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Embolectomy for acute embolic occlusion of the internal carotid artery bifurcation
Embolectomy for Acute Embolic Occlusion of the Internal Carotid Artery Bifurcation Hajime Touho, M.D., Toshitaka Morisako, M.D., Youichi Hashimoto, M.D., and Jun Karasawa, M.D. Department of Neurosurgery, Osaka Neurological Institute, Toyonaka, Osaka, Japan
Touho H, Morisako T, Hashimoto Y, Karasawa J. Embolectomy for acute embolic occlusion of the internal carotid artery bifurcation. Surg Neurol 1999;51:313–20.
KEY WORDS
Cerebral infarction, embolism, internal carotid artery, embolectomy.
BACKGROUND
Acute occlusion of the distal intracranial segment of the internal carotid artery (ICA) causes sudden severe hemispheric ischemia. A low rate of recanalization and a high mortality rate for this condition have been noted, even with endovascular treatment. METHODS
We report the results of emergency embolectomy in six patients with acute embolic occlusion of the internal carotid artery (ICA) bifurcation. All six patients were admitted to our institute within 2 h of the onset of symptoms. Computed tomography (CT) scans on admission revealed no low-density or high-density regions in any patients. The time between onset of symptoms and completion of angiography ranged from 2 to 4 h (2.8 6 0.7 h). RESULTS
Emergency embolectomy was performed for each patient. Recanalization was confirmed angiographically in four of the patients. In the remaining two patients, massive infarction in the territory of the ICA was detected on the CT scans obtained the day of the operation, and postoperative angiography was not performed in these two cases. These two patients died of uncal herniation 6 days after onset. Two of the six patients were able to walk with a cane 2 months after surgery. The remaining two patients were unable to walk or attend to their own bodily needs without assistance. The time elapsed between onset of symptoms to reopening of the occluded vessel was within 6 h in the four surviving patients. The recanalization rate was 66.7% (4/6) for the embolectomy procedure, significantly higher than that (12.5%) of the thrombolytic therapy reported in a previous study. CONCLUSIONS
In summary, open embolectomy can be performed when the time after onset of symptoms is less than 6 h. © 1999 by Elsevier Science Inc.
Address reprint requests to: Dr. Hajime Touho, Department of Neurosurgery, Osaka Neurological Institute, 2-6-23 Shonai Takara-machi, Toyonaka, Osaka 561-0836 Japan. Received July 25, 1996; accepted June 23, 1997. © 1999 by Elsevier Science Inc. 655 Avenue of the Americas, New York, NY 10010
hromboembolic occlusion remains the most common cause of ischemic stroke [3]. Recent favorable clinical studies with thrombolytic agents have suggested that such agents may be useful for the treatment of acute stroke [6,18,29]. A few preliminary controlled safety studies have shown variable degrees of thrombolytic efficacy [31]. Based on these encouraging results, various multicenter randomized trials using intravenous tissue plasminogen activator (a relatively fibrin-specific agent) have begun and are now in progress [33]. Recent advances in techniques of intracranial vascular catheterization have made possible the direct delivery of thrombolytic agents intraarterially into a thrombus. Experimental studies have demonstrated that intraarterial administration produces more rapid thrombolysis at a lower dose than does intravenous administration [21]. Clinical cardiac thrombolysis studies suggest that intraarterial delivery may have less risk of systemic hemorrhagic complications [5]. Acute occlusion of the distal intracranial segment of the internal carotid artery (ICA) causes sudden severe hemispheric ischemia. A low rate of recanalization and a high mortality rate for this condition have been noted, even with endovascular treatment. We report here the results of emergency embolectomy for acute embolic occlusion of the internal carotid artery bifurcation.
T
Materials and Methods From July 1993 to February 1996, six patients with acute embolic occlusion of the ICA bifurcation were 0090-3019/99/$–see front matter PII S0090-3019(97)00423-0
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Summary of the Six Patients Treated by Emergency Embolectomy of the Internal Carotid Artery
CASE AGE NO. (YR) SEX 1
72
2
57
3
64
4
83
5
67
6
68
F
SYMPTOMS
lt hemiplegia, conjugate deviation of the eyes, stupor M rt hemiplegia, conjugate deviation of the eyes, stupor M lt hemiplegia, conjugate deviation of the eyes, stupor F lt hemiplegia, conjugate deviation of the eyes, stupor M rt hemiplegia, conjugate deviation of the eyes, stupor F rt hemiplegia, conjugate deviation of the eyes, stupor
ADMISSION OCCLUSION (HR) SIDE COLLATERALS
ELAPSED TIME POST-OP POST-OP (HR) COMPLICATIONS RS
2.0
rt
poor
6.0
massive infarction
6
2.0
lt
poor
7.0
6
1.5
rt
fair
6.0
1.0
rt
fair
5.0
0.5
lt
fair
6.0
massive hemorrhagic infarction cortical and subcortical infarction cortical and subcortical infarction subcortical infarction
1.0
lt
fair
5.5
cortical and subcortical infarction
3 4 3 4
RS, Rankin scale; op, operation; F, female; m, male; lt, left; rt, right.
treated with emergency embolectomy at the site of the occluded ICA. All six patients had atrial fibrillation at admission, and the embolic occlusion of the ICA was attributable to cardiogenic embolization. All six patients were admitted to our institute within 2 h of the onset of symptoms. Each patient’s neurological status was determined at admission, and after 4 weeks it was documented using the modified Rankin scale (RS0–RS5), scoring death as 6 [28]. Criteria for use of emergency embolectomy were as follows: 1. Sudden appearance of hemiparesis/hemiplegia with disturbance of consciousness and conjugate deviation of the eyes to the contralateral side of the hemipalsy. 2. Arrival at our institute within 6 h of the onset of symptoms. 3. No low- or high-density regions on pretreatment computed tomography (CT) studies. 4. Angiographic evidence of complete embolic occlusion of the internal carotid artery bifurcation. 5. Informed consent from the patient’s relatives. The first CT was performed a mean of 1.3 6 0.5 h after the onset of symptoms with a Quantex RX (Yokogawa Medical System, Tokyo, Japan) using a section thickness of 10 mm throughout the brain. No low- or high-density regions were found on the initial CT scans in any of the patients. Four-vessel selective cerebral angiography via the transfemoral artery was then performed. In each case, angiogra-
phy disclosed embolic occlusion of the internal carotid artery bifurcation. Angiographic collateral circulation patterns were classified using the following criteria: 1. Good: Almost all cortical branches (M4 segment) of the middle cerebral artery (MCA) were visualized, and the distal portion of the first segment of the MCA filled and emptied rapidly. 2. Fair: Cortical branches (M4 segment) could be visualized only slowly and/or partially. 3. Poor: Cortical branches (M4 segment) could not be visualized, or if they were, they remained so even during the late venous phase. Just after completion of the cerebral angiography, the second CT studies were performed, in which again no low- or high-density regions were found in any of the patients. The time between onset of symptoms and the completion of the angiography ranged from 2 to 4 hours (mean, 2.8 6 0.7 h). Emergency surgery with embolectomy was then performed in each case (Table 1). PREOPERATIVE NEUROLOGICAL STATUS AND ANGIOGRAPHICAL FINDINGS All six patients were stuporous with hemiplegia and conjugate deviation of the eyes to the side of the affected cerebral hemisphere on admission. Cere-
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Intraoperative photographs before (left) and after (right) embolectomy (Case 3). An embolus was found in the intradural segment of the right internal carotid artery (ICA) and the first segments of the anterior (A1) and middle cerebral arteries (M1). Temporary clips were placed on the right ICA (arrow), A1 (curved arrow), M1 (arrowhead), and the right posterior communicating artery (double arrowheads). Arteriotomy of the M1 segment was performed first, followed by the right ICA (left). After total removal of the embolus, the proximal arteriotomy was closed with 6-0 nylon interrupted sutures and the distal arteriotomy with 10-0 nylon interrupted sutures. Complete reperfusion was obtained (right).
1
bral angiography disclosed embolic occlusion of the ICA in all cases, and development of leptomeningeal collaterals was classified as poor in two cases (Cases 1 and 2) and as fair in the other four cases (Cases 3, 4, 5, and 6) (Table 1). GENERAL ANESTHESIA AND INTRAOPERATIVE CEREBRAL PROTECTION Operation was performed under general anesthesia. Nitrous oxide, narcotic (fentanyl), and volatile anesthetic (isoflurane) technique was used in all six patients. Anesthesia was maintained with nitrous oxide (50%), oxygen and isoflurane (0.5–2.0%), with repeated intravenous injections of fentanyl (50 –100 mg/hr). Thiopental was used for cerebral protection and for reducing intracranial pressure and cerebral edema [15,25]. Thiopental was continuously infused at a rate of 4 to 5 mg/kg/hr beginning just after induction of anesthesia, and continued for 24 to 48 h postoperatively. Systolic blood pressure was maintained over 100 mm Hg with or without intravenous infusion of dopamine (3– 6 mg/kg/min) for 24 to 48 h postoperatively. Hypothermia was not introduced for cerebral protection in the present study.
Operations A frontotemporal skin incision was performed followed by a frontotemporal craniotomy on the side of the occlusion of the ICA. The dura mater was
opened and the Sylvian fissure was then opened widely. In each case, an embolus was visible through the ICA, MCA, and the anterior cerebral artery (ACA), and those vessels were occluded from the supraclinoid segment of the ICA to the first segment of the ACA (A1 segment) and to the second segment of the MCA (M2 segment) in all patients except Case 3. In Case 3, the distal end of the embolus was found in the distal portion of the first segment of the MCA (M1 segment). Temporary clips were placed on the second segment of the ICA, the A1 segment, and the M2 segment in all patients except Case 3. In Case 3, distal clips were placed at the A1 segment and at the M1 segment (Figure 1, left). An arteriotomy one-quarter the circumference of the involved vessel(s) (bifurcation of the ICA and/or distal portion of the M1 segment) was then performed over the embolus. From these arteriotomies, a portion of the embolus was extracted using tumor forceps. Then the proximal clip was removed and a portion of the embolus was pulled out free with good bleeding via an arteriotomy, followed by placement of the proximal clip. If back-flow was encountered via the anterior choroidal and/or posterior communicating (Pcom) arteries, a new temporary clip(s) was placed at the anterior choroidal and/or Pcom arteries. The distal temporary clip was then removed and the rest of the embolus was milked free with good back-bleeding at the A1 and M1 segment, followed by placement of the distal clips. After total removal of the embolus, the proximal arteriotomy was then closed with 6-0 nylon
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Massive hemorrhagic infarction developed in Case 2 (left) and massive infarction in Case 1 (right).
2
interrupted sutures. The distal arteriotomy was closed with 10-0 nylon interrupted sutures (Figure 1, right). The total time elapsed from onset of symptoms to re-establishment of blood flow to the ipsilateral cerebral hemisphere ranged from 5 to 7 h (mean: 5.9 6 0.6 h) (Table 1). Postoperative angiography was performed 3 to 7 days after the operation for all patients except Cases 1 and 2. Follow-up CT scans were performed and neurological status was determined one month postoperatively.
Results Recanalization was confirmed angiographically in four of the patients (Cases 3, 4, 5, and 6). In the remaining two patients (Cases 1 and 2), massive infarction with or without hemorrhage in the territory of the ICA was detected on the CT scans obtained the day of the operation, and postoperative angiography was therefore not performed in these two cases. The recanalization rate in our study (66.7%) was significantly higher than that (12.5%) for thrombolytic therapy reported by Jansen et al [7] (Fisher’s exact probability test, p , 0.02). POSTOPERATIVE CT FINDINGS AND CLINIAL OUTCOME Case 1 suffered massive infarction postoperatively and died of uncal herniation six days after onset (Figure 2, right). Case 2 suffered hemorrhagic infarction postoperatively and died of uncal herniation 6 days after onset (RS6) (Figure 2, left). Two patients (Cases 3 and 5) had evidence of cortical and/or subcortical infarction on CT scans 1 month
after surgery. However, they were able to walk with a cane 2 months after surgery (RS3). Cases 4 and 6 also had evidence of cortical and subcortical infarction on follow-up CT scans, and were unable to walk or attend to their own bodily needs without assistance (RS4) (Table 1). ILLUSTRATIVE CASE CASE 5. A 67-year-old man was admitted to our institute for sudden onset of right hemiplegia, conjugate deviation of the eyes to the contralateral side of the palsy, and stupor. The time elapsed between the onset of symptoms and admission was 0.5 h. CT scans were performed immediately and disclosed no abnormalities except a small and old cortical infarction in the left frontal lobe (Figure 3, upper). Cerebral angiography disclosed an embolic occlusion of the left ICA with fair collateralization (Figure 4, upper). The second set of CT scans were obtained just after completion of the angiography, and disclosed no additional abnormalities. Emergency embolectomy was performed, and reestablishment of the cerebral circulation in the left cerebral hemisphere was achieved 6.0 h after the onset of ischemic symptoms. Three days after the operation, he regained normal consciousness and could lift his right upper and lower extremities. Postoperative angiography revealed complete establishment of reperfusion via the left ICA 3 days after onset (Figure 4, lower). Follow-up CT scans performed 2 months after onset revealed a very small low-density region in the left internal capsule with subdural effusion over the left frontal lobe (Figure 3, lower). At that time, the patient could walk with a cane, and he was
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Pre- and postoperative angiograms of the left internal carotid artery (ICA) in Case 5. Preoperative angiography demonstrated complete occlusion of the ICA (upper), and postoperative angiography revealed complete reperfusion of the left ICA and the ipsilateral anterior choroidal artery (lower). Left: antero-posterior views; right: lateral views
4
Pre- and postoperative computed tomography (CT) scans in Case 5. Preoperative CT scans revealed an old cortical infarction in the left frontal lobe (upper), and postoperative CT scans demonstrated a very small infarction in the left internal capsule with subdural effusion over the left frontal lobe (lower). R: right; L: left
3
transferred to another hospital for rehabilitation 65 days after onset.
Discussion Acute occlusion of the distal intracranial segment of the internal carotid artery causes sudden severe hemispheric ischemia. This type of arterial occlusion most often is embolic [34]. It may extend from the supraclinoid portion of the carotid siphon into the proximal segments of the anterior and middle cerebral arteries, thus obstructing not only the intracranial internal carotid artery bifurcation with the two major arteries that supply the cerebral hemisphere, but frequently also the ostia of the posterior communicating artery and the anterior choroidal artery as well as the lenticulostriate arteries. Such occlusion results in massive ischemic edema and infarction of the basal ganglia; internal
capsule; and the frontal, temporal, and parietal lobes; and sometimes the occipital lobe, and causes severe hemispheric neurologic syndrome. Neither the symptomatology of this type of stroke nor its natural course have received much attention in the literature. A few studies have shown that intracranial internal carotid artery stenosis is a dangerous lesion, and commonly leads to death caused by stroke [1,4,12]. The mortality of patients with middle cerebral artery occlusion has ranged in different studies from 5% to 45% [9,19,22]. This wide range of mortality rates can be explained by the lack of angiographic control and the inclusion of a wide variety of types of occlusions. A higher mortality rate has been found for patients with complete embolic intracranial internal carotid artery occlusion, particularly with inclusion of the middle cerebral artery trunk, which results in more severe and more extensive ischemic edema. For acute embolic occlusion of the ICA bifurcation, thrombolysis with intravenous or intraarterial administration of various thrombolytic drugs has proven to be ineffective [7]. The purpose of thrombolytic therapy for intracranial vascular occlusion is to preserve threatened cerebral tissue, not to repair tissue that is already damaged. After sudden embolic occlusion of a major cerebral artery, infarc-
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tion of cortical and subcortical structures can be prevented by rapid opening of the already occluded vessel. In one study, the mean rate of recanalization was 32% with intravenous alteplase and 63% with intraarterial urokinase or streptokinase for middle cerebral artery occlusion or basilar artery occlusion [30]. On the other hand, the mean rate of recanalization for intracranial carotid artery occlusion has been only 11% in previous studies [6,13, 17,24,27,33,35,36]. The latter value was much lower than those for the recanalization rates of the middle cerebral artery or basilar artery. Jansen et al, observed no delayed spontaneous recanalization in 32 patients with acute occlusion of the intracranial carotid artery bifurcation [7]. They explained the low recanalization rate for intracranial carotid artery bifurcation by the size and composition of the embolus lodged in the bifurcation. A large, organized, rigid clot probably occludes a large proximal vessel or the bifurcation itself. Small emboli or large soft emboli are capable of passing the internal carotid bifurcation and lodging at the middle cerebral artery bifurcation. The mortality rate for patients with acute occlusion of the internal carotid artery bifurcation was very high, 53.1% (17/32), in their study. Boysen et al., also reported that recanalization of the internal carotid artery may be even more difficult than that of the basilar artery, probably attributable to its length and lack of branching arteries, and the rate of partial recanalization was 56% [2]. The first report of the use of emergency embolectomy for acute occlusion of the middle cerebral artery was by Welch in 1956 [32]. Since then, 35 patients treated with emergency embolectomy for acute occlusion of the middle cerebral artery have been reported [10,11,14,20,23,26]. On the other hand, emergency embolectomy for acute occlusion of the internal carotid artery bifurcation has been reported in only one case, by Kakinuma et al [8]. That patient had no neurological deficits on discharge, and the time elapsed from onset of symptoms to completion of embolectomy was 4.5 h. In our study, two patients (33.3%) died of uncal herniation attributable to massive cerebral infarction with or without hemorrhage. The other four patients survived; their neurological scores were between 3 and 4 at discharge. The recanalization rate, angiographically confirmed, was 66.7% (4/6). However, it was thought to be 100% (6/6), because reperfusion could be observed intraoperatively even in the two patients who died of uncal herniation. The mortality rate (33.3%) for the embolectomy
Touho et al
procedure was not significantly lower than that (53.1%) for thrombolytic therapy reported by Jansen et al [7]. However, the 66.7% (4/6) recanalization rate for the embolectomy procedure was significantly higher than that (12.5%) for thrombolytic therapy reported by Jansen et al (Fisher’s exact probability test, p , 0.02). Jansen et al reported a post-thrombolytic therapy hemorrhage rate of 31.3% [7]. In the present study, only one patient suffered hemorrhagic complications postoperatively. However, no significant difference was found between these two values (Fisher’s exact probability test). Infusing thrombolytic material at both the proximal and distal ends of the embolus may better dissolve the embolus than infusing this material from the proximal end alone. However, Jansen et al reported that in only 30% of cases of occlusion at the internal carotid artery bifurcation could a microcatheter be passed beyond the area of the occlusion, and that this technique could therefore be used in only a minority of patients [7]. On the other hand, open embolectomy at the internal carotid artery bifurcation was achieved in all patients in our study. If circulation can be re-established within 6 h of the onset of symptoms, massive infarction can be avoided, and patients can survive. During surgery, nitrous oxide, fentanyl, isoflurane, and thiopental were used in these six patients. Michenfelder et al reported a significantly lower incidence of ischemic changes on electroencephalogram during carotid endarterectomy with isoflurane anesthesia (18%) than with either halothane (25%) or enflurane (26%) [16]. Despite the relatively few studies demonstrating the efficacy of barbiturates in protecting against temporary focal ischemia, we introduced continuous barbiturate administration for protection of ischemic brain and for decreasing intracranial pressure and cerebral edema [15,25]. In summary, sudden occlusion of the internal carotid artery bifurcation is a life-threatening event, and the rate of complete recanalization after open embolectomy obtained in the present study was much higher than that after endovascular thrombolytic therapy reported in previous studies. Open embolectomy can be performed when the time elapsed from onset of symptoms to reopening of the occluded vessel is less than 6 h. REFERENCES 1. Bogousslavsky J, Regli F. Prognosis of symptomatic intracranial obstruction of internal carotid artery. Eur Neurol 1983;22:351– 8.
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COMMENTARY
This is an interesting manuscript in which the authors demonstrate that emergency embolectomy for embolus to the internal carotid artery bifurcation can be performed in a timely fashion with reasonably good technical success. In their anecdotal experience, they were able to restore flow in four of six patients. It is their impression that restoration of flow did lead to improvement in neurological outcome. The rapid time between patient arrival to the emergency room, angiography, and surgical embolectomy is quite impressive.
In my experience, most emboli to the ICA bifurcation extend both proximally and distally up the middle cerebral artery. For this reason, it would be my tendency to refer the patient to interventional radiology for attempted intra-arterial thrombolysis. It seems that intra-arterial thrombolysis is able to achieve technical success with restoration of vessel patency in a high number of cases. Since the radiologist is already performing the diagnostic angiogram, the effort and required time to attempt intraarterial thrombolysis is not great. Fredric B. Meyer, M.D. Department of Neurologic Surgery Mayo Clinic Rochester, Minnesota
he ideology of market fundamentalism is profoundly and irredeemably flawed. To put the matter simply, market forces, if they are given complete authority even in the purely economic and financial arenas, produce chaos and could ultimately lead to the downfall of the global capitalist system. There is a widespread presumption that democracy and capitalism go hand in hand. In fact the relationship is much more complicated. Capitalism needs democracy as a counterweight because the capitalist system by itself shows no tendency toward equilibrium. The owners of capital seek to maximize their profits. Left to their own devices, they would continue to accumulate capital until the situation became unbalanced.
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—George Soros “The Crisis of Global Capitalism” (1998)
Touho H, Morisako T, Hashimoto Y, Karasawa J. Embolectomy for acute embolic occlusion of the internal carotid artery bifurcation. Surg Neurol 1999;51:313–20.
KEY WORDS
Cerebral infarction, embolism, internal carotid artery, embolectomy.
BACKGROUND
Acute occlusion of the distal intracranial segment of the internal carotid artery (ICA) causes sudden severe hemispheric ischemia. A low rate of recanalization and a high mortality rate for this condition have been noted, even with endovascular treatment. METHODS
We report the results of emergency embolectomy in six patients with acute embolic occlusion of the internal carotid artery (ICA) bifurcation. All six patients were admitted to our institute within 2 h of the onset of symptoms. Computed tomography (CT) scans on admission revealed no low-density or high-density regions in any patients. The time between onset of symptoms and completion of angiography ranged from 2 to 4 h (2.8 6 0.7 h). RESULTS
Emergency embolectomy was performed for each patient. Recanalization was confirmed angiographically in four of the patients. In the remaining two patients, massive infarction in the territory of the ICA was detected on the CT scans obtained the day of the operation, and postoperative angiography was not performed in these two cases. These two patients died of uncal herniation 6 days after onset. Two of the six patients were able to walk with a cane 2 months after surgery. The remaining two patients were unable to walk or attend to their own bodily needs without assistance. The time elapsed between onset of symptoms to reopening of the occluded vessel was within 6 h in the four surviving patients. The recanalization rate was 66.7% (4/6) for the embolectomy procedure, significantly higher than that (12.5%) of the thrombolytic therapy reported in a previous study. CONCLUSIONS
In summary, open embolectomy can be performed when the time after onset of symptoms is less than 6 h. © 1999 by Elsevier Science Inc.
Address reprint requests to: Dr. Hajime Touho, Department of Neurosurgery, Osaka Neurological Institute, 2-6-23 Shonai Takara-machi, Toyonaka, Osaka 561-0836 Japan. Received July 25, 1996; accepted June 23, 1997. © 1999 by Elsevier Science Inc. 655 Avenue of the Americas, New York, NY 10010
hromboembolic occlusion remains the most common cause of ischemic stroke [3]. Recent favorable clinical studies with thrombolytic agents have suggested that such agents may be useful for the treatment of acute stroke [6,18,29]. A few preliminary controlled safety studies have shown variable degrees of thrombolytic efficacy [31]. Based on these encouraging results, various multicenter randomized trials using intravenous tissue plasminogen activator (a relatively fibrin-specific agent) have begun and are now in progress [33]. Recent advances in techniques of intracranial vascular catheterization have made possible the direct delivery of thrombolytic agents intraarterially into a thrombus. Experimental studies have demonstrated that intraarterial administration produces more rapid thrombolysis at a lower dose than does intravenous administration [21]. Clinical cardiac thrombolysis studies suggest that intraarterial delivery may have less risk of systemic hemorrhagic complications [5]. Acute occlusion of the distal intracranial segment of the internal carotid artery (ICA) causes sudden severe hemispheric ischemia. A low rate of recanalization and a high mortality rate for this condition have been noted, even with endovascular treatment. We report here the results of emergency embolectomy for acute embolic occlusion of the internal carotid artery bifurcation.
T
Materials and Methods From July 1993 to February 1996, six patients with acute embolic occlusion of the ICA bifurcation were 0090-3019/99/$–see front matter PII S0090-3019(97)00423-0
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Summary of the Six Patients Treated by Emergency Embolectomy of the Internal Carotid Artery
CASE AGE NO. (YR) SEX 1
72
2
57
3
64
4
83
5
67
6
68
F
SYMPTOMS
lt hemiplegia, conjugate deviation of the eyes, stupor M rt hemiplegia, conjugate deviation of the eyes, stupor M lt hemiplegia, conjugate deviation of the eyes, stupor F lt hemiplegia, conjugate deviation of the eyes, stupor M rt hemiplegia, conjugate deviation of the eyes, stupor F rt hemiplegia, conjugate deviation of the eyes, stupor
ADMISSION OCCLUSION (HR) SIDE COLLATERALS
ELAPSED TIME POST-OP POST-OP (HR) COMPLICATIONS RS
2.0
rt
poor
6.0
massive infarction
6
2.0
lt
poor
7.0
6
1.5
rt
fair
6.0
1.0
rt
fair
5.0
0.5
lt
fair
6.0
massive hemorrhagic infarction cortical and subcortical infarction cortical and subcortical infarction subcortical infarction
1.0
lt
fair
5.5
cortical and subcortical infarction
3 4 3 4
RS, Rankin scale; op, operation; F, female; m, male; lt, left; rt, right.
treated with emergency embolectomy at the site of the occluded ICA. All six patients had atrial fibrillation at admission, and the embolic occlusion of the ICA was attributable to cardiogenic embolization. All six patients were admitted to our institute within 2 h of the onset of symptoms. Each patient’s neurological status was determined at admission, and after 4 weeks it was documented using the modified Rankin scale (RS0–RS5), scoring death as 6 [28]. Criteria for use of emergency embolectomy were as follows: 1. Sudden appearance of hemiparesis/hemiplegia with disturbance of consciousness and conjugate deviation of the eyes to the contralateral side of the hemipalsy. 2. Arrival at our institute within 6 h of the onset of symptoms. 3. No low- or high-density regions on pretreatment computed tomography (CT) studies. 4. Angiographic evidence of complete embolic occlusion of the internal carotid artery bifurcation. 5. Informed consent from the patient’s relatives. The first CT was performed a mean of 1.3 6 0.5 h after the onset of symptoms with a Quantex RX (Yokogawa Medical System, Tokyo, Japan) using a section thickness of 10 mm throughout the brain. No low- or high-density regions were found on the initial CT scans in any of the patients. Four-vessel selective cerebral angiography via the transfemoral artery was then performed. In each case, angiogra-
phy disclosed embolic occlusion of the internal carotid artery bifurcation. Angiographic collateral circulation patterns were classified using the following criteria: 1. Good: Almost all cortical branches (M4 segment) of the middle cerebral artery (MCA) were visualized, and the distal portion of the first segment of the MCA filled and emptied rapidly. 2. Fair: Cortical branches (M4 segment) could be visualized only slowly and/or partially. 3. Poor: Cortical branches (M4 segment) could not be visualized, or if they were, they remained so even during the late venous phase. Just after completion of the cerebral angiography, the second CT studies were performed, in which again no low- or high-density regions were found in any of the patients. The time between onset of symptoms and the completion of the angiography ranged from 2 to 4 hours (mean, 2.8 6 0.7 h). Emergency surgery with embolectomy was then performed in each case (Table 1). PREOPERATIVE NEUROLOGICAL STATUS AND ANGIOGRAPHICAL FINDINGS All six patients were stuporous with hemiplegia and conjugate deviation of the eyes to the side of the affected cerebral hemisphere on admission. Cere-
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Intraoperative photographs before (left) and after (right) embolectomy (Case 3). An embolus was found in the intradural segment of the right internal carotid artery (ICA) and the first segments of the anterior (A1) and middle cerebral arteries (M1). Temporary clips were placed on the right ICA (arrow), A1 (curved arrow), M1 (arrowhead), and the right posterior communicating artery (double arrowheads). Arteriotomy of the M1 segment was performed first, followed by the right ICA (left). After total removal of the embolus, the proximal arteriotomy was closed with 6-0 nylon interrupted sutures and the distal arteriotomy with 10-0 nylon interrupted sutures. Complete reperfusion was obtained (right).
1
bral angiography disclosed embolic occlusion of the ICA in all cases, and development of leptomeningeal collaterals was classified as poor in two cases (Cases 1 and 2) and as fair in the other four cases (Cases 3, 4, 5, and 6) (Table 1). GENERAL ANESTHESIA AND INTRAOPERATIVE CEREBRAL PROTECTION Operation was performed under general anesthesia. Nitrous oxide, narcotic (fentanyl), and volatile anesthetic (isoflurane) technique was used in all six patients. Anesthesia was maintained with nitrous oxide (50%), oxygen and isoflurane (0.5–2.0%), with repeated intravenous injections of fentanyl (50 –100 mg/hr). Thiopental was used for cerebral protection and for reducing intracranial pressure and cerebral edema [15,25]. Thiopental was continuously infused at a rate of 4 to 5 mg/kg/hr beginning just after induction of anesthesia, and continued for 24 to 48 h postoperatively. Systolic blood pressure was maintained over 100 mm Hg with or without intravenous infusion of dopamine (3– 6 mg/kg/min) for 24 to 48 h postoperatively. Hypothermia was not introduced for cerebral protection in the present study.
Operations A frontotemporal skin incision was performed followed by a frontotemporal craniotomy on the side of the occlusion of the ICA. The dura mater was
opened and the Sylvian fissure was then opened widely. In each case, an embolus was visible through the ICA, MCA, and the anterior cerebral artery (ACA), and those vessels were occluded from the supraclinoid segment of the ICA to the first segment of the ACA (A1 segment) and to the second segment of the MCA (M2 segment) in all patients except Case 3. In Case 3, the distal end of the embolus was found in the distal portion of the first segment of the MCA (M1 segment). Temporary clips were placed on the second segment of the ICA, the A1 segment, and the M2 segment in all patients except Case 3. In Case 3, distal clips were placed at the A1 segment and at the M1 segment (Figure 1, left). An arteriotomy one-quarter the circumference of the involved vessel(s) (bifurcation of the ICA and/or distal portion of the M1 segment) was then performed over the embolus. From these arteriotomies, a portion of the embolus was extracted using tumor forceps. Then the proximal clip was removed and a portion of the embolus was pulled out free with good bleeding via an arteriotomy, followed by placement of the proximal clip. If back-flow was encountered via the anterior choroidal and/or posterior communicating (Pcom) arteries, a new temporary clip(s) was placed at the anterior choroidal and/or Pcom arteries. The distal temporary clip was then removed and the rest of the embolus was milked free with good back-bleeding at the A1 and M1 segment, followed by placement of the distal clips. After total removal of the embolus, the proximal arteriotomy was then closed with 6-0 nylon
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Massive hemorrhagic infarction developed in Case 2 (left) and massive infarction in Case 1 (right).
2
interrupted sutures. The distal arteriotomy was closed with 10-0 nylon interrupted sutures (Figure 1, right). The total time elapsed from onset of symptoms to re-establishment of blood flow to the ipsilateral cerebral hemisphere ranged from 5 to 7 h (mean: 5.9 6 0.6 h) (Table 1). Postoperative angiography was performed 3 to 7 days after the operation for all patients except Cases 1 and 2. Follow-up CT scans were performed and neurological status was determined one month postoperatively.
Results Recanalization was confirmed angiographically in four of the patients (Cases 3, 4, 5, and 6). In the remaining two patients (Cases 1 and 2), massive infarction with or without hemorrhage in the territory of the ICA was detected on the CT scans obtained the day of the operation, and postoperative angiography was therefore not performed in these two cases. The recanalization rate in our study (66.7%) was significantly higher than that (12.5%) for thrombolytic therapy reported by Jansen et al [7] (Fisher’s exact probability test, p , 0.02). POSTOPERATIVE CT FINDINGS AND CLINIAL OUTCOME Case 1 suffered massive infarction postoperatively and died of uncal herniation six days after onset (Figure 2, right). Case 2 suffered hemorrhagic infarction postoperatively and died of uncal herniation 6 days after onset (RS6) (Figure 2, left). Two patients (Cases 3 and 5) had evidence of cortical and/or subcortical infarction on CT scans 1 month
after surgery. However, they were able to walk with a cane 2 months after surgery (RS3). Cases 4 and 6 also had evidence of cortical and subcortical infarction on follow-up CT scans, and were unable to walk or attend to their own bodily needs without assistance (RS4) (Table 1). ILLUSTRATIVE CASE CASE 5. A 67-year-old man was admitted to our institute for sudden onset of right hemiplegia, conjugate deviation of the eyes to the contralateral side of the palsy, and stupor. The time elapsed between the onset of symptoms and admission was 0.5 h. CT scans were performed immediately and disclosed no abnormalities except a small and old cortical infarction in the left frontal lobe (Figure 3, upper). Cerebral angiography disclosed an embolic occlusion of the left ICA with fair collateralization (Figure 4, upper). The second set of CT scans were obtained just after completion of the angiography, and disclosed no additional abnormalities. Emergency embolectomy was performed, and reestablishment of the cerebral circulation in the left cerebral hemisphere was achieved 6.0 h after the onset of ischemic symptoms. Three days after the operation, he regained normal consciousness and could lift his right upper and lower extremities. Postoperative angiography revealed complete establishment of reperfusion via the left ICA 3 days after onset (Figure 4, lower). Follow-up CT scans performed 2 months after onset revealed a very small low-density region in the left internal capsule with subdural effusion over the left frontal lobe (Figure 3, lower). At that time, the patient could walk with a cane, and he was
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Pre- and postoperative angiograms of the left internal carotid artery (ICA) in Case 5. Preoperative angiography demonstrated complete occlusion of the ICA (upper), and postoperative angiography revealed complete reperfusion of the left ICA and the ipsilateral anterior choroidal artery (lower). Left: antero-posterior views; right: lateral views
4
Pre- and postoperative computed tomography (CT) scans in Case 5. Preoperative CT scans revealed an old cortical infarction in the left frontal lobe (upper), and postoperative CT scans demonstrated a very small infarction in the left internal capsule with subdural effusion over the left frontal lobe (lower). R: right; L: left
3
transferred to another hospital for rehabilitation 65 days after onset.
Discussion Acute occlusion of the distal intracranial segment of the internal carotid artery causes sudden severe hemispheric ischemia. This type of arterial occlusion most often is embolic [34]. It may extend from the supraclinoid portion of the carotid siphon into the proximal segments of the anterior and middle cerebral arteries, thus obstructing not only the intracranial internal carotid artery bifurcation with the two major arteries that supply the cerebral hemisphere, but frequently also the ostia of the posterior communicating artery and the anterior choroidal artery as well as the lenticulostriate arteries. Such occlusion results in massive ischemic edema and infarction of the basal ganglia; internal
capsule; and the frontal, temporal, and parietal lobes; and sometimes the occipital lobe, and causes severe hemispheric neurologic syndrome. Neither the symptomatology of this type of stroke nor its natural course have received much attention in the literature. A few studies have shown that intracranial internal carotid artery stenosis is a dangerous lesion, and commonly leads to death caused by stroke [1,4,12]. The mortality of patients with middle cerebral artery occlusion has ranged in different studies from 5% to 45% [9,19,22]. This wide range of mortality rates can be explained by the lack of angiographic control and the inclusion of a wide variety of types of occlusions. A higher mortality rate has been found for patients with complete embolic intracranial internal carotid artery occlusion, particularly with inclusion of the middle cerebral artery trunk, which results in more severe and more extensive ischemic edema. For acute embolic occlusion of the ICA bifurcation, thrombolysis with intravenous or intraarterial administration of various thrombolytic drugs has proven to be ineffective [7]. The purpose of thrombolytic therapy for intracranial vascular occlusion is to preserve threatened cerebral tissue, not to repair tissue that is already damaged. After sudden embolic occlusion of a major cerebral artery, infarc-
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tion of cortical and subcortical structures can be prevented by rapid opening of the already occluded vessel. In one study, the mean rate of recanalization was 32% with intravenous alteplase and 63% with intraarterial urokinase or streptokinase for middle cerebral artery occlusion or basilar artery occlusion [30]. On the other hand, the mean rate of recanalization for intracranial carotid artery occlusion has been only 11% in previous studies [6,13, 17,24,27,33,35,36]. The latter value was much lower than those for the recanalization rates of the middle cerebral artery or basilar artery. Jansen et al, observed no delayed spontaneous recanalization in 32 patients with acute occlusion of the intracranial carotid artery bifurcation [7]. They explained the low recanalization rate for intracranial carotid artery bifurcation by the size and composition of the embolus lodged in the bifurcation. A large, organized, rigid clot probably occludes a large proximal vessel or the bifurcation itself. Small emboli or large soft emboli are capable of passing the internal carotid bifurcation and lodging at the middle cerebral artery bifurcation. The mortality rate for patients with acute occlusion of the internal carotid artery bifurcation was very high, 53.1% (17/32), in their study. Boysen et al., also reported that recanalization of the internal carotid artery may be even more difficult than that of the basilar artery, probably attributable to its length and lack of branching arteries, and the rate of partial recanalization was 56% [2]. The first report of the use of emergency embolectomy for acute occlusion of the middle cerebral artery was by Welch in 1956 [32]. Since then, 35 patients treated with emergency embolectomy for acute occlusion of the middle cerebral artery have been reported [10,11,14,20,23,26]. On the other hand, emergency embolectomy for acute occlusion of the internal carotid artery bifurcation has been reported in only one case, by Kakinuma et al [8]. That patient had no neurological deficits on discharge, and the time elapsed from onset of symptoms to completion of embolectomy was 4.5 h. In our study, two patients (33.3%) died of uncal herniation attributable to massive cerebral infarction with or without hemorrhage. The other four patients survived; their neurological scores were between 3 and 4 at discharge. The recanalization rate, angiographically confirmed, was 66.7% (4/6). However, it was thought to be 100% (6/6), because reperfusion could be observed intraoperatively even in the two patients who died of uncal herniation. The mortality rate (33.3%) for the embolectomy
Touho et al
procedure was not significantly lower than that (53.1%) for thrombolytic therapy reported by Jansen et al [7]. However, the 66.7% (4/6) recanalization rate for the embolectomy procedure was significantly higher than that (12.5%) for thrombolytic therapy reported by Jansen et al (Fisher’s exact probability test, p , 0.02). Jansen et al reported a post-thrombolytic therapy hemorrhage rate of 31.3% [7]. In the present study, only one patient suffered hemorrhagic complications postoperatively. However, no significant difference was found between these two values (Fisher’s exact probability test). Infusing thrombolytic material at both the proximal and distal ends of the embolus may better dissolve the embolus than infusing this material from the proximal end alone. However, Jansen et al reported that in only 30% of cases of occlusion at the internal carotid artery bifurcation could a microcatheter be passed beyond the area of the occlusion, and that this technique could therefore be used in only a minority of patients [7]. On the other hand, open embolectomy at the internal carotid artery bifurcation was achieved in all patients in our study. If circulation can be re-established within 6 h of the onset of symptoms, massive infarction can be avoided, and patients can survive. During surgery, nitrous oxide, fentanyl, isoflurane, and thiopental were used in these six patients. Michenfelder et al reported a significantly lower incidence of ischemic changes on electroencephalogram during carotid endarterectomy with isoflurane anesthesia (18%) than with either halothane (25%) or enflurane (26%) [16]. Despite the relatively few studies demonstrating the efficacy of barbiturates in protecting against temporary focal ischemia, we introduced continuous barbiturate administration for protection of ischemic brain and for decreasing intracranial pressure and cerebral edema [15,25]. In summary, sudden occlusion of the internal carotid artery bifurcation is a life-threatening event, and the rate of complete recanalization after open embolectomy obtained in the present study was much higher than that after endovascular thrombolytic therapy reported in previous studies. Open embolectomy can be performed when the time elapsed from onset of symptoms to reopening of the occluded vessel is less than 6 h. REFERENCES 1. Bogousslavsky J, Regli F. Prognosis of symptomatic intracranial obstruction of internal carotid artery. Eur Neurol 1983;22:351– 8.
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COMMENTARY
This is an interesting manuscript in which the authors demonstrate that emergency embolectomy for embolus to the internal carotid artery bifurcation can be performed in a timely fashion with reasonably good technical success. In their anecdotal experience, they were able to restore flow in four of six patients. It is their impression that restoration of flow did lead to improvement in neurological outcome. The rapid time between patient arrival to the emergency room, angiography, and surgical embolectomy is quite impressive.
In my experience, most emboli to the ICA bifurcation extend both proximally and distally up the middle cerebral artery. For this reason, it would be my tendency to refer the patient to interventional radiology for attempted intra-arterial thrombolysis. It seems that intra-arterial thrombolysis is able to achieve technical success with restoration of vessel patency in a high number of cases. Since the radiologist is already performing the diagnostic angiogram, the effort and required time to attempt intraarterial thrombolysis is not great. Fredric B. Meyer, M.D. Department of Neurologic Surgery Mayo Clinic Rochester, Minnesota
he ideology of market fundamentalism is profoundly and irredeemably flawed. To put the matter simply, market forces, if they are given complete authority even in the purely economic and financial arenas, produce chaos and could ultimately lead to the downfall of the global capitalist system. There is a widespread presumption that democracy and capitalism go hand in hand. In fact the relationship is much more complicated. Capitalism needs democracy as a counterweight because the capitalist system by itself shows no tendency toward equilibrium. The owners of capital seek to maximize their profits. Left to their own devices, they would continue to accumulate capital until the situation became unbalanced.
T
—George Soros “The Crisis of Global Capitalism” (1998)