Urgent Carotid Artery Repair: Retrospective Study of 21 Cases

Original Articles

Urgent Carotid Artery Repair: Retrospective Study of 21 Cases Jean-Luc Gay, MD, Alain Curtil, MD, Sabine Buf®ere, MD, Jean-Pierre Favre, MD, and Xavier Barral, MD, Saint Etienne, France

The purpose of this retrospective study was to assess the outcome of urgent surgical repair in patients with symptomatic carotid artery lesions. The study population included 21 patients who underwent carotid artery repair less than 24 hr after diagnostic work-up. Indications included crescendo transient ischemic attacks in 5 cases, ¯uctuating neurological de®cits in 11, and stroke in evolution in 5. Immediate mortality was 9.5%. Mean follow-up was 55 months. Actuarial survival rates at 1 and 5 years were 90% and 62%, respectively. Actuarial neurological de®citfree rates at 1 and 5 years were 95% and 76%, respectively. The results of this study document the effectiveness of urgent carotid artery repair for treatment of acute cerebral ischemia. Although higher than elective surgery, morbidity and mortality are acceptable, given the severity of illness in this patient population.

INTRODUCTION In 1969 the Joint Study of Extracranial Arterial Occlusion showed that urgent carotid artery repair was associated with a morbidity/mortality rate of 42%.1 Poor outcome was attributed to progression of symptoms from focal ischemic to extensive hemorrhagic cerebral infarction, especially in patients with stroke in evolution.2 On the basis of these ®ndings, use of urgent carotid artery repair in patients presenting with acute neurological attacks was limited to only a few indications. With major progress in cerebrovascular imaging technology in the 1980s and 1990s and in particular with the advent of cerebral CT scanning,3 the issue of urgent carotid artery repair has resurfaced. This retrospective study was undertaken in an efService de Chirurgie Cardiovasculaire, HoÃpital Nord, Centre Hospitaller Universitaire, Saint Etienne, France. Correspondence to: J.L. Gay, MD, Service de Chirurgie Cardiovasculaire, HoÃpital Nord, 42055 Saint Etienne CeÂdex 2, France. Ann Vasc Surg 2002; 16: 401±406 DOI: 10.1007/s10016-001-0227-0 Ó Annals of Vascular Surgery Inc. Published online: 3 July 2002

fort to gain further insight into the indications for urgent carotid artery repair. The ®les of 21 patients treated within 24 hr after diagnostic work-up for transient ischemic attacks or stroke related to carotid artery occlusion in the Cardiovascular Surgery Department of the Saint Etienne University Hospital Center were reviewed.

PATIENTS AND METHODS From January 1, 1983 to December 31, 1997, a total of 1339 carotid endarterectomy procedures were performed in the Cardiovascular Surgery Department of the Saint Etienne University Hospital Center. In this series, 21 patients (1.6%) were treated urgently, i.e., within 24 hr after diagnostic work-up. Patients requiring re-intervention due to postoperative ischemic attacks were excluded from study. There were 13 men (61.9%) and 8 women (38.1%). Mean age was 69.7 years (range, 51.4 to 82.8 years). Habitual risk factors for atherosclerosis were observed in 20 patients. Concurrent conditions included respiratory insuf®ciency in 11 401

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Annals of Vascular Surgery

Table I. Arterial involvement

Normal Stenosis <75% Stenosis 75-95% Stenosis >95% Occlusion Ulceration Aneurysm Unknown

Treated carotid artery

Contralateral carotid artery

Ipsilateral vertebral artery

Contralateral vertebral artery

0 0 3 11 3 4 0 0

10 2 2 0 4 0 1 2

13 3 1 0 0 0 0 4

15 2 0 0 0 0 0 4

patients, coronary artery disease in 7, obesity in 6, and renal insuf®ciency (creatinine level >250 l/L) in 2 patients. The mean number of cardiovascular risk factors was two per patient. The mean number of morbidity factors was 1.6 per patient. Nineteen patients (90.5%) never undergone previous cardiovascular surgery. Three had undergone previous cardiovascular surgery, including respectively aortic repair, coronary bypass, and bilateral carotid surgery, in whom urgent carotid artery repair was performed for restenosis. All patients were symptomatic. Indications for emergency carotid artery repair were classi®ed into three groups. Crescendo transient ischemic attacks were the indication in ®ve patients (23.8%). In this group, treatment was undertaken within at least 24 hr after appearance of the ®rst de®cit embolic event and all patients recovered fully. Fluctuating neurological de®cit was the indication in 11 cases (52.4%), including 2 patients with disturbances of consciousness. Stroke in evolution was the indication for emergency carotid artery repair in ®ve cases (23.8%). All patients in this group were hospitalized at the time of stroke for severe urinary infection (n = 1) or diagnostic work-up for carotid artery disease (n = 4). The diagnostic procedure being performed at the time of stroke was angiography of the supraaortic vessels in three patients and Doppler ultrasonography of the neck in one. In all cases occurrence of stroke within the hospital setting allowed rapid intervention. These ®ve cases can be considered a high-risk subgroup since three patients presented with disturbances of consciousness. Overall, 5 of the 21 patients in this series (23.8%) had neurological manifestations during arteriography and 5 had disturbances of consciousness at the time of emergency carotid artery repair. Since carotid artery repair was undertaken urgently, full diagnostic work-up, including Doppler ultrasound of the neck, arteriography of the supraaortic vessels, and cerebral CT scan, could not be performed in every case. Diagnostic work-up in-

cluded Doppler ultrasound of the neck in 15 cases (71.4%) and arteriography of the supraaortic vessels in 18 (85.7%). Incomplete work-up explains the missing data for four cerebral artery vessels presented in Table I. Preoperative CT scanning was performed in only 15 cases (71.4%) with injection of contrast material in 4 cases (26.6%) and without contrast injection in 11 (73.3%). Cerebral infarction was noted in 13 cases (86.7%). In two cases (13.3%), cerebral CT scan ®ndings were considered normal or to show evidence of previous ischemic events. All procedures were carried out under general anesthesia with monitoring of arterial blood pressure. The internal carotid artery was exposed beneath the digastric muscle. The carotid bulb was dissected after heparinization by the systemic route at a dose of 1 mg/kg. As a precaution against embolization during dissection, a clamp was placed on the internal carotid artery. In three patients, opening of the artery revealed the presence of thrombosis. The repair procedure was endarterectomy in 16 cases, including 4 with patch closure, venous bypass in 3 cases, and prosthetic bypass in 2 cases. A Javid shunt was used for cerebral protection in nine cases (42.8%). Assessment of outcome was based on follow-up control examinations and contact with the attending physician or the family, especially if the patient had died. Outcome was assessed for the immediate postoperative period de®ned as the ®rst month after surgery and for the late period up until January 30, 1998 or until the date of death. Data on survival, neurological events, and patency were studied directly and then analyzed using actuarial curves according to the Kaplan-Meier method.

RESULTS Immediate mortality within the ®rst month after emergency carotid artery repair was 9.5% (2/21). The causes of death were rupture of the carotid

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Fig. 1. Actuarial survival curve.

suture line, induced by coughing 12 hr after carotid repair in an unprepared smoker (n = 1), and major lung congestion in a patient who had hemiplegia with disturbances of consciousness that did not resolve after the procedure (n = 1). One patient was lost from follow-up. Mean follow-up was 55 months (range, 1 to 148 months). During long-term follow-up, 9 of the 19 patients (47.3%) who were alive at the end of the postoperative period died. The mean duration of survival for these patients was 61 months. No death was related to carotid artery repair. The actuarial survival curve is shown in Figure 1. Neurological status was evaluated upon recovery from anesthesia, at 1 month after surgery, and at the end of follow-up. Upon recovery from anesthesia, 6 patients (28.6%) were stable and presented no change in neurological status in comparison with status prior to induction of anesthesia. Partial or full resolution of neurological de®cits was observed in seven (33.3%) and ®ve (23.8%) patients, respectively. In the remaining three patients, neurological status worsened. Neurological deterioration was attributed to clamping in one of these patients and reoperation was not undertaken. In the other two patients, reoperation revealed no evidence of technical defect. Worsening was attributed to reperfusion edema, which responded to treatment with mannitol and corticosteroids. The morbidity rate upon recovery from anesthesia was 14.3%. At 1 month after surgery, no deterioration of neurological status was noted in any of the 19 surviving patients, and no further neurological morbidity occurred. Of the 15 patients who presented with de®cits prior to surgery, partial or total recovery was observed in 6 and 9 patients, respectively. At the end of follow-up (mean duration, 55 months), all surviving patients underwent Doppler ultrasound which showed no thrombosis in the treated carotid artery. One patient suffered infarc-

Urgent carotid artery repair 403

Fig. 2. Actuarial neurological event±free curve.

tion in the posterior region of the brain at 46 months, which was attributed to ulceration in the left vertebral artery. This patient was treated by direct reimplantation of the vertebral artery into the common carotid artery. One patient had a transient ischemic attack with aphasia at 59 months. Angiography demonstrated high-grade stenosis of the operated carotid artery, which was treated by a vein graft from the common carotid to the left internal carotid. One patient suffered a stroke at 8 months in the region supplied by the operated carotid artery. Diagnostic work-up show no abnormality involving the surgically treated segment. Overall, one stroke related to urgent carotid repair occurred during follow-up in this study. Another stroke occurred in the area supplied by the surgically treated carotid artery but was not related to surgery. The third stroke observed during follow-up did not occur in the area supplied by the treated carotid artery. Thus, in this series, 76.2% of patients had neurological de®cits at the time of induction of anesthesia and 66.6% were asymptomatic at the time of death or end of follow-up. The actuarial neurological de®cit±free curve is shown in Figure 2.

DISCUSSION Urgent repair has been used in situations involving ongoing carotid artery disease processes that threaten to cause irreversible destruction of cerebral parenchyma in the minutes or hours following diagnosis. Since this strategy supposes a demonstrable relation between the symptoms and carotid lesion, all candidates present with neurological manifestations.4 Indications can be classi®ed into three main groups: crescendo transient ischemic attacks, ¯uctuating neurological de®cits, and stroke in evolution. Crescendo transient ischemic attacks are generally related to carotid artery lesions associated with

404 Gay et al.

embolic events. The purpose of emergency repair in these cases is to suppress the source of emboli. Reported outcomes5-10 have validated the usefulness of this treatment strategy in this situation, which is considered a compelling indication by most authors. Delay is dangerous because repeated transient ischemic attacks result in an unstable neurological status with a constant high risk of frank stroke. Fluctuating neurological de®cit and stroke in evolution are the two other situations in which emergency carotid artery repair may be used. In both cases, the goal of surgery is to stabilize the patient by removing the threat of ischemia. However the relative roles of functional ischemia and ischemia-related necrosis in determining the de®cit are not quanti®able in daily practice. Differentiation of these two mechanisms has obvious implications for surgical indications and for assessment of outcome. In patients with functional ischemia, surgical repair can reestablish normal tissue perfusion and thus correct oligemia. The risk of reperfusion can be controlled by maintaining blood pressure at safe levels. In patients with ischemicrelated necrosis of brain tissue, prognosis is less favorable, with little or no likelihood of recovery and an enhanced risk of deterioration after reperfusion. In this regard, CT scanning has no predictive value.5,6,8,11,12 Although it is dif®cult to compare results from various reports including this type of indication and there are no large randomized series, authors tend to agree on the following points: (1) patients suffering ongoing attacks with moderate de®cits are acceptable candidates for urgent carotid artery repair, even if the CT scan depicts infarction5,6,8,11,12 (2) patients suffering ongoing attacks with severe de®cits should be evaluated on a case-by-case basis; and (3) patients suffering a frank stroke with severe immediate symptoms probably have ischemia-related necrosis of cerebral tissue and thus are beyond the reach of urgent carotid artery repair. It should be recalled, however, that the mean time between cerebral artery occlusion and brain infarction in humans is 6 hr.13 In this race against the clock, two factors besides the speed of intervention could argue against surgical treatmentÐdisturbances in consciousness12 and detection of distal lesions, if angiography 1 can be performed. Thus time to possible infarction, which may be dif®cult to ascertain with certainty, is not the only criterion to be taken into account in 2 deciding on treatment for these patients. In this series, Doppler ultrasound of the neck and/or arteriography of the supraaortic vessels were used to document the implication of the carotid artery lesion in cerebral hypoperfusion and

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the CT scan was used to assess the state of the brain parenchyma. The effectiveness of CT scanning in an emergency setting is limited. In the future, more reliable assessment of brain parenchyma will probably be achieved using MRI with diffusion/ perfusion,14 which allows accurate determination of the extent of brain damage at an early stage. Use of this technique should enable more ef®cient selection of surgical indications. From a technical standpoint, several points should be emphasized. In our opinion, general anesthesia provides better brain oxygenation in an emergency setting. However, this preference is purely conjectural. Administration of heparin has not been correlated with a more favorable outcome in patients with progressing ischemic attacks. However, since heparin does not increase the risk of cerebral hemorrhage, administration appears advisable in patients presenting with stroke in evolution or ¯uctuating neurological de®cit, provided that hemorrhage has been ruled out by CT scan.15 Conversely, heparin administration should be discontinued in the postoperative period to avoid promoting hemorrhagic transformation. Routine systemic administration of mannitol and corticosteroids lowers the risk of brain swelling, which is much greater after surgical treatment that reestablishes perfusion immediately than after medical treatment.16 Shunt placement has three theoretical advantages. The ®rst is to shorten the duration of brain ischemia. The second is to permit more progressive cerebral reperfusion by limiting the initial ¯ow ac3 cording to shunt diameter. The third is to avoid barotrauma due to overloading when the clamp is removed.17 Reports in the literature offer con¯icting evidence on the value of shunt placement.5,8,17-19 Despite the lack of consensus, shunting seems to be a necessary precaution if the carotid artery is patent. In patients with acute occlusion (three cases in this series), spontaneous retrograde ejection of thrombus through the arteriotomy may occur due to re¯ux from the intracranial internal carotid artery. Spontaneous ejection is a sign of good residual pressure and of patency of the circle of Willis. Intraoperative arteriography should nevertheless be performed to rule out the presence of nonoccluding residual mural thrombus, which might produce emboli when the ¯ow is restored, and to evaluate branches of the internal carotid artery. Intraoperative arteriography is also important to detect residual mural thrombus in the circle of Willis or occlusion in the middle cerebral arteries. Either of these ®ndings may be an indication for thrombolysis in addition to proximal repair. The main

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arguments for in situ thrombolysis are immediate removal of thrombus, lower ®brinolytic agent dose requirements, and performance of concomitant arteriography to assess quality of distal runoff. The major argument against thrombolysis is enhancement of the risk of hemorrhage when ¯ow is reestablished in the carotid artery. In our opinion, thrombolysis is warranted if intraoperative arteriography demonstrates distal occlusion. Our technique consists in injecting 250,000 IU of streptokinase at the end of the procedure and repeating arteriography after a 20-min waiting period. If residual thrombus is found, we reinject a single dose and stop if arteriographic recovery is not achieved. Discontinuation of heparin is mandatory after revascularizaton. The patient should remain in the intensive care unit under general anesthesia with a systolic arterial pressure setting not exceeding 100 mmHg for at least 12 hr. The pitfalls and limitations of surgical treatment and the current trend toward noninvasive procedures have encouraged the use of intravenous ®brinolysis. Since 1995, several controlled trials have been carried out to study the ef®cacy of intravenous thrombolysis for management of acute ischemic stroke (MAST-I, MAST-E, ASK, ECASS, NINDS, ATLANTIS, ECASS 2). Morbidity and mortality rates (persistent handicap or death) have generally been >45%. All but one study (ECASS 2) showed a signi®cant increase in the incidence of symptomatic cerebral hemorrhage. Only one study (NINDS) documented the ef®cacy of intravenous thrombolysis in comparison to a placebo group.13,20 Since these trials included ischemic stroke resulting from a wide range of causes, comparison with our study, which included only stroke related to carotid artery disease, is dif®cult. Another difference is that intravenous thrombolysis is used in patients suffering from frank stroke rather than transient ischemic attacks. Only 16 patients in our series would have been candidates for intravenous thrombolysis. A major drawback of thrombolysis is leaving the carotid artery lesion in place. Use of the combination of carotid endarterectomy and in situ thrombolysis to reduce hemorrhagic risk is a new option for single-stage emergency treatment of stroke from carotid artery stenosis associated with distal occlusion, which has a poor prognosis if left in place.21

CONCLUSION This study con®rms the ef®cacy of emergency carotid artery repair in patients presenting with cre-

Urgent carotid artery repair 405

scendo transient ischemic attacks. The goal is to eliminate the cause of emboli and/or reduced cerebral blood ¯ow. Our ®ndings also indicate that emergency repair is justi®ed for lesions causing progressive, continuous, or ¯uctuating neurological de®cits not accompanied by disturbances of consciousness and/or extensive cerebral infarction documented by CT scan. The goal of surgery is to stabilize the patient by removing the threat of ischemia. The indication for emergency repair in patients suffering a stroke in evolution with immediately severe manifestations depends on the delay between the onset of clinical symptoms and surgery, which must be less than 6 hr, and on the presence or absence of disturbance of consciousness. Coma is a contraindication. In practice, these severe situations are rare, accounting for only 1.6% of the procedures in our series. Ideally, treatment should be started immediately on a multidisciplinary basis. REFERENCES 1. Blaisdell FW, Clauss RH, Gailbraith JG, Smith JA Jr. Joint Study of Extracranial Carotid Artery Occlusion. IV. Review of surgical considerations. JAMA 1969;209:1889-1895. 2. Mead GE, Murray H, Farrel A, et al. Pilot study of carotid surgery for acute stroke. Br J Surg 1997;84:990-992. 3. Barral X, Youvarlakis P, Chbib MA, et al. La chirurgie d'urgence dans les leÂsions atheÂromateuses carotidiennes. Arteres Veines 1987;6:43-46. 4. Koskas F, Samson Y, Rancurel G, Kieffer E. Chirurgie carotidienne d'urgence pour leÂsions non traumatiques. In: Kieffer E, ed. Urgences Vasculaires Non Traumatiques. Paris: AERCV 1998, pp 385-393. 5. Goldstone J, Effeney DJ. R^ ole de l'rendarteÂriectomie carotidienne dans le traitement des de®cits neurologiques aigus. Acquisitions Nouv Pathol Cardiovasc 1980;22:705719. 6. Mentzer RM, Finkelmeier BA, Crosby YK, Wellons HA. Emergency carotid endarterectomy for ¯uctuating neurologic de®cits. Surgery 1981;89:60-61. 7. Welling RE, Cranley JJ, Krause RJ, et al. Surgical therapy for recent total occlusion of the internal carotid artery. J Vasc Surg 1984;1:57-61. 8. Greenhalgh RM, Cuming R, Perkin GD, Mc Collum CN. Urgent carotid surgery for high risk patients. Eur J Vasc Surg 4 1993;7(Suppl A):25±32. 9. Wilson SE, Mayberg MR, Yatsu F, Weiss DG, and the Veterans Affairs Trialists. Crescendo transient ischemic attacks: a surgical imperative. J Vasc Surg 1993;17:249-256. 10. Gertler JP, Blankensteijn JD, Brewster DC, et al. Carotid endarterectomy for unstable and compelling neurologic conditions: do results justify an aggressive approach? J Vasc Surg 1994;19:32-42. 11. Benes V Jr. Emergency internal carotid artery desobliteration in patients with severe neurological de®cit. Zentralbl Neurochir 1987;48:1-8. 12. Eckstein HH, Schumacher H, Ringleb P, Allenberg JR. Indications de la chirurgie carotidienne chez les patients avec un eÂtat neurologique instable. In: Branchereau A, Jacobs

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