 cm/s. Increased systolic or diastolic blood pressure raised flow through the shunt significantly (P =.001). When two criteria used for selective shunt use were compared, only a moderate correlation was found between absolute middle cerebral artery velocity after carotid cross clamping and percentage change in middle cerebral artery velocity relative to preclamp values. Conclusions: The Pruitt-Inahara shunt is able to maintain adequate middle cerebral artery velocity in 98% of patients undergoing carotid endarterectomy. Alterations in blood pressure can significantly affect flow through the shunt. (J Vasc Surg 2000; 32:299-306.) From the Department of Surgery, Leicester Royal Infirmary. Competition of interest: nil. Reprint requests: Paul Hayes, FRCS(Ed), Department of Surgery, Clinical Sciences Building, Leicester Royal Infirmary, Leicester LE2 7LX, United Kingdom. Copyright 2000 by The Society for Vascular Surgery and The American Association for Vascular Surgery, a Chapter of the International Society for Cardiovascular Surgery. 0741-5214/2000/$12.00 + 0 24/1/107565 doi:10.1067/mva.2000.107565 Considerable controversy surrounds the issue of whether to use a shunt during carotid endarterectomy (CEA). 1-5 Even among those surgeons who believe in shunting, debate continues on whether to shunt routinely or selectively 2,3,6,7 and on which shunt to use. 8 There are two main types of shunt: some (eg, the Javid) have a greater mean luminal diameter but are relatively stiff and inflexible; others (eg, the Pruitt-Inahara) have a smaller proximal lumen but are generally more flexible. The largediameter shunts have been criticized because it is not always possible to insert them into the distal end of the internal carotid artery (ICA), given the small diameter of that vessel. 3 There are also occasional reports of these large-diameter shunts damaging vessel endothelium, 9 the result being embolism or even thrombosis. 10,11 The smaller shunts have been criticized on the basis of their smaller luminal diameter and, because flow is inversely proportional to the fourth power of the radius, their greater resistance to blood flow. 8,12 A study of 163 patients found that the Javid shunt failed to maintain preoperative middle cerebral artery velocities (MCAVs) in 41%; the corresponding figure for the Pruitt-Inahara device was 66%. 8 The present study was performed to examine MCAV changes in 548 patients who were routinely shunted with the Pruitt-Inahara shunt, examining not only the deviation from preoperative flow rates but also the relation between use of the shunt and markers of inadequate perfusion. 299

300 Hayes et al August 2000 PATIENTS AND METHODS CEA was performed in a standardized manner throughout the study period (September 1992 through September 1998). This is not a consecutive series, inasmuch as transcranial Doppler scan monitoring was not possible between October 1994 and October 1995 because of staffing levels. Data are presented for the 548 patients undergoing CEA in whom intraoperative transcranial Doppler (TCD) monitoring was possible. In no case did a patient undergo a bilateral CEA at a single operation. During the period in which intraoperative TCD monitoring was performed, there were 56 patients for whom no data were available. In 44 patients there was an inadequate temporal window. In three cases the wrong artery was insonnated (usually this was the posterior cerebral artery), and in seven cases the quality of the recorded data did not allow for accurate analysis. The operation was undertaken with the patient under normocarbic, normotensive general anesthesia through use of systemic heparinization. A Pruitt- Inahara shunt (Horizon Medical, Santa Ana, Calif) was used in all cases. The ICA and the common carotid artery (CCA) were temporarily clamped, and a short arteriotomy was performed. The distal end of the shunt was inserted into the CCA, and 0.75 to 1.25 ml of saline solution was used to gently inflate the proximal balloon. The shunt was then flushed through with blood from the CCA. The distal shunt was inserted into the ICA, the balloon inflated, and the shunt opened. The proximal balloon was gently held with a rubber sling to prevent dislodgement. The arteriotomy was then extended to the appropriate length and the endarterectomy performed. The proximal and distal intimal steps were tacked down with 7-0 Prolene (Ethicon, Inc, Somerville, NJ) and each arteriotomy was closed with a patch angioplasty. Completion angioscopy was performed in each case after removal of the shunt. Detection of retained luminal thrombus or an intimal flap (> 3 mm) was noted. Patients were reshunted for the correction of technical defects. Intraoperative TCD monitoring of the MCAV was performed by means of a 2-MHz fixed-head probe (SciMed UK Ltd, United Kingdom). The mean MCAV was calculated automatically by the software accompanying the TCD package. The calculation is based on integration of the velocity waveform over several cardiac cycles with a Fast Fourier transform (this approximates closely to the following formula: mean MCAV = diastolic MCAV + [systolic MCAV diastolic MCAV)/3]). The MCAV and systolic and diastolic blood pressures were prospectively recorded for all patients at the following time points: 1. during dissection before the first ICA clamping 2. after the first ICA clamping 3. after shunt insertion and restoration of flow 4. after the second ICA clamping 5. after shunt removal and restoration of flow through the endarterectomized vessel. All of the data were collected in the appropriate minute before or after each clamping or flow release. The MCAVs were recorded at the same time that the blood pressure and end-tidal carbon dioxide (ETCO 2 ) were recorded. Subsequent data analysis was performed blinded to patient outcome. The groups of data relating to changes in MCAV were compared with one another through use of the t test or the χ 2 test, as appropriate. Previous work has defined an MCAV of 15 cm/s as the point below which the cerebral perfusion is no longer adequate to maintain electric activity. 13 When the MCAV falls to less than 10 cm/s, the perfusion is inadequate to maintain the basic metabolic needs of the cerebral tissue. Other studies have defined a fall in MCAV of greater than 50% to 70% as a critical point in cerebral perfusion. 14,15 Falls of 50% and 60% have been compared with one another in this study. After October 1995, all patients were monitored for 3 to 6 hours postoperatively by means of the TCD device. Patients who exhibit either significant numbers of particulate emboli (> 25 in a 10-minute period) or distortion of the waveform in the middle cerebral artery are at risk of complete occlusion of the carotid artery. 16,17 These patients were treated with 10% dextran-40, beginning at a rate of 20 ml/h. If the number of emboli failed to decline, the rate of the dextran-40 infusion was increased by 5 ml/h every 10 minutes to a maximum rate of 40 ml/h. Once the rate of embolization had stabilized, the dextran-40 therapy was continued for 12 hours. Our unit protocol was that if the maximum dose of dextran-40 failed to control the embolization, the patient was to be reexplored; however, all cases of sustained embolization settled with the use of dextran-40. Any new neurologic deficit lasting longer than 24 hours was classified as a stroke. Each patient was assessed by means of computed tomography head scanning, carotid duplex scanning, and further TCD monitoring, with or without a return to the operating room for further exploration. The severity of the stroke was determined by a neurologist using the Oxford Handicap Scoring system. 18

Volume 32, Number 2 Hayes et al 301 RESULTS All patients in the study were shunted through use of a Pruitt-Inahara looped outlying shunt. In 17 patients (3.1%), the shunt required physical manipulation after initial insertion. The surgeon performing the operation was alerted to the need for shunt adjustment by changes in the MCAV monitored with the TCD device. A common cause of poor initial MCAV was overinflation of the distal balloon within the ICA; another was impaction of the shunt lumen on a distal kink or loop, occluding shunt outflow. Movement of the shunt during the operation occasionally impaired flow, and again this was quickly detected by a fall in the MCAV detected with the TCD device, allowing corrective action to be taken. There were no strokes or deaths directly attributable to shunt use in this series of patients. The morbidity and mortality figures are shown in Table I. The mortality rate was 1.3%. The disabling stroke rate was 0.9%, and the nondisabling stroke rate was 1.3%. Each of the 2 on-table thromboses was reopened before the patient left the operating room, and thrombus was found within the endarterectomy zone in the absence of technical error. Before implementation of our policy of postoperative monitoring and selective dextran-40 therapy, there were four postoperative carotid thromboses, and on reexploration, thrombus was found adherent to the endarterectomized vessel. Two patients had sustained embolization, which was prevented from proceeding to thrombosis by the use of dextran-40 therapy. There were 3 patients in whom no cause for the postoperative stroke could be identified, despite the use of carotid duplex scanning, further TCD monitoring, reexploration, and computed tomography head scanning. In none of these patients was a thrombus or intimal flap identified outside the endarterectomy zone that could have been responsible for the stroke. None of these three patients awoke with a neurologic deficit, and their strokes occurred in the postoperative period. Thus, embolization through the shunt during surgery was not the cause of these deficits. In addition, each of the three patients had an MCAV greater than 25 cm/s with the shunt in place, making hypoperfusion a very unlikely source of the neurologic deficit. Changes in MCAV during CEA. Table II summarizes the changes that take place in MCAV during five separate stages of CEA. In the pre-ica clamping, or dissection, phase, only four patients (1%) had Table I. Morbidity and mortality in 548 patients undergoing CEA No. of events Intraoperative events On-table carotid thrombosis 2 Postoperative events Vein patch rupture 2 Intracranial hemorrhage 2 MI or cardiac failure 3 Hyperperfusion syndrome 1 Carotid thrombosis 4 Stroke caused by sustained embolization 2 Impossible to identify cause 3 MCAVs below 15 cm/s and none had an MCAV below 10 cm/s. After clamping of the ICA for the first time, the MCAV fell below the critical 15 cm/s level in 169 patients (31%). With placement of a flexible looped Pruitt-Inahara shunt, the MCAV rose to above 15 cm/s in 159 (94%) of these patients. One patient s MCAV remained at 9.7 cm/s for 1 minute after shunt insertion. This was partially due to a low systolic blood pressure (SBP), and the MCAV rose above 10 cm/s when the anesthetist pharmacologically corrected the blood pressure. Of the 10 patients whose MCAVs remained below 15 cm/s, none had a neurologic deficit on waking from anesthesia. The mean MCAVs during the five stages of the CEA are shown in Table III. There are significant falls in MCAV after both ICA clampings relative to the preclamp values (P <.001). The average fall in velocity was 42% after the first clamping and 38% after the second clamping. During shunting, velocities fell only 10% relative to preclamping values, from 39.5 cm/s to 34.2 cm/s. There was a significant correlation between the MCAV before clamping and the MCAV seen with the shunt open (R = 0.68; P <.01). The MCAV showed a high degree of correlation (R = 0.89; P <.005) between the first and second clampings. There were significantly more MCAVs less than 10 cm/s after the first clamping than after the second (97 vs 79; χ 2 = 108.2; P =.01). The mean velocity of 50 cm/s seen in the MCA after clamp release is significantly greater (33% average increase; P <.001) than the preclamp values. Patients with no flow in their MCAs during the first (46 patients) or second (34 patients) ICA clamping had a significantly greater percentage increase in MCAV on clamp release than was seen in patients with measurable MCAV on clamping (50% vs 33%; P <.05).

302 Hayes et al August 2000 Table II. Numbers of patients with different ranges of MCAV for five phases of CEA No. of patients (%) MCAV (cm/s) Preclamping First ICA clamp During shunting Second ICA clamp Flow restoration < 10 0 (0) 97 (18) 1 (0) 79 (15) 0 (0) 10.1-15 4 (1) 72(13) 9 (2) 67 (13) 2 (0) 15.1-20 17 (3) 83 (15) 47 (9) 75 (14) 9 (2) 20.1-30 128 (23) 159 (29) 169 (31) 154 (29) 53 (10) 30.1-40 187 (34) 83 (15) 177 (32) 96 (18) 122 (23) 40.1-80 201 (37) 42 (8) 145 (26) 60 (11) 309 (58) 80+ 11 (2) 1(0) 0 (0) 0 (0) 36 (7) Totals 548 (100) 537 (99) 548 (100) 531 (100) 531 (100) Table III. Mean MCAV during five stages of CEA and percentage changes relative to preclamp values Preclamp First clamp Shunt open Second clamp ICA release Mean MCAV (cm/s) 39.5 22.1 34.2 23.7 50 ± SD 14.9 13.7 12.5 13.5 18.3 Percent fall relative to 41.8 10.1 37.5 32.9 preclamp values Table IV. Relative increases in blood pressure during five stages of CEA relative to preclamp values Preclamp First clamp Shunt open Second clamp ICA release Mean SBP (mm Hg) 124 129 133 139 129 ± SD 22.9 23.8 21.2 24.1 20.1 Percent change relative to 6.4 9.8 14.9 6.8 preclamp values P value <.005 <.001 <.001 <.005 The MCAV data were studied to determine whether there was a relationship between MCAV and CO 2, a known vasodilator. There was no significant difference between patients with low MCAVs and patients with high MCAVs during shunting and ETCO 2. The correlation coefficient between MCAV and ETCO 2 was 0.09 during dissection, 0.19 during clamping, and 0.14 with the shunt in situ. The ETCO 2 did not vary significantly between the various stages of the CEA (4.3% during dissection and 4.4% with the shunt open; P =.84). Changes in blood pressure during CEA. The changes in SBP during CEA are shown in Table IV. The average SBP was significantly (P <.005) elevated during clamping, shunting, and ICA release relative to pre-ica clamp levels. These changes in SBP are mirrored by changes in diastolic and mean blood pressure (data not shown). In the 176 patients in whom SBP fell between the first ICA clamping and the second, there was an average fall in MCAV of 2.5 cm/s. In the patients who had a rise in SBP between clampings, there was a significant increase in average MCAV of 15.2 cm/s (P <.001). There was no correlation with ETCO 2 and blood pressure changes during the operation. The data were examined to determine whether those patients who had low MCAVs when their ICAs were clamped also had low blood pressures to account for their low velocities. Those patients who had MCAVs less than 15 cm/s had a mean SBP of 130 mm Hg; this compared with a mean SBP of 128 mm Hg for patients with higher MCAVs (P =.3). The data were similarly examined during shunting. In each of 10 patients, the MCAV was below 15 cm/s after the shunt had been open for 1 minute. The mean systolic pressure in this group was unchanged in comparison with that for the patients with higher MCAVs (137 vs 133; P =.52). Similar negative results were obtained when diastolic and mean blood pressures were examined. Analysis of data with respect to selective shunting. Throughout this study, a policy of routine shunt use in all CEAs was adhered to. Many units, however, used a policy of selective shunt use, and the study data have been analyzed accordingly. The suitability of using pre ICA clamp MCAV values to pre-

Volume 32, Number 2 Hayes et al 303 Table V. Comparison of absolute change in MCAV against percent change in MCAV MCAV > 15 cm/s No. of patients MCAV < 15 cm/s <50% fall in MCAV 311 23 >50% fall in MCAV 71 137 Boldface indicates that these patients would have been shunted only through use of one criterion or the other. dict which patients would have low flows after ICA clamping was assessed. Patients with MCAVs of 0 after ICA clamping were found throughout the full range of preclamping MCAV values. There were two patients with high preclamp MCAVs (89 and 94 cm/s) whose MCAVs fell to 0 on ICA clamping. At only 0.16, the R 2 correlation coefficient between preclamp and postclamp (first and second) MCAV values was not significant. On the basis of TCD monitoring of the MCAV, two types of criteria have been specified as indicating which patients should be selectively shunted. 19,20 These are (1) a specified drop (of either 50% or 60%) in MCAV after ICA clamping and (2) a fall in the actual MCAV after clamping to a velocity below 15 cm/s. Comparison of the patients actual MCAVs after ICA clamping against the percentage change with clamping shows a significant correlation (R 2 = 0.58; P <.001) between these groups. However, closer examination of the data reveals that there are a number of patients who would require shunting by one definition of inadequate flow but not by the other. These data are presented in Tables V and VI. Table VII gives the sensitivities, specificities, and predictive values of using 50% and 60% falls in MCAV as indicators for selective shunting. DISCUSSION In this series of 548 patients, in whom data relating to shunt usage and intraoperative shunt flows were collected prospectively, there were no strokes directly related to shunt use. There were two on-table thromboses and four postoperative thromboses in the series. One objection raised against shunt usage is that strokes can arise as a result of damage caused by the shunt to the endothelium in the lumen of the distal or proximal vessel. However, consideration of the point makes this unlikely. If the shunt does cause some minor damage to the endothelial lining, the thrombotic potential of the area is massively outweighed by the 5 or 6 cm of endarterectomized vessel in which the Table VI. Comparison of absolute change in MCAV against percent change in more than 60% fall in MCAV after ICA clamping as indicator of need for shunting MCAV > 15 cm/s No. of patients MCAV < 15 cm/s < 60% fall in MCAV 124 39 > 60% fall in MCAV 31 121 Boldface indicates that these patients would have been shunted only through use of one criterion or the other. Table VII. Predictive power of using either 50% or 60% fall in MCAV to predict need for shunt insertion Percent fall in MCAV indicating need to insert shunt > 50% > 60% Sensitivity 85.6 78.1 Specificity 81.4 91.9 Positive predictive value 65.8 78.2 Negative predictive value 93.1 90.6 entire subendothelium is exposed. Indeed, in each of our two on-table thromboses, exploration of the vessel revealed thrombus attached to the endarterectomy zone and not in the normal vessel. Before the introduction of the postoperative TCD monitoring and selective dextran-40 therapy, there were four symptomatic carotid thromboses, and these were reexplored; in each case, platelet-rich thrombus was found adherent to the endarterectomy zone and not within an area of the vessel damaged by the use of the shunt. Insertion of the looped, outlying Pruitt-Inahara shunt was possible in all patients. The concomitant use of intraoperative TCD monitoring of the MCAV was useful on a number of occasions when it identified patients in whom the shunt had been dislodged from its original position and required adjustment. In patients in whom only low MCAVs were obtained after shunt opening, the TCD device was able to detect an improvement in flow if the distal shunt balloon had been overinflated and was then partially deflated. TCD monitoring also allowed the blood pressure to be manipulated to adjust flow through the shunt. In one patient the initial MCAV after shunt opening remained below 10 cm/s; after anesthetic intervention to raise the blood pressure, the MCAV rose above the critical 10 cm/s. The use of intraoperative TCD monitoring is a useful adjunct to routine shunt use.

304 Hayes et al August 2000 Fifteen centimeters per second has previously been identified as velocity below which normal electric activity in the brain is replaced by abnormal focal bursts of activity. 13 Below a velocity of 10 cm/s, blood flow is inadequate for the metabolic demands of the brain tissue. In this study, 169 patients (31%) had MCAVs below 15 cm/s after their ICAs were clamped for the first time, and 97 patients (18%) had flows below 10 cm/s. These results are in keeping with those of Sundt et al, 21 who believed that without shunting approximately 30% of patients would be at risk of cerebral ischemia. However, it is unlikely that all of these patients were at risk of developing ischemic stroke, inasmuch as a number of centers have reported series of patients with contralateral stenosis in whom no shunt was used and the incidence of perioperative stroke was acceptable. 4,5 Studies using local anesthetic and response to clamping have found that approximately 10% of patients have a deficit requiring subsequent shunting. 7,19 There are data demonstrating that reduction of cerebral perfusion below a critical level in some patients does place them at risk for developing intraoperative ischemic stroke. 3,13-15,21-23 At present, it is not possible to predict with 100% sensitivity and specificity which patients will have ischemic stroke if not shunted, so it would seem prudent to maintain patients MCAVs as close to normal as possible during the procedure. Although complications from the failure of cerebral perfusion may be relatively uncommon, the consequences can be severe. The data in Table II demonstrate that flows were restored above the critical limit of 10 cm/s by insertion of the Pruitt-Inahara shunt in all but one patient, who required blood pressure intervention. In only 2% of patients did the shunt fail to raise the MCAV above the level of 15 cm/s. After the first clamping of the ICA, the mean MCAV fell by 41.8% in comparison with preclamp values. This reduction in mean MCAV was reduced fourfold by the opening of the shunt. With the shunt open, the mean MCAVs were only 10.1% lower than the preclamp values; 98% of them were within the normal range. A recent article criticized the Pruitt-Inahara shunt on the basis of its hemodynamic performance. 8 That study found that only 34% of patients had their MCAVs returned to preclamp levels after opening of the Pruitt-Inahara shunt; this compared with 59% of those with the Javid shunt. The fact that in the present study 98% of patients had MCAVs within the normal range is probably more important than the number of patients whose MCAVs actually returned to their preclamp levels. The average fall in MCAV of 10.1% in comparison with preclamp values is probably of much less importance. The MCAVs during the second period of ICA clamping were significantly better than those during the first clamping. A total of 97 patients had MCAVs below 10 cm/s after the first ICA clamping; this compared with 79 patients after the second ICA clamping (χ 2 = 108.2; P =.01). This is almost certainly due to an increase in the SBP between the two times (Table IV) rather than to any preconditioning induced by the first period of ischemia. There is a significant rise in MCAV between preclamp values and those seen in the clamp release period. This may represent failure of cerebral autoregulation, in which the cerebral vasculature has been maximally vasodilated for a chronic period of time to facilitate the suboptimal levels of flow that may be experienced with severe carotid disease. Interestingly, the patients who exhibited the greatest increase in MCAV between preclamp and release were those who had no crossover flow on clamping of the ICA during the procedure. This confirms the findings of a smaller previous study. 20 The question of whether shunt flow can be altered by changes in blood pressure was also examined, because this may have implications for those patients in whom adequate shunt flows cannot be obtained by the insertion of a shunt alone. Blood pressure was able to influence the shunt flow. In those patients in whom the SBP fell between the first and second ICA clampings, there was a mean reduction in MCAV of 2.5 cm/s. In those patients whose SBP rose between the time of the first clamping and the time of the second, there was a mean increase in MCAV of 15.2 cm/s (P <.001). For those centers that shunt but do not use TCD devices to monitor MCAV, these data indicate that maintenance of an adequate blood pressure by the anesthetist may help to maintain adequate shunt flows. Blood pressure is not wholly responsible for maintaining shunt flow, however. Those patients who had the lowest MCAVs (< 15 cm/s) during clamping or shunting had the same SBP as the rest of the group. Similar results were obtained with diastolic and mean blood pressures as well. All of the patients in our series were routinely shunted. However, some centers shunt patients on a selective basis. The data were examined to determine whether there was a good correlation between two different methods of determining the need for insertion of a shunt: either an absolute reduction in

Volume 32, Number 2 Hayes et al 305 MCAV after ICA clamping below 15 cm/s or the reduction of MCAV by a given percentage relative to preclamp levels (either 50% or 60%). Examination of the data suggests that there is only a moderate correlation between these two methods (R = 0.395). Closer inspection of the data indicates that although there is a good overall correlation between the two methods, there is relatively poor discrimination in those patients whose values approach the cutoff points for shunting or no shunting. That is to say, there are many patients with MCAVs around the absolute value of 15 cm/s, but these are equally dispersed on either side of the relative decrease in MCAV of 50%. The negative and positive predictive values of 50% and 60% falls in MCAV as indicators for shunt insertion are shown in Table VII. Although the specificity of the 60% cutoff point is good at 91.9%, its sensitivity is relatively poor at 78.1%. In selecting patients who are at risk of cerebral ischemia during CEA, sensitivity is more important than specificity. If a fall of the MCAV to below 15 cm/s were taken as a true indicator of need for shunt use, then to achieve a sensitivity of 100% using relative fall in MCAV as an indicator for shunting, all of the 447 patients (81.6%) with falls of more than 12.8% would have to be shunted. If the situation were reversed and a 50% fall in MCAV were taken as the true indicator for shunt insertion, then all of the 487 patients (88.9%) with MCAVs less than 37.6 cm/s would have to be shunted to achieve 100% sensitivity. With such a large percentage of patients needing to be shunted to maintain a 100% sensitivity, it would appear logical to routinely shunt all patients and stop worrying about the criteria for selective shunting. The use of routine shunt insertion allows the surgeon to develop a routine for these procedures and breeds familiarity with the technique in the operating room staff. The data presented here indicate that routine use of the Pruitt-Inahara shunt allows the maintenance of adequate MCAV during shunting in 98% of patients. There are a small proportion of patients in whom the shunt cannot maintain adequate flow; it may be that modification of the shunt design will enable surgeons to overcome this problem. Manipulation of blood pressure can influence MCAV with the shunt in position. There is only moderate agreement between the two criteria used for selective shunting. Most important, in the 548 patients in this study who were routinely shunted, no strokes occurred that were attributable to the use of a shunt. REFERENCES 1. Gumerlock MK, Neuwelt EA. CEA: to shunt or not to shunt. Stroke 1988;19:1485-90. 2. Halsey JH Jr. Risks and benefits of shunting in CEA. The International Transcranial Doppler Collaborators. Stroke 1992;23:1583-7. 3. Sandmann W, Kolvenbach R, Willeke F. Risks and benefits of shunting in carotid endarterectomy. Stroke 1993;24:1098-9. 4. Andrikopoulos V, Antoniou I, Papacharalambous G, Panousis P. Our experience with carotid endarterectomy without a patch and shunt. Int Angiol 1996;15:307-11. 5. Samson RH, Showalter DP, Yunis JP. Routine carotid endarterectomy without a shunt, even in the presence of a contralateral occlusion. Cardiovasc Surg 1998;6:475-84. 6. Salvian AJ, Taylor DC, Hsiang YN, et al. Selective shunting with EEG monitoring is safer than routine shunting for carotid endarterectomy. Cardiovasc Surg 1997;5:481-5. 7. Cao P, Giordano G, Zannetti S, et al. Transcranial Doppler monitoring during carotid endarterectomy: is it appropriate for selecting patients in need of a shunt? J Vasc Surg 1997;26:973-9. 8. Wilkinson JM, Rochester JR, Sivaguru A, Cameron IC, Fisher R, Beard JD. Middle cerebral artery blood velocity, emobolisation, and neurological outcome during CEA: a prospective comparison of the Javid and Pruitt-Inahara shunts. Eur J Vasc Endovasc Surg 1997;14:399-402. 9. McCaughan JJ Jr, Young JM. Intra-arterial occlusion in vascular surgery. Ann Surg 1970;171:695-703. 10. Beezley MJ. Safer shunt insertion during CEA. J Vasc Surg 1985;2:607-9. 11. Browse NL, Ross-Russell R. CEA and the Javid shunt: the early results of 215 consecutive operations for transient ischaemic attacks. Br J Surg 1984;71:53-7. 12. Aufiero TX, Thiele BL, Rossi JA, Miller CA, Neumeyer MM. Haemodynamic performance of carotid artery shunts. Am J Surg 1989;158:95-100. 13. Halsey JH, McDowell HA, Gelmon S, Morawetz RB. Blood velocity in the middle cerebral artery and regional cerebral blood flow during CEA. Stroke 1989;20:53-8. 14. Arnold M, Sturzenegger M, Schaffler L, Seiler RW. Continuous intra-operative monitoring of middle cerebral artery blood flow velocities and EEG during carotid endarterectomy. Stroke 1997;28:1345-50. 15. Jansen C, Vriens EM, Eikelboom BC, Vermeulen FEE, van Gijn J, Ackerstaff RGA. Carotid endarterectomy with TCD and EEG monitoring. Stroke 1993;24:665-9. 16. Lennard N, Smith JL, Abbott R, et al. Prevention of post-operative thrombotic stroke after carotid endarterectomy: the role of trans-cranial Doppler ultrasound. J Vasc Surg 1997;26:579-84. 17. Levi CR, Roberts AK, Fell G, et al. Transcranial Doppler microembolus detection in the identification of patients at high risk of peri-operative stroke. Eur J Vasc Endovasc Surg 1997;14:170-6. 18. Bamford JM, Sandercock PAG, Warlow CP, Slattery J. Interobserver agreement for the assessment of handicap in stroke patients. Stroke 1989;20:828. 19. Giannoni MF, Sbarigia E, Panico MA, et al. Intraoperative transcranial Doppler sonography monitoring during carotid surgery under locoregional anaesthesia. Eur J Vasc Endovasc Surg 1996;12:407-11. 20. Naylor AR, Whyman MR, Wildsmith JA, et al. Factors influencing the hyperaemic response after carotid endarterectomy. Br J Surg 1993;80:1523-7.

306 Hayes et al August 2000 21. Sundt TM Jr. The ischaemic tolerance of neural tissue and the need for monitoring and selective shunting during CEA. Stroke 1983;14:93-8. 22. McCarthy WJ, Park AE, Koushanpour E, Pearce WH, Yao JS. Carotid endarterectomy. Lessons from a intra-operative monitoring: a decade of experience. Ann Surg 1996;224: 297-305. 23. Pistolese GR, Ippoliti A, Appolloni A, Ronchey S, Faraglia V. Cerebral haemodynamics during cross clamping. Eur J Vasc Endovasc Surg 1993;7 Suppl A:33-8. Submitted Oct 12, 1999; accepted Feb 11, 2000. LIFELINE FOUNDATION E. J. Wylie Traveling Fellowship Guidelines: The primary purpose of the E. J. Wylie Traveling Fellowship is to provide the recipient with the opportunity to visit a number of excellent vascular surgery centers in the United States and abroad. Though brief, these visits stimulate academic inspiration, promote international exchange, and foster development of fraternal fellowship in vascular surgery. The achievement of these objectives will enhance the development of the fellow s career in vascular surgery. This award is not intended to support specific research interests but rather to assist the fellow in a unique opportunity for travel and professional exchange within established vascular centers in this country and abroad. Eligibility for Selection: 1. Be under age 40 at the time of the award 2. Have completed a postgraduate vascular training program or have considerable experience in vascular surgery supplemental to surgical training 3. Be committed to an academic career in vascular surgery and have obtained an academic appointment in a medical school or freestanding clinic devoted to excellence in medical education 4. Have a demonstrated record of success in pursuing clinical or basic science research sufficient to ensure academic excellence in his or her pursuit of a career in vascular surgery Selection will be made without regard to the candidate s geographic location. Requirements for Consideration: A candidate submitting documentation for consideration for selection must furnish an up-to-date curriculum vitae; a list of publications, research projects, and current research support; and a list of the centers that he or she wants to visit. Three letters of recommendation are required, including one from the division head and another from the chairman of the department of surgery of the institution in which the candidate holds a faculty appointment. A 500-word essay describing the objectives of the candidate s travel plans and linking these to his or her career goals must be appended. Report to Committee: A report covering your experience should be prepared and forwarded to the Chairman of the Research & Education Committee within 3 months of completion of your fellowship travel. This report should be five to eight double-spaced typewritten pages and should summarize your activities during the fellowship. Although factual statements of activities should be included, you are encouraged to place these within an overall context of their impact on your education and maturation. The format of the report and its content should be suitable for consideration by the Committee for publication in the Journal of Vascular Surgery. Financial Support: The generosity of W. L. Gore & Associates, Inc, has allowed the establishment of this fellowship. Their graciousness ensures the noncommercial nature of the award and its continuation in years to come. The E. J. Wylie Traveling Fellowship of the Lifeline Foundation will pay up to $12,000 for expenses of travel, research, and clerical help. The fellowship monies may not be used for other purposes. Application: No application forms are required. A letter demonstrating interest in applying for the E. J. Wylie Traveling Fellowship or nominating a candidate may be sent to the Chairman of the Research and Education Committee. Details of the application should include the materials requested above. The deadline for receiving applications is January 15. Decisions regarding the award will be mailed to the applicants by mid April. A letter of nomination or intent should be directed to: Chairman Research and Education Committee Lifeline Foundation 13 Elm Street Manchester, MA 01944