(Stroke. 1999;30:1288.)
© 1999 American Heart Association, Inc.
Letters to the Editor |
Transcranial Doppler Monitoring of Carotid Artery Occlusion During Endarterectomy
Division of Neurology, Department of Medicine, Queen Mary Hospital Hong Kong
To the Editor:
I read with great interest the article, "Predicting the Effect of Carotid Artery Occlusion During Carotid Endarterectomy: Comparing Transcranial Doppler Measurements and Cerebral Angiography," by Doblar and colleagues.1 In this study, 45 patients were separated into 3 groups according to the presence of collaterals on 4-vessel cerebral angiography, and mean flow velocity (FVm) over the middle cerebral artery and EEG were continuously monitored during carotid endarterectomy. The collaterals are the anterior communicating artery (ACoA) and the posterior communicating artery (PCoA) on the side of surgery. I would like to raise the following comments.
First, evidence-based guidelines for carotid endarterectomy are available.2 The surgery is highly effective in preventing stroke among patients with symptomatic high-grade carotid artery stenosis but much less beneficial in patients with asymptomatic high-grade stenosis.3 4 In the study by Doblar and colleagues,1 41 of 45 patients did not have ischemic symptoms before carotid endarterectomy, the mildest stenosis was only 35%, and 5 perioperative strokes were encountered (see their Table 1). I am interested to know the indications of carotid endarterectomy in the patients with only 35% stenosis as well as the degree of stenosis and symptomatic status of the 5 patients who developed perioperative strokes.
Second, absence of collaterals on cerebral angiography may represent an adequate arterial system (ie, no need for collateral) or inadequate collaterals despite a high-grade stenosis. This is why cerebral angiography is an excellent anatomic but a poor functional tool. In the study of Doblar and colleagues,1 all group 3 patients had a nonfunctioning ACoA or anatomic hypoplasia or stenosis of the A1 segment of the anterior cerebral artery on cerebral angiography. The findings suggest inability to derive a good blood flow from the ACoA even if more collaterals are need physiologically. This, together with a significantly greater severity of contralateral internal carotid artery stenosis, probably account for the findings on transcranial Doppler studies.
Third, the definitions of the "minimum FVm during occlusion," the "prerelease FVm during occlusion," and the "maximum FVm after release" do not have any physiological basis, because FVm varies continuously. The findings of a "significant" difference between the "average FVm during occlusion" and the "minimum FVm during occlusion," between the "prerelease FVm during occlusion" and the "minimum FVm during occlusion," and between the "average FVm 2 minutes after release" and the "maximum FVm after release" in group 1 and/or group 2 probably reflected greater variability of FVm in these groups when compared with that in group 3 (see Table 2 of Doblar et al1 ); there is no evidence of "progressive recruitment of collaterals during the occlusion period."
Fourth, the mean arterial blood pressure was highest in group 3 during occlusion when FVm was lowest (see their Table 3). In contrast to the authors' interpretations in the discussion, the findings probably indicated the physiological response to low FVm resulting from carotid clamping and poor collaterals.
Finally, EEG can provide physiological evidence of cerebral ischemia, and EEG was continuously monitored in the study.1 Nevertheless, EEG results were not provided in the article. I wonder whether the EEG results correlated well with the transcranial Doppler information and whether the EEG data predicted the occurrence of perioperative ischemia.
References
1.
Doblar DD, Plyushcheva NV, Jordan W, McDowell H.
Predicting the effect of carotid artery occlusion during carotid
endarterectomy: comparing transcranial
Doppler measurements and cerebral angiography. Stroke. 1998;29:2038–2042.
2.
Moore WS, Barnett HJM, Beebe HG, Bernstein EF, Brener
BJ, Brott T, Caplan LR, Day A, Goldstone J, Hobson RW II, Kempczinski
RF, Matchar DB, Mayberg MR, Nicolaides AN, Norris JW, Ricotta JJ,
Robertson JT, Rutherfold RB, Thomas D, Toole JF, Trout HH III,
Wiebers DO. Guidelines for carotid endarterectomy:
a multidisciplinary consensus statement from the Ad Hoc Committee,
American Heart Association. Stroke. 1995;26:188–201.
3. North American Symptomatic Carotid Endarterectomy Trial Collaborators. Beneficial effect of carotid endarterectomy in symptomatic patients with high-grade carotid stenosis. N Engl J Med. 1991;325:445–453.[Abstract]
4.
Executive Committee for the Asymptomatic
Carotid Atherosclerosis Study.
Endarterectomy for asymptomatic carotid
artery stenosis. JAMA. 1995;273:1421–1428.
Response
Departments of Anesthesiology and Biomedical Engineering
Department of Anesthesiology
Department of Surgery, University of Alabama, Birmingham, Alabama
Key Words: carotid artery occlusion • carotid
endarterectomy • collateral circulation
We thank Dr Cheung for his interest in our study.1
We published the article to illustrate value of knowing the functional
status of the cerebral collateral pathway(s) in predicting the response
of mean middle cerebral artery blood flow velocity (FVm) to acute
internal carotid artery (ICA) occlusion and release during carotid
endarterectomy (CEA). Our study population was too
small to draw conclusions regarding risks and benefits of operating on
patients with combinations of symptomatic versus
asymptomatic, high-grade, or low-grade ICA
stenosis. Such a study, the ACAS multicenter CEA
trial,2 has been published and has increased the impetus
for surgeons to operate on asymptomatic patients with ICA
stenoses of 
60%. Two of our patients had low-grade ICA
stenosis. The group 1 patient with occluded bilateral vertebral
arteries and an occluded left subclavian artery had transient arm
weakness in the postoperative period. The group 2 patient was
symptomatic with transient ischemic attacks before
surgery and had no postoperative deficit.
One patient of 45 suffered a stroke (Table 11 ); there were not 5 strokes in the study, as stated in Dr Cheung's letter. The rate of 1/45 (2.2%) is consistent with American Heart Association guidelines for CEA.3 The patient who suffered a postoperative stroke was symptomatic with transient ischemic attacks before surgery, had 99% stenosis of the ICA, lacked a functional ACoA, and was dependent on the ipsilateral PCoA for collateral blood flow. Back-bleeding from the arteriotomy site was noted to be abnormal during the surgical procedure, and an emboli shower lasting 2.5 seconds occurred during surgical dissection before carotid artery occlusion. Forty-one discrete emboli were seen. Baseline FVm was 36 cm/s, with a blood pressure of 133/76 mm Hg. FVm ranged from 19 to 33 cm/s during the 10-minute occlusion, and blood pressure was maintained above baseline at 158/88 mm Hg. Seven emboli were detected after reperfusion. No hyperemia was observed. The EEG was abnormal due to a shift to lower frequencies.
Four patients experienced reversible ischemic neurological deficits and not strokes (Table 1). In the first, the patient with a transiently weak arm, 3 emboli were detected after release of the cross-clamp and complete restoration of middle cerebral artery flow without hyperemia. The second, who presented with amaurosis fugax before CEA and suffered a stroke after diagnostic angiography in preparation for CEA, experienced mild transient mental status changes after CEA. There were significant EEG changes during the 7-minute period of occlusion, accompanied by a 74% reduction in FVm. Blood flow velocity was unstable during the occlusion. This is a rare occurrence in our experience and was suggestive of severely compromised collateral circulation. Ipsilateral FVm was 30% above preocclusion baseline following release of the cross-clamp for <1 minute. Two emboli were detected after cross-clamp release. The third patient was confused and experienced a seizure postoperatively without EEG changes or emboli. The fourth patient experienced asymmetry in the EEG with slowing and amplitude changes during cross-clamping. Mild hyperemia persisted for 20 minutes after release of the clamp.
Dr Cheung suggests that the FVm measurements summarized in our Table 3 "have no physiological basis, because FVm varies continuously." We agree that FVm does change during the various stages of CEA surgery and during the occlusion period. This is the reason we reported the data in this fashion. We believe that it is important to specify precisely when the measurements were taken when reporting such data. Whether or not Dr Cheung agrees with our interpretation of the change in FVm during the occlusion period, ie, "recruitment of collaterals," it is clear from our data that there is a statistically significant increase in FVm as the occlusion period progresses (Table 2). Beat-to-beat FVm data, not presented in the manuscript, demonstrate in some cases 2 components of the response after the initial decrease with cross-clamping: a small but immediate increase in FVm followed by a progressive increase in FVm. We have observed that the compensatory response of the collateral circulation has at least 2 time constants: the short time constant response may be a function of vascular compliance and the longer time constant is related to the redistribution of flow in the collateral circulation.
Dr Cheung further stated that the blood pressure was higher during occlusion when FVm was the lowest, indicating "the physiological response to low FVm resulting from carotid clamping and poor collaterals." We are in partial agreement on this point also, because it does not occur in all patients. We have observed that carotid cross-clamping in both anesthetized and awake patients results in a spontaneous increase in systolic blood pressure in the range of 20 mm Hg in approximately 25% of patients (authors' unpublished clinical data, 1995–1999). Anesthesiologists routinely take measures to increase blood pressure in anticipation of carotid cross-clamping. We either administer intravenous phenylephrine or decrease the depth of anesthesia to increase blood pressure to the desired level during carotid occlusion. This detail of the anesthetic management of these patients was inadvertently not discussed in our "Subjects and Methods" section1 because "it is universally accepted that the blood pressure during carotid occlusion should be maintained at or up to 20% higher than the patient's highest resting blood pressure when awake."4
Regarding the EEG data, there were ischemic changes in the EEG in 6 patients. Two of those patients experienced postoperative neurological deficits. One was the patient with postoperative stroke, and the second was the patient who experienced a stroke after angiography. Four other patients developed asymmetry and mild loss of amplitude and/or slowing in the EEG during the occlusion period that returned to baseline upon reperfusion. There was no correlation between the FVm value during occlusion and EEG changes. Persistent changes, not transient correctable changes, in EEG are associated with stroke.5 In our institution, EEG is primarily used as an indicator for the insertion of an intra-arterial shunt in the anesthetized patients.
In summary, the nature of the functional collateral pathway(s) influence the response to carotid occlusion (see our Table 2). Our data suggest that clinical studies of the cerebrovascular response to carotid cross-clamping should include consideration of the primary pathways of collateral circulation. Otherwise, pooling of data from patients with significantly different functional collateral pathways could lead to misinterpretation of the cerebrovascular response to occlusion.
References
1. Doblar DD, Plyushcheva NV, Jordan W, McDowell H. Predicting the effect of carotid artery occlusion during carotid endarterectomy: comparing transcranial Doppler measurements and cerebral angiography. Stroke. 1998;29:2038–2042.
2. Executive Committee for the Asymptomatic Carotid Atherosclerosis Study. Endarterectomy for asymptomatic carotid artery stenosis. JAMA. 1995;273:1421–1428.
3. Moore WS, Barnett HJ, Beebe HG, Bernstein EF, Brener BJ, Brott T, Caplan LR, Day A, Goldstone J, Hobson RW II, Kempczinski RF, Matchar DB, Mayberg MR, Nicolaides AN, Norris JW, Ricotta JJ, Robertson JT, Rutherford RB, Thomas D, Toole JF, Trout HH III, Wiebers DO. Guidelines for carotid endarterectomy: a multidisciplinary consensus statement from the ad hoc Committee, American Heart Association. Stroke. 1995;26:188–201.
4. Beattie C, Frank SM, Walker GV, Siex NW. Anesthesia for major vascular surgery. In: Longnecker DE, Tinker JH, Morgan GE, eds. Principles and Practice of Anesthesiology. St Louis, MO: Mosby; 1998:1841–1880.
5. Sundt TW, Sharborough FW, Piepgras DG, Kearns TP, Messick JM Jr, O'Fallon WM. Correlation of cerebral blood flow and electroencephalographic changes during carotid endarterectomy with results of surgery and hemodynamics of cerebral ischemia. Mayo Clin Proc. 1981;56:533–543.[Medline] [Order article via Infotrieve]
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