Common carotid artery occlusion with internal and external carotid arteries: Diagnosis and surgical management

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1 Common carotid artery occlusion with internal and external carotid arteries: Diagnosis and surgical management patent Michael Belkin, MD, William C. Mackey, MD, Michael S. Pessin, MD, Louis R. Caplan, MD, and Thomas F. O'Donnell, MD, Boston, 2~lass. Purpose: Occlusion of the common carotid artery (CCA) is generally associated with occlusion of the ipsilateral internal carotid artery (ICA) and external carotid artery (ECA). Occasionally, however, collateral circulation to the ECA may preserve patency of the ICA via retrograde perfusion through the bulb. These patients may suffer ongoing transient ischemic attacks and risk for stroke. Recognition of this pathologic variant may allow for effective surgical intervention. Methods: We have performed seven operations in six patients with occluded CCAs and patent ECA and ICAs. The occluded CCA was on the left side in each case (p < 0.01). Six of the operations were performed for ischemic symptoms, including amaurosis fugax in five patients, hemispheric TIA in one patient, and profound global ischemia in two patients who had concomitant occlusions of other extracranial vessels. In the five most recent cases the patent ECA and ICA above the occluded CCA were recognized by preoperative duplex scanning, which prompted cerebral angiography. A variety of reconstructive procedures were used, depending on the pathologic anatomy. These procedures included subclavian or axillary artery to carotid artery bypass with carotid endarterectomy (five), carotid endarterectomy with thrombectomy of the proximal CCA (one), and ascending aorta to carotid artery bypass (one). Results: There were no strokes associated with the surgery, although one patient had transient neurologic symptoms and a seizure associated with documented reperfusion edema. Three of the patients had preoperative and postoperative transcranial Doppler studies that documented significant improvement in intracranial hemodynamics. Five of the patients have had continuously patent grafts with relief of symptoms for an average of 40 months (range 3 to 155 months). The remaining patient had graft occlusion after 72 months and underwent repeat operation for amaurosis fugax and global ischemia. His second graft remains patent, and he is symptom free 21 months later. Conclusions: Recognition of patent distal vessels above a CCA occlusion depends on a high index of suspicion, careful investigation of the carotid bulb with duplex scanning, and delayed arteriographic views of the bulb allowing for late collateral vessel filling. The favorable results in this small series of patients supports an aggressive surgical approach when patients with symptoms are encountered with patent distal vessels above an occluded CCA. (J VASC SURe 1993;17: ) Carotid endarterectomy for symptomatic carotid bifurcation atherosclerosis has become a wellestablished and nearly universally accepted proce- From the Departments of Surgery and Neurology, New England Medical Center, Tufts University School of Medicine, Boston. Presented at the Nineteenth Annual Meeting of the New England Society for Vascular Surgery, Dixville Notch, N.H., Sept , Reprint requests: Michael Belkin M_D, Box 1015, New England Medical Center, 750 Washington St., Boston, MA Copyright 1993 by The Society for Vascular Surgery and International Society for Cardiovascular Surgery, North American Chapter /93/$ /6/45116 dure. ~ Relatively little has been written, however, on the management of occlusive disease of the common carotid artery (CCA). The incidence of CCA occlusion in patients with symptomatic cerebrovascular disease has been found to be from 1% to 5%. 2.4 Occlusion of the CCA is usually associated with occlusion of the ipsilateral internal carotid artery (ICA). Occasionally, however, collateral circulation to the external carotid artery (ECA) may preserve patency of the ICA via retrograde perfusion through the carotid bulb. These patients may have ongoing transient ischemic attacks and risk for stroke. The recognition and surgical treatment of this pathologic 1019

2 1020 Belkin et al. June 1993 TaMe I. Demographic information and presenting symptoms of the six patients who underwent seven operations Associated Patient Sex~age (yr) Risk factors Presenting symptoms brachiocephalic disease Operation Follow-up 1 M/51 History of smok- Global/VB RICA occlusion, LCEA with LSCA Patent 27 mo ing, CAD, hy- bilateral vert oc- to LCCA bypertension, dia- clusion (shunt pass-ptfe 2 M/65 betes mellitus required) History of smok- Hemispheric L vert occlusion R LCEA with LSCA Patent 5 mo ing, CAD, hy- TIA vert stenosis to LCCA bypertension, dia- pass-ptfe betes mellitus 3 F/65 History of smok- Left TMB RICA stenosis, LCEA with LCCA, Patent 38 mo ing, CAD, by- 75% thrombectomy pertension 4 F/63 History of smok- Left TMB RCCA and RICA LCEA with L axil- patent 155 mo ing, CAD, hy- occlusion lary to LCCA pertension bypass - vein 5 M/65 History of smok- Left TMB RICA stenosis, LCEA with L axil- Patent 3 mo ing, CAD, hy- 70% lary to LCCA pertension bypass- PTFE 6 M/51 History of smok- Bilateral TMB RCCA stenosis, Bilateral CEA, As- Failed between ing, CAD 90% cending aortic 72 and 144 mo bifurcation graft to CCAs 6 (second M/63 History of smok- Global, left RCCA and RICA LCEA with RSCA Patent 21 mo operation) ing, CAD, hy- TMB occlusion, Bilat- to LCCA bypass pertension eral vert stenosis PTFE CAD, Coronary artery disease; Global, global hypoperfusion; VB, vertebrobasilar symptoms; TMB, transient monocular blindness; R/CA, right internal carotid artery; RSCA, tight subclavian artery; vert, vertebral artery; RCCA, right common carotid artery; LSCA, left subclavian artery; LCCA, left common carotid artery; LCEA, left carotid endarterectomy; T/A, transient ischemic attack. variant has rarely been reported in the vascular surgery literature. Several isolated cases have been described as part of larger series of brachiocephalic arterial reconstructions, s-8 Other series focusing specifically on the surgical management of the occluded CCA have also identified such patients.4,9 These early series have largely relied on blind exploration of the carotid bifurcation in an attempt to identify patent ICAs. More recently, color-enhanced duplex scanning has facilitated evaluation of the carotid bulb, allowing preoperative recognition and guided arteriography of patients with patent ICAs above CCA occlusions. 10 We have performed seven operations in six patients with occluded CCAs and patent ICAs and ECAs. This report reviews the preoperative evaluation, surgical treatment, hemodynamic results, and clinical course of these patients. Emphasis is placed on the need for careful investigation of the carotid bulb with duplex scanning and delayed arteriographic views of the bulb, allowing for collateral vessel filling. Because of concurrent occlusive disease of the other brachiocephalic vessels, a variety of reconstructive procedures may be necessary to restore inflow beyond the occluded CCA. PATIENTS AND METHODS Demographics and presenting symptoms. From March 1978 to October 1992, six patients underwent seven operations to restore inflow to patent ICAs and ECAs above occluded CCAs. One patient originally operated on in March 1978 underwent a second procedure in December 1990 after his first reconstruction failed. The hospital charts, office records, arteriograms, and noninvasive laboratory records of each patient were reviewed. Table I includes the patients' demographic informarion and their presenting symptoms. There were four men and two women with an average age of 61 years (range 51 to 65 years) at the rime of surgery. All of the patients had a history of smoking, coronary artery disease, and hypertension. Two of the patients had diabetes meuitus. All seven operations were performed for symptomatic cerebrovascular disease. Five of the opera-

3 JOURNAL OF VASCULAR SURGERY Volume 17, Number 6 Belkin et al Fig. 1. A, Longitudinal duplex scan of occluded CCA with reconstimtion of turbulent flow at carotid bulb. B, Longitudinal image from above the bifurcation where retrograde flow down ECA (red) can be seen adjacent to antegrade flow up ICA (blue). tions were performed for left hemispheric transient ischemic attacks or left amaurosis fugax. The two remaining operations were undertaken for severe symptoms of global hypoperfusion. Both of these patients had bilateral carotid artery occlusions and associated vertebral artery disease (Table I, patients 1 and 6). One of these patients had symptoms of vertigo and repetitive episodes of syncope. The second patient had rapid progression of poor concentration, difficulty with word finding, and simple reading comprehension. This patient also had a single episode of left amaurosis fugax. Preoperative evaluation. The two patients admitted before 1980 were evaluated with only preop-

4 1022 Belkin et al. June 1993 Fig. 2. Lateral (A) and anteroposterior (B) arteriograms of left carotid artery that demonstrate prompt filling of ICA through prominent ECA collateral vessels. erative biplanar aortic arch and four-vessel selective arteriography. The five patients admitted after May 1990 underwent initial noninvasive evaluation with color-enhanced duplex scanning of the carotid bifurcation. (Ultramark 9-HDI, Advanced Technology Laboratories, Bothell, Wash.) In each of these five cases an occluded left CCA was identified, with a patent ECA demonstrating retrograde flow through the bulb into the ICA, which was patent with antegrade flow toward the brain. Fig. 1, A, shows a longitudinal duplex scan of an occluded left CCA, with turbulent flow appearing at the level of the bulb. Fig. 1, B, shows a more distal view of the same patient where retrograde flow down the ECA (red) is shown adjacent to antegrade flow up the ICA (blue). Three of these five patients also had preoperative hemodynamic evaluation with transcranial Doppler studies (TC2000, Eden Medical Electronics, Dantec Medical, Inc., Santa Clara, Calif.). On the basis of the duplex scan evaluation, the five patients underwent aortic arch and four-vessel selective arteriography with both standard cut films and digital subtraction arteriography. Fig. 2 demonstrates the prompt filling of a patent left ICA via ECA collateral vessels that was visualized in two of the five patients. In the three other patients, however, visualization of the patent ICA was more difficult. In these cases the information supplied by duplex scanning was pivotal in leading to delayed views that showed the patent ICA. Fig. 3 shows a delayed DSA image that demonstrates the subtle reconstitution of the left carotid bulb and ICA, which was missed on the initial run. Table I includes the arteriographic findings for the six patients and seven operations. In addition to the occluded left CCA with patent ECA and ICA, most noteworthy is the prevalence of contralateral carotid artery disease. In five of the six patients the contralateral right carotid artery was either occluded (two) or severely stenosed (three). Operative approach. All operations were performed with electroencephalograph monitoring for cerebral ischemia. In addition to restoration of inflow to the left carotid bulb, each patient underwent endarterectomy of the carotid bifurcation. The op-

5 JOURNAL OF VASCULAR SURGERY Volmne 17, Number 6 Belkin et al Fig. 3. Digital subtraction arteriogram that demonstrates ~;ubtle and delayed reconstitution of the left carotid bifurcation and internal carotid artery (arrow). Fig. 4. Postoperatix~e arteriogram of left subclavian to carotid artery bypass performed with 8 mm PTFE. erative approach to revascularization varied, depending on the pathologic anatomy and the best available inflow vessel. In four patients the ipsilateral subclavian (two) or axillary (two) artery was used as an inflow vessel for bypass to the carotid bulb. Three of these bypasses were performed with polytetrafluroethylene (PTFE) (8 ram, ringed) graft material (Fig. 4), and one was performed with reversed saphenous vein (Fig. 5). One of the patients that had a PTFE bypass had severe electroenccphalograph changes with crossclamping of the carotid artery and underwent intraluminal shunting from the subclavian artery (via the PTFE graft) to the ICA. All electroencephalograph changes reversed with opening of the shunt. No other patient had electroencephalograph changes during surgery. The fifth patient underwent exploration of the distal left CCA and bifurcation after the preoperative arteriogram revealed a 2 cm snamp of the proximal left CCA off the aorta without a significant origin stenosis. This patient was presumed to have occlusion of a progressive distal left CCA stenosis. Exploration of the distal left CCA revealed extensive localized atherosclerotic plaque with proximal thrombus. Thrombectomy of the proximal carotid artery restored normal inflow to the bulb that was endarterectomized. The sixth patient underwent two operations. The first operation in 1978 was for bilateral symptomatic disease caused by a right proximal CCA stenosis and a left CCA occlusion. He underwent an ascending aortic bifurcation graft to the distal right and left CCAs and bifurcation endarterectomies. This graft was known to be patent until 1984, when the patient was lost to follow-up. He was readmitted in 1990 with a thrombosed graft and symptoms of global hypoperfusion and left amaurosis fugax. Duplex scanning and arteriography showed that the left ECA and ICA remained patent. Because his left subclavian

6 1024 Belkin et al JOURNAL OF VASCULAR SURGERY lune 1993 Fig. 5. Postreconstruction artenogram of left axillary artery to carotid artery bypass. artery was occluded, the patient underwent a right subclavian to left CCA bypass with PTFE. Postoperative follow-up. Patients were monitored after operation by their operating surgeons. Patients were questioned about the return of preoperative symptoms. Patency of the bypass grafts were monitored by physical examination and serial duplex scanning. The five most recent patients also underwent postoperative transcranial Doppler studies to assess the effects of the left CCA reconstruction on cerebral hemodynamics. RESULTS Operative complications. There were two perioperative surgical complications. One patient who underwent a left CCA thrombectomy and bifurcation endarterectomy had a postoperative wound hematoma that was drained the second postoperative day. She had an otherwise uneventful recovery. The second complication occurred in a patient who was discharged on the fifth postoperative day after a left subclavian to left CCA bypass with PTFE. His postoperative course was marked by headaches and intermittent hypertension. He was readmitted on the tenth postoperative day with right-sided focal motor seizures that were followed by right arm weakness. An arteriogram (Fig. 4) revealed his subclavian to CCA bypass was widely patent with no irregularities. Serial computed tomography scans of the head revealed left hemispheric edema that resolved over 7 days along with the patient's symptoms. He is presumed to have had reperfusion hyperemia with secondary edema, seizure activity, and transient neurologic deficit. A previous case report has been written of hyperperfusion-induced seizures in a patient after an identical operation for the same vascular disease. ~ Patency of CCA reconstructions. The follow-up on all patients is complete and has averaged 66 months (range 3 to 155 months). Of the seven CCA reconstructions there has been one failure during long-term follow-up. This was the failure of an ascending aortic bifurcation graft to both CCAs. Graft failure occurred sometime between the sixth postoperative year, when the patient was lost to follow-up with a patent graft, and the twelfth postoperative year, when the patient returned with symptomatic graft failure (leading to repeat operation). The remaining six CCA reconstructions have remained patent for a mean of 42 months (range 3 tc~ 155 months). Clinical and hemodynamic results. All six patients were relieved of their neurologic symptoms after operation and have remained stroke free throughout the follow-up period. Four of the six patients have remained neurologically symptom free during follow-up. Two patients (both with right CCA and ICA occlusion) have had transient symptoms referable to the right cerebral hemisphere despite a patent left CCA reconstruction. One patient has had intermittent right amaurosis fugax beginning 1 year after surgery. The other patient had a right hemispheric transient ischemic attack 7 years after her initial operation. Arteriography at that time confirmed an occluded right CCA and a patent left axillary to left CCA bypass. In three patients both preoperative and postoperative transcranial Doppler studies were available to assess the hemodynamic effects of surgery. The combined results for all patients is shown in Table II. In each patient the preoperative transcranial Doppler scanning demonstrated decreased flow velocities in the anterior circulation vessels ipsilateral to the

7 Volume 17, Number 6 Belkin et al 1025 Table II. Transcranial Doppler results Artery Carotid siphon Ophthalmic artery )I~CA ACA Normal (cm/sec) Preoperative (cm/sec) Postoperative (cm/sec) Values are expressed as mean value + one SEM. MCA, Middle cerebral artery; ACA, anterior cerebral artery. occluded left CCA. Postoperative studies demonstrated that these velocities were corrected after left CCA revascularization. Table II reveals that the postoperative velocities were above the normal range, consistent with reperfusion hyperemia. DISCUSSION Most patients presenting with symptomatic extracranial cerebrovascular disease are found to have atherosclerotic occlusive disease of the carotid bifurcation and ICA. The natural history of this disease and the results of carotid endarterectomy are well established? Conversely, relatively tittle is known about the natural history and optimal treatment of patients presenting with symptomatic occlusion of the CCA. This is especially true of patients who have patent ECAs and ICAs beyond a CCA occlusion. During the 13-year interval over which these six operations were performed for reconstruction of occluded CCAs, 1080 conventional carotid endarterectomies were performed by our vascular surgery service. The incidence of CCA occlusion in patients presenting with symptomatic cerebrovascular occlusive disease has varied from 1% to 5%. 2-4 Interestingly, the incidence of left CCA occlusion has been equal to or higher than right CCA occlusion in nearly every study, accounting for 50% to 89% of cases. 12 The Joint Study of Extracranial Arterial Occlusion documented left CCA occlusions or stenoses in 2.2% and 4.8% of patients, respectively? In this study all operations were performed for left CCA occlusion, with no patients identified with tight CCA occlusion and patent ECAs and ICAs. The chance of this occurring because of chance alone is p < This is consistent with other surgical reports where, with few exceptions, 7'9 reported cases have involved the left CCA. ~ The mechanism of CCA occlusion may be either a thrombotic occlusion of a bifurcation plaque with retrograde thrombosis or left CCA origin thrombosis with antegrade thrombosis to the bulb. It has been *References 3,6,10,11,13,14. previously suggested that the former mechanism is usually operative, as The marked prevalence of left over right CCA occlusion with patent distal vessels in this and other series, however, is more consistent with the latter mechanism. Possible contributing factors to increased left CCA origin occlusion include hemodynamic differences between the two CCAs, differences in arterial length, and direct encroachment of aortic plaque into the CCA origin on the left. The high incidence of other associated brachiocephalic disease in our patients and in other series is also consistent with left CCA origin disease as the initiating event in CCA occlusion. 4,6,12 The mechanism of cerebrovascular symptoms may be multifactorial. In some patients hemodynamic factors may predominate with cerebral or ocular hypoperfusion, resulting in transient ischemic attacks or distal field infarcts. In other patients the cul de sac at the end of the CCA occlusion may serve as a source of cerebral emboli similar to the "stump" of an occluded ICA. a6 Whatever the mechanism the presenting symptoms may be quite variable. Although most patients have ipsilateral hemispheric transient ischemic attacks or amaurosis fugax, a significant proportion may present with vertebrobasilar symptoms or those of global hypoperfusion. This myriad of presentations may be attributed to associated brachiocephalic disease and complex patterns of collateral perfusion. This wide variation of presenting symptoms has been universally recognized in surgical series of patients treated for brachiocephalic disease, s,6'8 The preoperative identification and surgical treatment of patients with occluded CCAs and patent distal vessels has been infrequently reported in the vascular surgery literature. Several cases have appeared as part of larger series of brachiocephalic reconstructions, ss The report by Zelenock et al.6 of 71 complex brachiocephalic arterial reconstructions included one case of bypass of an occluded left CCA. Similarly, Vogt et al.8 reported the Cleveland clinic experience with 100 brachiocephalic reconstructions, including one documented case of an occluded left CCA that was treated with proximal endarterectomy

8 1026 Belkin et al. lune 1993 Fig. 6. Magnetic resonance arteriogram confirms presence of occluded (3CA and a patent ICA (arrow) in symptom-free patient. and reimplantation into the left subclavian artery. Other series have specifically addressed the management of the occluded CCA. 4,9,13 Podre et al. 4 reported on the successful revascularization of six carotid bifurcations in 12 patients presenting with CCA occlusion. Riles et al.9 were able to revascularize 11 ICAs in 24 patients explored for CCA occlusion. Both of these authors found preoperative arteriography to be insensitive (33% and 17%) to identifying patent ICAs above occluded CCAs. Thus these authors relied heavily on "blind" exploration of the carotid " bulb for identification of the patent distal vessels. Since the publication of these reports the duplex scan evaluation of the carotid bulb has been refined. The addition of color-enhanced duplex imaging has further advanced our ability to accurately delineate carotid anatomy. Case reports of the utility of the duplex scanning in identifying the patent CCA above a CCAocctusion have appeared. I Our experience confirms the utility of duplex scanning in this regard. Armed with the information supplied by duplex scanning and modern angiographic techniques, neuroangiographers should be able to identify the patent'distal ECA and ICA with high sensitivi W. In our opinion "blind" explorations of the carotid bifurcation should seldom be necessary with current imaging methods. Over the past year we have identified three additional symptom-free patients with occluded left CCAs with patent distal vessels. With the current widespread application of duplex scanning, the identification of this pathologic variant will undoubtedly increase. What role other new imaging methods may play in identifying and evaluating these patients remains speculative. Fig. 6 demonstrates a magnetic resonance arteriogram of a recent patient confirming antegrade flow up the ICA above a CCA occlusion. In summary, the favorable graft patencies and clinical results in this series and others support an aggressive surgical approach in patients presenting with symptomatic CCA occlusion and patent distal vessels. This is further supported by the postreconstructive improvement in cerebrovascular hemodynamics demonstrated in this series by transcranial Doppler studies. The recognition of patent distal vessels above an occluded CCA depends on a high index of suspicion (especially with a left CCA occlusion), careful investigation of the carotid bulb and distal vessels with the duplex scan, and directed arteriographic views of the carotid bulb, allowing for late collateral filling. Once identified, the surgeon must maintain a flexible approach, tailoring the operation to the patient's particular disease and available inflow source. REFERENCES 1. North American Symptomatic Carotid Endarterectomy Trial collaborators. Beneficial effect of carotid endarterectomy in

9 Volume 17, Number 6 Belkin et al symptomatic patients with high-grade carotid stenosis. N Engl J Med 1991;325: Hass WK, Fields WS, Noah RR, Kricheff II, Chase NE, Bauer RB. Joint study of extracranial carotid occlusions, II: arteriography, techniques, sites and complications. JAMA 1968;201: Collice M, D'Angelo V, Areno O. Surgical treatment of common carotid occlusion. Neurosurgery 1983;12: Podre PC, Rob CG, DeWeese JA, Green RM. Chronic common carotid occlusion. Stroke 1981;12: Crawford ES, Stowe CL, Powers RW. Occlusion of the innominate, common carotid and subclavian arteries: longterm results of surgical treatment. Surgery 1983;94: Zelenock GB, Cronenwetr JL, Graham LM, et al. Brachiocephafic arterial occlusions and stenoses. Arch Surg 1985;120: Perler BA, Williams GM. Carotid-subclavian bypass-a decade of experience. J VASC SURG 1990;12: Vogt DP, Hertzer NR, O'Hara PJ, Beven EG. Brachiocephalic arterial reconstruction. An n Surg 1982;196: Riles TS, Imparato AM, Posner MP, Eikelboom BC. Common carotid occlusion: assessment Of distal vessels. Ann Surg 1984;199: Berby AJ, Hines GL. Total occlusion of the common carotid artery with a patent internal carotid artery; identification by duplex ultrasonography: report of a case. J VAsc SURG 1989; 10: Ammar AD. Seizures following subclavian-carotid bypass. J VASC SURG 1987;5: Levine SR, Welch KM. Common carotid artery occlusion. Neurology 1989;39: Keller HM, Valavanis, Imhof HG, Turina M. Patency of external and internal carotid artery in the presence of an occluded common carotid artery: noninvasive evaluation with combined cerebrovascular doppler examination and sequential computertomography. Stroke 1984;15: Ziomek S, Quifiones-Baldrich WJ,. Busittil RW, et al. The superiority of synthetic arterial grafts over autologous veins in carotid-subclavian bypass. J VAsc SURG 1986;3: Moore WS, Blaisdell FW, Hall AD. Retrograde thrombectomy for chronic occlusion of the common carotid artery. Arch Surg 1967;95: Barnett HJ, Peerless SJ, Kanfman JC. "Stump" of internal carotid artery-a source for fu~her cerebral embolic ischemia. Stroke 1978;9: Submitted Oct. 8, 1992; accepted Dec. 19, DISCUSSION Dr. David B. Pilcher (Burlington, Vt.). You report six CCA occlusion reconstructions and one neurologic event. My review of the literature shows more than 200 cases of ~,.CA occlusion or severe stenosis with patent distal vessels that have undergone surgical reconstruction with 10 neurologic incidents and five deaths, so the perioperative morbidity rate in that group is 7.5%. Given the superb results of carotid endarterectomy at your institution, if you had an ICA stenosis contralateral to a CCA occlusion, as two of your patients did, wouldn't you repair the ICA stenosis rather than perform this more complex graft procedure? In our series of CCA occlusions, with patent distal vessels, the right side was involved in two of seven cases- you emphasized the left side- so we concurred with that in our smaller series. However, in 150 cases from the literature, the right CCA was involved in 41% of the cases, so I don't believe you really can make a case that the left side predominates. With short carotid artery to subclavian bypass grafts that we perform for subclavian stenosis, synthetic grafts or transposition have been the standard, but these subclavian to carotid artery grafts are longer. They go from the subclavian or the axillary to the bulb, and they're much longer. In the literature saphenous veins and synthetic vessels have been used with almost equal frequency, and there really haven't been good long-term studies to show long-term follow-up. Do you have a choice of conduit, or do you see an advantage of one conduit over the other? And why did you use PTFE in most of your cases? Color-flow Doppler ultrasonography is highly successfill in demonstrating this in all the other reports. Usually color-flow scanning shows you antegrade ICA flow and retrograde ECA flow, and it has usually been reported with low velocities, as in this case. You can also detect with Doppler scanning the high velocities that tell you that there is a stenosis in the ICA distal to this. In one of our cases severe plaque in the ICA was associated by very low flow distally. It was open on the angiogram, but at operation, the ICA was not suitable for reconstruction, and we had to reconstruct to the ECA, which did in fact relieve symptoms. You showed one case of selective subclavian angiography. In my review, in our series, and in your series, angiography can show these lesions without performing duplex scanning to show that there is a patent bulb if the angiographers are aware that, if they see a CCA occlus!on, they should perform delayed scanning. They should perform left subclavian or innominate or right subclavian injections to try to demonstrate these collateral vessels. My review suggests that the vertebra l thyrocervical collateral vessels, are far more frequent than cross-the-neck ECA to ECA collateral vessels. - Dr. Michael Belkin. You raise the question about how to treat a patient with left hemispheric symptoms with right carotid artery stenosis and an occluded left CCA with a patent ECA and ICA. We prefer to reconstruct the side that's causing the symptoms, although I think that a high-grade stenosis on the contralateral side could be treated on its own merits.

10 1028 Belkin et al June 1993 Regarding the incidence of left-sided versus right-sided occlusion, it's true that when you look at series discussing the incidence of right versus left CCA occlusion, there is a 41% incidence of right CCA occlusion. When you look at this series of reconstructive surgery for carotid artery occlusion with patent distal vessels, however, there is a much higher incidence of left side. I could find only two reported cases, and yours adds another case, of right-sided occlusions with patent distal vessels. You mentioned your concern about our choice of conduit, suggesting that a carotid subclavian bypass graft is a short graft and represents a good situation for PTFE. Conversely, a subclavian to carotid artery bypass, as a "longer bypass," is perhaps better done with vein. I think that "long bypass" is a relative term, and we are talking about a 7 versus a 4 cm graft. I do believe that this is an excellent application for synthetic graft because we're able to use a large-caliber, 8 ram, ring PTFE graft in a high-flow situation, and we've been quite satisfied with it. I think that if your choice is to use vein, it is completely acceptable. I agree with you that a competent arteriographer will almost always identify this lesion. It's almost moot because everyone will go through duplex scanning before they perform cerebral arteriography. Dr. Robert W. Hopkins (Providence, R.I.). The inferior thyroid artery may be enlarged and have a nice ICA signal, and it could be shown to anastomose directly with the superior thyroid artery in the external carotid artery with reverse of the flow. Obviously these are not common cases. I think that we mistook the inferior thyroid artery for the vertebral artery on several occasions. I think it is important to look for in the noninvasive diagnosis of the patency of the ICA and ECA above the occluded CCA. Dr. Belkin. I agree that the ipsilateral subclavian artery generally fills the patent carotid bulb above the occluded carotid artery. Cross filling from right external to left external branches was noted in only one of our patients. Dr. K. Craig Kent (Boston, Mass.). We are using magnetic resonance imaging increasingly at our institution to image the carotid artery circulation, and with this technique we have identified a subset of patients that have CCA occlusion and an open ICA. Many of these patients undergo duplex scanning that suggests ICA occlusion, and magnetic resonance imaging may turn out to be a more sensitive test for this entity. Because many of these patients have had just one transient ischemic attack, and because the morbidity and mortality rates of the operations that you are suggesting may be higher than that of conventional carotid endarterectomy, should I recommend operation to all patients that have had just one transient ischemic attack? Dr. Belkin. That's a good question, and I don't think that this surgery has been performed enough to know what the results will be. We did not have any strokes in our series, but we had a transient neurologic deficit that we believe was related to cerebral edema from reperfusion syndrome. So we are thus far satisfied and will continue to be aggressive with this operation. It may turn out, as more of this surgery is being done and this disease is more widely recognized, that the results may not warrant such aggressive intervention. Dr. Nancy L. Cantelmo (Boston, Mass.). I have a question about that patient that underwent reperfusion. We haven't had any reperfusion in the patients undergoing endarterectomy that we have studied, but I was wondering if that patient had a very marked rise in the transcranial Doppler scanning after operation, which some suggest is warning that this patient may then have reperfusion syndrome. Dr. Belkin. That particular patient demonstrated middle cerebral artery flow velocities in the postoperative period that were three times the preoperative baseline. Dr. Cantelmo. So you suspect that may have happened? Dr. Belkin. Correct, and we're looking at this prospectively now. All of our patients are undergoing preoperative transcranial Doppler scanning and transcranial Doppler scanning immediately after operation and at 3 weeks after operation to sort out who is at risk for headaches and reperfusion syndrome. It seems we've had three cases that we can identify over the past 6 years who had frank seizures and cerebral edema by computerized axial tomography scan, which resolved very quickly, which we, at this point, are attributing to this syndrome. Dr. Magruder Donaldson (Boston, Mass.). I wanted to ask about your opinion on another surgical option that I have used once. I think you are correct in pointing out that many of these occlusions are based on disease at the aortic arch with propagated thrombus to the bulb that may, in many cases, be normal. I think that with duplex scanning you can pick up whether there is calcium at that location. Is there a possibility of simply using the CCA as a thromboendarterectomized conduit swung to the subclavian or even the other carotid artery? Dr. Belkin. I think it is. One of our patients underwent preoperative arteriography, which showed a 2 cm stump off the aorta of a left CCA that was normal without an origin stenosis. At the time of exploration of the carotid bulb, we presumed there would be a more distal lesio~/ There was a very tight atherosclerotic lesion about 2 cm proximal to the bulb. That was removed, and the vessel was thrombectomized. When a proximal CCA lesion is noted, reimplantation of the CCA is an acceptable but perhaps more difficult option.