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(Stroke. 1997;28:685-691.)
© 1997 American Heart Association, Inc.

Articles

Transcranial Doppler Monitoring and Causes of Stroke From Carotid Endarterectomy

Merrill P. Spencer, MD

From Sound Vascular Monitoring and the Institute of Applied Physiology and Medicine, Seattle, Wash.

Correspondence to Merrill P. Spencer, MD, Institute of Applied Physiology and Medicine, 701 16th Ave, Seattle, WA 98122.

	Abstract

Top Abstract Introduction Subjects and Methods Results Discussion References

 
Background and Purpose The value of carotid endarterectomy (CEA) depends on the safety of the operation. Transcranial Doppler ultrasound (TCD) was used to evaluate the possibilities of hypoperfusion, hyperperfusion, and embolization as causes of stroke and to evaluate the significance of Doppler microembolic signals (DMES).

Methods Five hundred CEAs were monitored with TCD of the ipsilateral middle cerebral artery during various phases of CEA to determine hemodynamic changes and incidence of DMES. Complications were graded according to their severity, and their probable cause was determined from TCD criteria and review of hospital charts.

Results We observed 24 cerebrovascular complications (4.8%), including 9 with transient ischemic attacks and 15 (3%) with permanent deficits. Among all cerebrovascular complications, embolism was judged to be responsible in 13 (54%; P<.02 compared with hypoperfusion), hyperperfusion in 7 (29%; P<.14 compared with hypoperfusion), and hypoperfusion in 4 (17%; P<.08 compared with embolism plus hyperperfusion). The surgeons responded to TCD information by several strategies depending on the TCD information. The incidence of permanent deficits diminished from 7% in the first 100 operations to 2% in the last 400 (P.01). Shunting was more strongly associated with cerebrovascular complications than nonshunting, but this difference was not significant (P=.24). Intraoperative prevalence of DMES was strongly associated with cerebrovascular complications (P=.02).

Conclusions Embolism is the principal cause of cerebrovascular complications from CEA; hyperperfusion and hypoperfusion are also important causes. TCD provides information that allows prompt identification and treatment of these three major causes of stroke from this operation. The perioperative stroke rate can be reduced by appropriate measures, taken by the surgeons, based on findings of TCD monitoring.

Key Words: carotid endarterectomy • Doppler • embolism

	Introduction

Top Abstract Introduction Subjects and Methods Results Discussion References

 
Surgical excision of atherosclerotic plaque at the bifurcation of the CCA is performed to prevent CVCs; however, CEA itself can produce CVCs, including disabling stroke and death. Many intraoperative monitoring techniques have been used to warn the surgeon of the possibility of an adverse outcome,^{1 2 3 4 5} but these, including self-monitoring under regional block, address only the possibility of brain hypoperfusion during the time of cross-clamping of the carotid arteries. Other major recognized causes include hyperperfusion after release of the clamps⁶ and embolism.⁷ Recent reports have expanded our understanding of the basic causes of CVCs.^{8 9 10} In a study of the causes of perioperative stroke after 3062 CEAs, 20 different mechanisms were identified, mainly categorized into ischemia from carotid artery clamping, postoperative thrombosis and embolism, and intracerebral hemorrhage.¹⁰

The hemodynamic and embolic information provided by TCD monitoring offers the opportunity to identify, in real time, these major causes of stroke so that preventive measures can be undertaken. The first reports on TCD in CEA appeared in the late 1980s,^{11 12 13 14 15 16 17 18} and many authors argued for and against its usefulness^{19 20 21 22 23} in measuring hemodynamic and embolic parameters. TCD with simultaneous electroencephalography^{24 25 26 27} also provided useful indications of flow in the MCA and perfusion of the cortex. Although embolization is generally agreed to be the main cause of cerebral complications during CEA, it was not until 1990^{28 29} that TCD was reported to detect particulate as well as bubble emboli in this operation. This report relates our experience with TCD monitoring in determining the hemodynamic and embolic causes and prevention of CVCs through alterations in surgical techniques and management.

	Subjects and Methods

Top Abstract Introduction Subjects and Methods Results Discussion References

 
Included in this report are the first 500 CEAs of the ICA performed between October 1985 and July 1994 in which an ipsilateral temporal bone ultrasonic window could be found, in which the technologist was able to obtain TCD data throughout the surgery, and in which complete hospital chart review was obtainable. All charts were completely reviewed and complications identified by the author. In addition, observations regarding complications were always made in the recovery room by the author, the TCD technologist, and the nursing staff. No patients were included who underwent CEA of the external carotid artery only, and none underwent other concurrent surgical procedures. Indications for CEA were symptomatic and asymptomatic carotid artery stenosis. Several patients were operated with stenosis <60% for reasons including repeated TIAs, radiologist diagnosis of ulceration, radiologist overestimation of stenosis compared with micrometer diameter measurements of the angiograms (eg, area percentage versus diameter percentage), and occlusion of the contralateral artery. Forty-four patients underwent a previous CEA of the contralateral ICA. Eight underwent repeated CEA on the same ICA, and one patient underwent contralateral CEA as well as a repeated CEA.

The preoperative symptoms of the patients were classified and coded as follows: patient denies all symptoms of cerebrovascular insufficiency over the past 6 months (A) or complains of nonlateralizing cerebral symptoms (D); transient unilateral monocular blindness (TAF); TIA (T) or RIND (R): transient lateralizing symptoms of cerebrovascular insufficiency and speech deficits but not including unilateral monocular blindness; and stroke (S): recent persistent unilateral symptoms of cerebrovascular insufficiency.

Twenty-one operations were performed under sedation and regional anesthesia. The remainder were conducted under general anesthesia with nitrous oxide in oxygen and isoflurane or enflurane after induction with thiopental. The operations were performed by 23 vascular surgeons in seven community hospitals of three western counties of the state of Washington. Shunting of the endarterectomy site was performed in 297 operations (59%), including 9 incomplete attempts. One hundred twenty-seven operations (25%) were performed without angiography, with the severity of stenosis based on the highest frequencies found with 5-MHz continuous-wave Doppler. The following scale was verified in 222 of the cases in which both angiograms and Doppler examinations were performed: <3 kHz, 0% stenosis; 3 kHz, 10%; 4 kHz, 20%; 5 to 6 kHz, 30%; 7 to 8 kHz, 40%; 9 to 10 kHz, 50%; 11 to 13 kHz, 60%; 14 to 15 kHz, 70%; 16 to 18 kHz, 80%; and >18 kHz, 90% stenosis.

The MCA flow velocity signals were monitored with a 2-MHz pulsed Doppler probe (Transpect; Medasonics Inc) placed over the temporal bone, on the operated side, and focused on the MCA at a depth of 45 or 50 mm with a focal length of 20 mm. A special headband was used to hold a ball-shaped transducer with a position-locking mechanism, which allowed hands-off monitoring. Positive identification of the MCA was confirmed by responses on the Doppler spectrum to finger oscillations of the cervical CCA or intraoperative surgical manipulations of the carotid arteries.

TCD monitoring phases were defined as follows: preoperative (before anesthesia); dissection (during surgical exposure of the carotid arteries up to the time of cross-clamping of the CCA); cross-clamping (including shunting, if performed); release (5 minutes after removal of the carotid artery clamps); closure (the period after release up to final closure of the skin incision); recovery (the following period until recovery from anesthesia); and follow-up (after recovery from the anesthetic, including the following day).

At the time of cross-clamping of the CCA, the decrease in mean MCA velocity was calculated as the percent remaining velocity compared with the pre–cross-clamp velocity²³ after 10 seconds were allowed for autoregulation adjustment. Upon release of the cross-clamp, after the arteriotomy was closed, the percent increase in velocity was calculated as the velocity after 15 seconds compared with the pre–cross-clamp velocity. The Doppler signals, voice annotations, and spectral signals were recorded on audio/video tape for detailed analysis.

DMES in the MCA were recognized by previously published combined audio and spectral criteria,^{29 30} and their numbers and the observation time were recorded for each phase. DMES occurring within the release phase were considered to primarily represent bubbles of air, but particulate matter may have been present. If they occurred before the artery was opened or after the release phase, they were considered to represent particulates. The surgeons were informed of relevant information during the surgery, and their responses were recorded. The tape recordings were analyzed postoperatively for velocity changes and DMES. The abstracted TCD measurements were entered into an analytical database. We performed statistical analyses using the ² test and two-tailed Student's t test. Statistical significance was considered at P<.05.

During the first 100 operations, TCD criteria were developed to identify the risks of intraoperative hypoperfusion, hyperperfusion, and embolism as well as strategies for cerebral protection. Surgeons were continuously informed of TCD information throughout all operations. Causal criteria analyzed to determine the etiology of CVCs were as follows: (1) hypoperfusion: intraoperative MCA velocities <30% of the pre–carotid cross-clamp value for >5 minutes; 40% of the pre–cross-clamp value can be tolerated indefinitely²³ intraoperatively, as well as postoperatively, if carotid artery occlusion occurs; (2) hyperperfusion: persistence of MCA velocities >1.5 times the pre–cross-clamp values during shunting or after final release of the carotid cross-clamps, without adequate corrective measures; and (3) embolism: failure to meet the previous two hemodynamic criteria and the persistence of DMES during the intraoperative and recovery phases, except for the release phase, or postoperatively without adequate preventive measures. No special limitations on the microembolic numbers or rates were established, but the surgeons became sensitive to their occurrence and measures were frequently taken to minimize their numbers.

CVCs were identified during the postsurgical hospitalization beginning in the recovery room and by examination of all hospital chart notes of the anesthesiologist, surgeon, and nurses and progress notes, consultation notes, and discharge summaries. CVCs were graded according to severity of clinically evident injury, as follows: grade I, TIA or RIND; grade II, residual deficits not impairing ordinary daily activities; grade III, impairment necessitating assistance with some ordinary activities; grade IV, impairment necessitating assistance with all ordinary activities; and grade V, coma or death.

CVCs were considered to occur intraoperatively if symptoms were noted upon the patient's recovery from the anesthetic. CVCs were considered to occur postoperatively if symptoms developed after recovery from the anesthetic. The probable cause of each CVC was determined by the following: (1) TCD criteria; (2) reopening the arteriotomy and inspecting for thrombus or occlusion; (3) postoperative ultrasound examination to confirm ICA and MCA patency; and (4) cranial CT findings and opinions from consultation with a neurologist (when available).

	Results

Top Abstract Introduction Subjects and Methods Results Discussion References

 
There were no deaths among the 500 CEAs, but 24 CVCs occurred (4.8%; 95% confidence interval, 2.9% to 6.7%). There were 15 permanent deficits, beyond the 9 TIAs, for a stroke rate of 3% (95% confidence interval, 1.5% to 4.5%). Fourteen complications occurred intraoperatively and 10 postoperatively. Table 1 lists all CVCs with the principal hemodynamic, embolic, and other data used to determine the probable cause of the complications. Among all CVCs, embolism was judged to be responsible in 13 (54%; P<.02 compared with hypoperfusion), hyperperfusion in 7 (29%; P<.14 compared with hypoperfusion), and hypoperfusion in 4 (17%; P<.08 compared with embolism plus hyperperfusion). More than one causal factor sometimes appeared to be involved, but the primary cause was usually identifiable.

View this table: [in this window] [in a new window]   Table 1. Probable Causes and Relevant Information in 24 CVCs From CEA

During the cross-clamp phase, MCA velocities decreased below 30% of their pre–cross-clamp values in 81 operations (16%). The surgeons responded to the threat of hypoperfusion by shunting or attempted shunting except in three cases in which no shunt was used and no CVC resulted. The time without shunting in these three cases was 17, 21, and 21 minutes, with residual cross-clamp MCA velocities of 7%, 18%, and 28%, respectively. The arterial pressure was increased in these patients to improve perfusion. Presumably cortical collateral played a role in providing adequate perfusion in all three subjects. Other responses to hypoperfusion included adjustment of an occluded shunt, intermittent release of the clamps when extra time was needed for suturing of the arteriotomy, and reopening and reinspecting of the operative site for intimal flaps or an occluding thrombus. Surgeons whose policy was to routinely shunt began to rely on TCD information for selective shunting. Those surgeons who used a shunt selectively, based on stump pressure measurements, eventually abandoned the pressure technique and relied solely on the TCD velocity information to decide for or against use of a shunt.

After release of the cross-clamps, MCA velocities abruptly increased above pre–cross-clamp values and then usually decreased toward the pre–cross-clamp values. In 73 operations (15%) they persisted at values more than twice the pre–cross-clamp values. There were subsequent complications in 3 (4%) of these. In 2 of the 3, hyperperfusion was considered the primary cause, and in the third it was considered a secondary cause. Measures to prevent hyperperfusion included intraoperative temporary partial occlusion of the CCA, lowering of the arterial pressure, induction of hypocarbia by increased pulmonary ventilation, and infusion of nitroprusside or other hypotensive agent. The Figure illustrates the sequence of events in a patient with hyperperfusion and treatment by control of arterial blood pressure. This patient was a 71-year-old normotensive man who preoperatively had a left hemispheric TIA. Angiograms were interpreted to represent 80% to 90% narrowing of the left ICA, but micrometer measurements of the ICA revealed 50% diameter stenosis. Doppler and duplex examinations diagnosed 30% stenosis. When the surgeons were notified of the danger of hyperperfusion, they lowered the arterial pressure and partially pinched off the CCA to decrease the MCA velocities. No postoperative headache or CVC occurred in this patient.

View larger version (70K): [in this window] [in a new window]   Figure 1. Changes in MCA velocity during several phases of CEA and results of actions to prevent hyperperfusion. The vertical scale maximum for the top three panels equals 120 cm/s and for the bottom three panels equals 320 cm/s. The time base for all panels is 4 seconds. V indicates velocity (systolic/end diastolic); P, systemic arterial pressure (systolic/diastolic); and T, time of day (PM).

The prevalence and number of DMES during the perioperative phases are shown in Table 2. For this analysis all intraoperative phases including dissection, cross-clamping, release, and closure were grouped together. The preoperative prevalence of one or more DMES in the MCA in all 500 cases was 16%. However, when we analyzed those monitored for more than 5 minutes to eliminate trivial monitoring times, the preoperative prevalence in 443 cases increased to 19%. In this group the difference between the preoperative number of DMES per minute in CVC cases and non-CVC cases was not significant (P=.95). During the intraoperative phases the DMES prevalence was 93%, and the difference in DMES between CVC and non-CVC cases was significant (P=.02). The difference during the recovery phase between CVC and non-CVC cases was marginally significant (P=.06). These statistics were computed with the two-tailed t test.

View this table: [in this window] [in a new window]   Table 2. MES and Perioperative Phases of CEA

When the surgeons released the external carotid artery and CCA clamps before release of the ICA, DMES were frequently detected in the MCA, presumably passing retrograde through the ophthalmic artery, which served as a collateral channel to the ICA. Although these were mainly considered bubbles and were not treated with the same seriousness as particulate DMES of other phases, the surgeons responded to release DMES by altering their techniques to more thoroughly eliminate intraluminal air before final closure of the arteriotomy. No decrease in MCA velocity was observed after any of the DMES. This observation suggests that they did not greatly obstruct MCA flow, individually or in clusters upon clamp release. Surgeons responded to the presence of particulate DMES during surgical maneuvers with more care during the dissection, early cross-clamping of the distal ICA before dissection of the CCA and external carotid artery, and administration of extra heparin. Surgeons responded to postoperative DMES by administration of heparin, intravenous dextran, and increased alertness to possible postoperative complications.

Table 3 indicates a tendency for embolism to be more strongly associated with lesser grades of CVCs and for hemodynamic factors to be associated with more severe grades of CVCs. Probabilities were as follows: for the distribution of CVCs found with embolization, hyperperfusion, and hypoperfusion, P<.07; for hypoperfusion and hyperperfusion, P<.14; for embolization and hypoperfusion, P<.08 and P=.17 with Bonferroni adjustment; for embolization and hypoperfusion, P<.02 (the distribution between these two causes is therefore statistically significant).

View this table: [in this window] [in a new window]   Table 3. Severity and Distribution of CVCs According to Probable Cause

Table 4 shows that shunting was more strongly associated with CVCs than nonshunting, although the difference was not statistically different (P=.24). CVCs from embolization appeared equally distributed among the shunted and nonshunted cases. Hyperperfusion accounted for the major difference between shunted and nonshunted operations: we observed 7 CVCs in the shunted operations, whereas none of the nonshunted operations involved hyperperfusion. This finding suggests that nonshunted subjects were adequately perfused before surgery and also during cross-clamping, with their collateral and autoregulation mechanisms adequate or unchallenged. In 9 of the shunted operations, placement was only partially successful, with the nonshunted duration of cross-clamping ranging from 10 to 58 minutes. There were 4 CVCs (44%) among these 9 partially shunted cases. Embolism was considered the primary cause in 3 and a secondary factor in 1. Table 1 indicates the secondary causes of CVCs when appropriate.

View this table: [in this window] [in a new window]   Table 4. Shunting and Causes of CVCs

Postsurgical occlusion of the operated ICA was found in 6 of the CVC patients, 3 occurring intraoperatively and 3 postoperatively. All ICA occlusions were confirmed by reopening of the arteriotomy with evidence of thrombosis of the ICA. Three of the 5 patients with ICA occlusion demonstrated microemboli in the recovery room before their return to the operating room. Embolization from the occluding thrombus was concluded to be the cause of complications in 5 of the 6 occlusions because cross-clamp velocities and stump pressures were considered adequate to maintain global perfusion even without protection of anesthesia. In the sixth patient hypoperfusion was concluded to be the cause, but large numbers of microemboli detected in the recovery room were thought to be a contributing factor.

One ipsilateral MCA occlusion (patient 347, Table 1) was thought to be due to primary thrombosis developing at the site of a 50% MCA stenosis detected by TCD and seen on the preoperative angiogram. This patient was initially referred to surgery for an RIND and a 90% stenosis of the ICA. Thrombosis of the MCA was completed 6 hours postoperatively when the patient became comatose and Doppler examination of the cervical ICA and the MCA confirmed MCA occlusion. In this patient only seven microembolic signals occurred during a 100-minute dissection phase and no microemboli were seen in a 60-minute recovery phase, suggesting that the occlusion was the result of primary thrombosis of the MCA and not embolization from the operative site. Three postoperative cranial CT examinations demonstrated old infarctions in the left posterior parieto-occipital area and no hemorrhage.

Table 5 discloses the CVCs by preoperative symptom category. There was no significant difference between the number of strokes in 238 asymptomatic patients and 262 symptomatic patients (P=.30). It appears that the most risk-free symptomatic category included those patients referred for amaurosis fugax, and patients referred for hemispheric symptoms sustained the highest rate of CVCs; however, 2x3 cross-tabulation analysis of the three symptomatic categories yielded P=.20. There were no complications among the 44 patients with a prior contralateral CEA. Among the 8 undergoing a repeated ipsilateral CEA, 1 patient had a grade I complication from the first operation and 1 patient had a grade III complication from the second CEA. One of the 8 patients sustained a grade III stroke due to a thrombus developing at the site of the cross-clamp of the CCA. There were no hospital complications among the 21 regional anesthesia patients, although only 6 were referred for hemispheric symptoms and the numbers of patients are insufficient for separate statistical analysis.

View this table: [in this window] [in a new window]   Table 5. CVCs From CEA According to Preoperative Symptoms

In 499 patients the percent stenosis was quantitated by either angiography or Doppler by the method that resulted in the greatest severity. Of the 499, 190 (38%) had stenosis <70% and 309 (62%) had stenosis 70%. Twelve CVCs occurred in the 190 patients with <70% stenosis for a 6.3% complication rate, and 12 CVCs occurred in the 309 patients with 70% stenosis for a 3.9% complication rate (P=.22). There was no statistically significant difference between symptomatic patients with 70% stenosis and patients with <70% stenosis: in 156 patients with 70% stenosis there were 8 CVCs (5.1%), whereas in 105 with <70% stenosis there were 7 CVCs (6.7%) (P=.61). Likewise there was no difference between asymptomatic patients with 60% stenosis and patients with <60% stenosis: in 200 patients with 60% stenosis there were 8 CVCs (4.0%), whereas in 38 patients with <60% stenosis there was 1 CVC (2.6%) (P=.68).

The proportion of patients in asymptomatic versus symptomatic categories was the same among the first 100 and the last 400 patients, ie, 48% were asymptomatic in both groups of cases. The incidence of permanent deficits diminished from 7% in the first 100 operations to 2% for the last 400 (P.01). For all CVCs the incidence diminished from 8% in the first 100 to 4% in the last 400 (P.11).

	Discussion

Top Abstract Introduction Subjects and Methods Results Discussion References

 
In this study it appears that embolization is the main cause of hospital cerebral complications from CEA and that hyperperfusion is the second major cause. Hypoperfusion is the least frequent cause of CVCs in this study in which 59% of subjects were shunted. Even so, this latter finding, along with the higher complication rate for shunted operations, suggests that shunting may be advisable only in highly selected cases and should be particularly avoided when difficulties in placement are anticipated. This conclusion was also reached by a previous large group study.³¹

Cortical collateral may account for tolerance to cross-clamping, with MCA velocities below the 30% level for extended periods in some patients. The residual MCA velocity after cross-clamping may be reduced by cortical collateral, the effect of which would be opposite that of the collateral from the circle of Willis. The presence of cortical collateral, however, does not invalidate the shunting criteria used here because any error from this effect is on the side of safety.

In this study no single embolus or combination of microemboli has been recognized that clearly produced embolic complications, but transient decreases in MCA velocity associated with embolic showers³² in the recovery room have led to CVCs. It was not possible in the present study to completely monitor the entire intraoperative and postoperative periods, and therefore a large embolus or group of particulate emboli may well have been missed. However, DMES are clearly more strongly associated with CVC cases than with non-CVC cases. Controlling the numbers of microemboli appears to prevent the development of large, clinically significant emboli and saves brain tissue from many small infarcts, as reported by others.³³ The size of microemboli cannot yet be measured, but multifrequency techniques show great promise.^{34 35}

The evidence presented here that TCD monitoring has reduced the incidence of cerebral injury is based on improvement of outcomes since our initial experience and also on the surgeons' actions on the basis of TCD information. A randomized, blinded study will be difficult to perform in this environment because many vascular surgeons believe that the technique represents good medical practice and believe that the findings from the monitored cases will be applied to those who were not monitored, thus rendering comparison difficult between monitored and nonmonitored patient groups. The work of others using TCD in CEA confirms the present results.^{36 37}

Problems with TCD monitoring of CEA patients mainly relate to finding and holding the MCA signal throughout the surgery because of the narrow and sometimes nonexistent temporal bone window. Fifteen percent of CEA patients (13% of women and 5% of men) do not have an adequate transtemporal window to allow insonation of the MCA. Improved headbands and application techniques are now available to stabilize the probe and allow hands-off bilateral monitoring in most cases.

Conclusions
We conclude the following: (1) Nineteen percent of CEA patients demonstrate microemboli in the MCA. (2) Embolism from the operative site during CEA is the principal cause of CVCs (P<.02), with hyperperfusion and hypoperfusion also significant causes. (3) Postarteriotomy occlusion of the ICA by thrombosis is a major cause of CVCs; the major mechanism is embolization from the thrombosed artery. (4) TCD monitoring provides relevant on-line information to allow prompt identification and treatment of the three major causes of CVCs from CEA. (5) TCD information provided to the vascular surgeon in the perioperative CEA period leads to alterations in surgical techniques and patient management. (6) The perioperative stroke rate can be reduced by appropriate measures by the surgeons, based on findings of TCD monitoring (P.01). (7) DMES are produced intraoperatively in >90% of all CEAs with or without CVCs. However, the number of intraoperative DMES is strongly associated with CVCs from CEA (P=.02). (8) TCD monitoring of CEAs provides important knowledge about the mechanisms of CVCs in CEA. (9) There is no statistically significant difference between the number of CEA strokes in asymptomatic and symptomatic patients (P=.30). (10) Shunting of the operative site may be associated with more complications than nonshunting, particularly when difficulties are encountered with insertion of the shunt. (11) Shunting is recommended in a small percentage of patients who can be selected on the basis of TCD-detected velocity changes after cross-clamping of the CCA.

	Selected Abbreviations and Acronyms

 

CCA = common carotid artery CEA = carotid endarterectomy CVCs = cerebrovascular complications DMES = Doppler microembolic signals ICA = internal carotid artery MCA = middle cerebral artery RIND = reversible ischemic neurological deficit TCD = transcranial Doppler ultrasound TIA = transient ischemic attack

	Acknowledgments

 
The author thanks Peter Mansfield, MD, Director of The Heart Center, Seattle Providence Medical Center, for assistance in statistical analysis.

Received December 26, 1996; revision received January 31, 1997; accepted January 31, 1997.

	References

Top Abstract Introduction Subjects and Methods Results Discussion References

 

1. Sundt TM, Sharbrough FW, Anderson RE, Michenfelder JD. Cerebral blood flow measurements and electroencephalograms during carotid endarterectomy. J Neurosurg. 1974;41:310-320. [Medline] [Order article via Infotrieve]
2. Larson CP, Ehrenfeld WK, Wade JG, Wylie EJ. Jugular venous oxygen saturation as an index of adequacy of cerebral oxygenation. Surgery. 1967;62:31-39.
3. Krul JMM, Ackerstaff RGA, Eikelboom BC, Vermeulen FEE. Stroke-related EEG changes during carotid artery surgery. Eur J Vasc Surg. 1989;3:423-428. [Medline] [Order article via Infotrieve]
4. Moore WS, Hall AD. Carotid artery back pressure, a test of cerebral tolerance to temporary carotid occlusion. Arch Surg. 1969;99:702-710. [Medline] [Order article via Infotrieve]
5. Archie JP. Technique and clinical results of carotid stump back-pressure to determine selective shunting during carotid endarterectomy. J Vasc Surg. 1991;13:310-326.
6. Schroeder T, Sillesen H, Sorensen O, Engell HC. Cerebral hyperperfusion following carotid endarterectomy. J Neurosurg. 1987;22:824-829.
7. van Alphen HAM, Polman CH. Carotid endarterectomy: how does it work? A clinical and angiographic evaluation. Stroke. 1986;17:1251-1253. [Abstract/Free Full Text]
8. McKinsey JF, Desai TR, Bassiouny HS, Piano G, Spire JP, Zarins CK, Gewertz BL. Mechanisms of neurologic deficits and mortality with carotid endarterectomy. Arch Surg. 1996;131:526-531. [Abstract]
9. Archie JP. The endarterectomy-produced common carotid artery step: a harbinger of early emboli and late restenosis. J Vasc Surg. 1996;23:932-939. [Medline] [Order article via Infotrieve]
10. Riles TS, Imparato AM, Jocbowitz GR, Lamparello PJ, Giangola G, Adelman MA, Landis R. The cause of perioperative stroke after carotid endarterectomy. J Vasc Surg. 1994;19:206-216. [Medline] [Order article via Infotrieve]
11. Ringelstein EB, Richert F, Bardos S, Minale C, Alsukun M, Zeplin H, Schöndube F, Zeumer H, Messmer B. Transkraniell-sonographisches monitoring des blutflusses der A. cerebri media während reanalisierender operationen an der extrakraniellen A. carotis interna. Nervenarzt. 1985;56:423-430. [Medline] [Order article via Infotrieve]
12. Padayachee TS, Gosling RG, Bishop CC, Burnand K, Browse NL. Monitoring middle cerebral artery blood velocity during carotid endarterectomy. Br J Surg. 1986;73:98-100. [Medline] [Order article via Infotrieve]
13. Padayachee TS, Gosling RG, Lewis RR, Bishop CC, Browse NL. Transcranial Doppler assessment of cerebral collateral during carotid endarterectomy. Br J Surg. 1987;74:260-262. [Medline] [Order article via Infotrieve]
14. Spencer MP, Aaslid R, Castillos F, McDaniel M. Intraoperative monitor for intracranial hemodynamics. In: Proceedings and abstracts of the 32nd Annual Convention of the American Institute of Ultrasound in Medicine; October 6-9, 1987; New Orleans, La.
15. Laman DM, Voorwinde A, Davies G, Van Duijin H. Intraoperative internal carotid artery restenosis detected by transcranial Doppler monitoring. Br J Surg. 1989;76:1314-1316.
16. Powers AD, Smith RR, Graeber MC. Transcranial Doppler monitoring of cerebral flow velocities during surgical occlusion of the carotid artery. Neurosurgery. 1989;25:383-389. [Medline] [Order article via Infotrieve]
17. Steiger HJ, Schäffler L, Boll J, Liechti S. Results of microsurgical carotid endarterectomy. Acta Neurochir (Wien). 1989;100:31-38. [Medline] [Order article via Infotrieve]
18. Powers AD, Smith RR. Hyperperfusion syndrome after carotid endarterectomy: a transcranial Doppler evaluation. Neurosurgery. 1990;26:56-60. [Medline] [Order article via Infotrieve]
19. Bernstein EF. Role of transcranial Doppler in carotid surgery: noninvasive diagnosis of vascular diseases. Surg Clin North Am.. 1990;70:225-234. [Medline] [Order article via Infotrieve]
20. Fisher DM, Fisher PA, Pietrzak NA. Efficacy of transcranial Doppler for monitoring middle cerebral arterial velocity during carotid endarterectomy. J Cardiovasc Tech. 1990;9:80-81.
21. Ackerstaff RGA, Jansen C, Moll FL. The pros and cons of TCD monitoring during carotid endarterectomy. Neurosonology. 1993;6:20-27.
22. Jørgensen L, Schroeder T, Knudsen L, Perko M. Transcranial Doppler monitoring and carotid artery blood pressure measurements during carotid endarterectomy. J Cardiovasc Tech. 1990;9:79-80.
23. Spencer MP, Thomas GI, Moehring MA. Relation between middle cerebral artery blood flow velocity and stump pressure during carotid endarterectomy. Stroke. 1992;23: 1439-1445.
24. Sollmann WP, Lorenz M, Gaab MR, Dorfmüller G, Hinrichs H, Feistner H. Intraoperative monitoring with TCD, EEG and evoked potentials in extracranial cerebrovascular surgery. J Cardiovasc Tech. 1989;8:174-176.
25. Thiel A, Russ W, Nestle HW, Hempelmann G. Early detection of cerebral ischemia during carotid endarterectomy using transcranial Doppler sonography and somatosensory evoked potentials. Thorac Cardiovasc Surg. 1989;37:115-118. [Medline] [Order article via Infotrieve]
26. Thiel A, Russ W, Zeiler D, Dapper F, Hempelmann G. Transcranial Doppler sonography and somatosensory evoked potential monitoring in carotid surgery. Eur J Vasc Surg. 1990;4:597-602. [Medline] [Order article via Infotrieve]
27. Steiger HJ, Schoch C, Zhong Y. The value of carotid surgery monitoring with TCD and EEG. J Cardiovasc Tech. 1990;9:315-316.
28. Spencer MP, Thomas GI, Nicholls SC, Sauvage LR. Detection of middle cerebral artery emboli during carotid endarterectomy. Stroke. 1990;21:415-423. [Abstract/Free Full Text]
29. Spencer MP. Detection of cerebral arterial emboli with transcranial Doppler. In: Newell DW, Aaslid R, eds. Transcranial Doppler. New York, NY: Raven Press Ltd; 1992:215-230.
30. Consensus Committee of the Ninth International Cerebral Hemodynamics Symposium. Basic identification criteria of Doppler microembolic signals. Stroke. 1995;26:1123. [Free Full Text]
31. Halsey JH Jr. Risks and benefits of shunting in carotid endarterectomy. Stroke. 1992;23:1583-1587. [Abstract/Free Full Text]
32. Gaunt ME, Ratliff DA, Martin PJ, Smith JL, Bell PRF, Naylor AR. Incipient carotid artery thrombosis during carotid endarterectomy by transcranial Doppler scanning. J Vasc Surg.. 1994;20:104-107. [Medline] [Order article via Infotrieve]
33. Jansen C, Ramos LMP, van Heesewijk JPM, Moll FL, van Gijn J, Ackerstaff RGA. Impact of microembolism and hemodynamic changes in the brain during carotid endarterectomy. Stroke. 1994;25:992-997. [Abstract]
34. Spencer MP, Klepper JR. Ultrasonic frequency dependence of Doppler detectability of arterial microemboli. FASEB J. 1992;6:A1357.
35. Moehring MA, Klepper JR. Pulse Doppler ultrasound detection, characterization and size estimation of emboli in flowing blood. IEEE Trans Biomed Eng. 1994;41:35-44.[Medline] [Order article via Infotrieve]
36. Jørgensen LG, Schroeder TV. Transcranial Doppler for detection of cerebral ischemia during carotid endarterectomy. Eur J Vasc Surg. 1992;6:142-147. [Medline] [Order article via Infotrieve]
37. Jansen C, Vriens EM, Eikelboom BC, Vermeulen FEE, van Gijn J, Ackerstaff RGA. Carotid endarterectomy with transcranial Doppler and electroencephalographic monitoring. Stroke. 1993;24:665-669.[Abstract/Free Full Text]

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