- Email: [email protected]
The Incidence of Ischemic Stroke versus Intracerebral Hemorrhage after Carotid Endarterectomy: A Review of 2452 Cases
Clinical Research The Incidence of Ischemic Stroke versus Intracerebral Hemorrhage after Carotid Endarterectomy: A Review of 2452 Cases Peter V. Wilson, MD, and Alex D. Ammar, MD, Wichita, Kansas
Carotid endarterectomy is a frequently performed vascular procedure. The most common major perioperative neurologic complication is ischemic stroke. Intracerebral hemorrhage has been traditionally viewed as less common. It has been recently proposed that as technical advances are made, the rate of ischemic stroke and other complications has decreased, causing hemorrhagic stroke to attain increasing importance as a perioperative complication. A review of 2452 consecutive endarterectomies performed by a single surgeon from 1983 to 2000 was performed and rates of ischemic and hemorrhagic strokes were analyzed. There were five hemorrhagic strokes for a rate 0.20% (13.5% of postoperative neurologic complications) and 32 with ischemic strokes for a rate of 1.31% (86.5% of postoperative neurologic complications). From these data we conclude that hemorrhagic stroke remains uncommon and ischemic stroke continues to be the most frequent cause of postoperative neurologic complication after carotid endarterectomy.
INTRODUCTION Carotid endarterectomy (CEA) is a commonly performed vascular procedure with a reported 108,275 cases performed in 1996.1 It has been shown to be beneficial therapy for the treatment of carotid stenosis.2,3 The perioperative complications of CEA include ischemic stroke, intracerebral hemorrhagic stroke (IHS), myocardial infarction, hematoma, infection, cranial nerve injury, and death. The most common perioperative major neurologic complication is ischemic stroke, with rates ranging from 1.8 to 14.5% over the last 30 years.4,5 Recently, the perioperative ischemic stroke rate for asymptomatic patients has been reported to be 0.5-1.4%.4,6 Reported rates of IHS have been 0.41-0.75%.6-10 Ouriel et al.6 reported an increased relative rate of IHS versus ischemic Department of Surgery, University of Kansas School of Medicine– Wichita, Wichita, KS. Correspondence to: Alex D. Ammar, MD, University of Kansas School of Medicine–Wichita, 818 N. Emporia, Suite 200, Wichita, KS 67214, USA, E-mail: [email protected] Ann Vasc Surg 2005; 19: 1-4 DOI: 10.1007/s10016-004-0131-5 Ó Annals of Vascular Surgery Inc. Published online: January 11, 2005
stroke and proposed that as advances in perioperative management and operative technique improved overall morbidity and mortality, IHS would attain increasing importance as a perioperative complication. The purpose of this study was to quantify the rates of perioperative ischemic strokes and IHS in a single surgeonÕs experience.
PATIENTS AND METHODS A written log of consecutive CEAs performed by a single surgeon from 1983 to 2000 was reviewed. This log contained patient name, date of operation, operation performed, and complications suffered. The total number of operations was quantified, as were the number of perioperative ischemic and hemorrhagic strokes. Outpatient clinic and hospital charts of patients experiencing these complications were reviewed and data including age, gender, percent ipsilateral and contralateral stenosis, incidence of coronary artery disease, hypertension, diabetes, history of smoking, previous stroke, and severity of perioperative stroke rate were recorded. All patients had either preoperative carotid arteriography or duplex ultrasound. The degree of 1
2 Wilson and Ammar
Annals of Vascular Surgery
Table I. Comparison of age, comorbidities, carotid stenosis rates, and mortality for patients suffering intracerebral hemorrhage or ischemic strokea Parameter
Intracerebral hemorrhage group
Ischemic stroke group
p
Patients (n) Age (years) Comorbidities Coronary artery disease Hypertension Diabetes Smoking history Previous cerebrovasular accident Degree of carotid artery stenosis Contralateral stenosis Ipsilateral stenosis Death
5 59.8 ± 8.9b
32 69.6 ± 8.9
0.0294
1 4 0 3 0
16 20 13 14 11
0.211 0.446 0.077 0.498 0.159
a
(20) (80) (0) (60) (0)
36% 90% 5 (100)
(50) (63) (41) (44) (34)
39% 72% 4 (13)
0.9056 0.0734 0.001
Data are numbers with percents in parentheses, except where indicated. Mean ± SD.
b
stenosis on arteriogram was calculated by subtracting from one, the ratio of the narrowest diameter at the stenosis to the diameter of the internal carotid artery distal to the stenosis, and multiplying by 100, similar to the method used in the North American Symptomatic Carotid Endarterectomy Trial (NASCET) Collaborators.11 The degree of stenosis was calculated using color duplex sonography in conjunction with internal carotidto-common carotid artery velocity ratios. In all patients with history of prior stroke, endarterectomy was delayed for at least 3 weeks from the time of the stroke, this interval depending on patientÕs clinical status (i.e., resolution of symptoms, degree of stenosis). The operations were performed under general anesthesia. Anticoagulation was attained using heparin (1.5 mg/kg) with partial reversal with protamine. Shunting was used for stump pressures of <50 mmHg, history of previous stroke, or contralateral carotid occlusion. Patch angioplasty with Hema-Shield knitted double-velour Dacron (Meadox, Boston Scientific, Wayne, NJ) was used on redo operations or for small carotid arteries, especially females or young patients with premature atherosclerosis. Low-molecular-weight Dextran was routinely infused intraoperatively and postoperatively since 1991, and all patients were placed on aspirin unless they had aspirin allergy or sensitivity. Postoperative intensive care (ICU) was routinely used prior to 1992. Subsequently, patients were followed in the recovery room for 2 hr and a decision was made regarding the need for ICU admission, usually for hypotension or hypertension or cardiac comorbidities. Stroke was diagnosed by clinical examination demonstrating
acute neurologic deficit. Computed tomography (CT) scans of the brain were performed to differentiate between IHS and ischemic stroke. Postoperative follow-up was between 2 and 3 months.
RESULTS A total of 2452 patients received CEA during the study period. Of these, 32 patients (1.31%) suffered ischemic strokes and 5 (0.20%) had IHS. This accounted for 86.5% and 13.5% of perioperative neurologic complications, respectively. Hemorrhage occurred on postoperative day 2 in one case, day 4 in three cases, and day 9 in one case. History and outcomes for patients suffering IHS versus ischemic stroke are compared in Table I. The average age of patients in the ischemic stroke group was 69.6 years vs. 59.8 for the IHS group. Coronary artery disease was present in 16 (50%) of the ischemic group vs. 1 (20%) in the IHS group. Twenty of the ischemic stroke patients (63%) suffered from hypertension whereas this was a comorbidity in four (80%) of the patients in the IHS group. A history of previous stroke was noted in 11 patients (34%) of the ischemic stroke group and none of the patients in the IHS group. Ipsilateral carotid artery stenosis averaged 90% in the IHS patients compared to 72% average stenosis in the ischemic stroke group. Whereas none of the IHS patients had diabetes, 13 (41%) of the ischemic stroke patients were diabetic. There was a 100% death rate in the IHS group compared to 12.5% of the patients in the ischemic stroke group. Intracerebral hemorrhagic stroke occurred between 2 and 9 days postoperatively, with the last occurring in 1996.
Vol. 19, No. 1, 2005
Ischemic stroke and intracerebral hemorrhage after CEA 3
DISCUSSION
years, it was shown that endarterectomy resulted in a 5.1% stroke rate vs. 11% for nonoperative therapy. Intracerebral hemorrhagic stroke is believed to result from a hyperperfusion syndrome,22 a situation in which long-standing hypoperfusion results in chronic dilatation and loss of the normal compensatory autoregulation and vasoconstriction of cerebral vasculature. With restored blood flow, these dilated vessels then experience supranormal flow rates resulting in rupture and hemorrhage. The rate of IHS has been documented ranging from 0.4 to 2%.6,8,10,23 IHS generally occurred between 1 and 24 days postoperatively. In addition to prior recent stroke, factors identified with IHS are hypertension, headache, and increased flow velocities noted on transcranial Doppler.22,23 Ouriel et al.6 added that younger age and severe cerebrovascular occlusive disease appeared to increase the risk of postoperative IHS. They further postulated that improved preoperative and postoperative management of cardiac disease and operative techniques resulting in decreased morbidity would cause the traditionally stable incidence of IHS to become a relatively more common complication. Our data suggest that IHS remains an infrequent complication. Furthermore, the data in this report agrees with those of Ouriel in that patients with IHS were younger (p = 0.0294) and tended to have more severe cerebrovascular disease. Interestingly, none of our IHS patients suffered a preoperative stroke. Although uncommon, IHS is very significant in that it is often fatal, with 100% mortality among those patients with hemorrhagic stroke in this study. Piepgras et al.9 reported 14 cases of postoperative hemorrhage with 8 deaths, 4 significant neurologic deficits, and 2 complete recoveries. This contrasts somewhat with OurielÕs data, which show that of 11 patients suffering postoperative hemorrhage, 4 died, 3 had partial residual neurologic deficit, and 4 had complete recovery. Reith et al.10 reported two cases, one with devastating neurologic deficit and one with hemiparesis. Despite the low frequency, post-endarterectomy IHS remains significant in terms of its morbidity and mortality. The best treatment for hemorrhagic stroke would appear to be prevention. Control of blood pressure and avoidance of anticoagulation and antiplatelet medication are important. Once IHS is documented, neurosurgical consultation is mandatory; however, the outlook is often poor. Clearly, further study is needed regarding the avoidance of this frequently fatal complication.
The first successful CEA procedures were reported in 195312 and 195413 for patients suffering transient ischemic attacks (TIAs) and mild strokes. Through the next decade, a greater number of these procedures were performed with unclear indications and less than satisfactory results. Historically, CEA was performed as a treatment for stroke on an emergent basis within 24-48 hr from the onset of symptoms. When CEA was performed prematurely after acute stroke, operative mortality ranged from 20 to 60%14-16 while the fraction of patients receiving benefit from this operation was less than 40%.17 The majority of these deaths were due to IHS. Subsequently, patients undergoing endarterectomy greater than 2 weeks after the onset of symptoms were noted to have a lower mortality of 17%.18 Currently, the role of CEA is felt to be preventative in asymptomatic patients or those with TIAs or mild strokes rather than for the treatment of acute severe stroke. Randomized studies definitively quantified the beneficial effect of CEA versus nonoperative treatment for the prevention of stroke in symptomatic patients. In 1991 the NASCET collaborators2 showed that endarterectomy was highly beneficial in preventing strokes in patients with history of stroke or TIA and 70-99% stenosis. Medical therapy yielded stroke rates of 26% over 2 years compared to a 9% rate in those undergoing operative therapy. In 1998 the NASCET collaborators19 published results suggesting that there was a benefit to CEA in symptomatic patients with 50-69% stenosis, with medical therapy resulting in 22.2% 5-year stroke rate vs. 15.7% with surgery. The benefits of endarterectomy were also recognized for asymptomatic patients with carotid stenosis. Although not randomized, a prospective study in 1978 detailed the beneficial effects of endarterectomy.20 Patients undergoing endarterectomy were followed up to 15 years and had symptoms at a rate of 1% per year vs. 3.8% per year for a group of comparable controls that did not undergo operation. In 1993 the results of the Veterans Administration Asymptomatic Trial21 were published as the first randomized study to show benefit in asymptomatic patients. The stroke plus TIA rate was 20.6% in the medical arm vs. 8% in the surgical group. The Asymptomatic Carotid Atherosclerosis Study3 in 1995 was a second randomized study that showed the beneficial effect of endarterectomy for asymptomatic patients with stenosis of >60%. With a follow-up period of 2.7
4 Wilson and Ammar
CONCLUSIONS CEA is a proven safe and effective treatment for symptomatic and asymptomatic carotid stenosis. The vast majority of strokes continue to be ischemic. Although IHS often has devastating results, its relative frequency has not increased. REFERENCES 1. Hsia DC, Moscoe LM, Krushat WM. Epidemiology of carotid endarterectomy among Medical beneficiaries: 1985-1996 update. Stroke 1998;29:346-350. 2. North American Symptomatic Carotid Endarterectomy Trial Collaborators. Beneficial effect of carotid endarterectomy in symptomatic patients with high-grade carotid stenosis. N Eng J Med 1991;325:445-453. 3. Executive Committee for the Asymptomatic Carotid Atherosclerosis Study. Endarterectomy for asymptomatic carotid artery stenosis. JAMA 1995;273:1421-1428. 4. Hertzer NR, OÕHara PJ, Mascha EJ, et al. Early outcome assessment for 2228 consecutive carotid endarterectomy procedures: the Cleveland Clinic experience from 1989 to 1995. J Vasc Surg 1997;26:1-10. 5. Easton JD, Sherman DG. Stroke and mortality rate in carotid endarterectomy: 228 consecutive operations. Stroke 1977;8. 565-568. 6. Ouriel K, Shortell CK, Illig KA, et al. Intracerebral hemorrhage after carotid endarterectomy: incidence, contribution to neurologic morbidity, and predictive factors. J Vasc Surg 1999;29:82-89. 7. Bruetman ME, Fields WS, Crawford ES, et al. Cerebral hemorrhage in carotid artery surgery. Arch NeuroI 1963; 147:458-467. 8. Solomon RA, Loftus CM, Quest DO, et al. Incidence and etiology of intracerebral hemorrhage following carotid endarterectomy. J Neurosurg 1986;64:29-34. 9. Piepgras DG, Morgan MK, Sundt TM, Jr, et al. Intracerebral hemorrhage after carotid endarterectomy. J Neurosurg 1988;68:532-536. 10. Reith HB, Edelmann M, Reith C. Spontaneous intracerebral hemorrhage following carotid endarterectomy. Experience of 328 operations from 1983-1988. Int Surg 1992;77:224-225.
Annals of Vascular Surgery
11. Golledge J, Ellis M, Sabharwal T, et al. Selection of patients for carotid endarterectomy. J Vasc Surg 1999;30. 122-130. 12. DeBakey ME. Successful carotid endarterectomy for cerebrovascular insufficiency. Nineteen-year follow-up. JAMA 1975;233:1083-1085. 13. Eastcott HH, Pickering GW, Rob CG. Reconstruction of internal carotid artery in a patient with intermittent attacks of hemiplegia. Lancet 1954;267:994-996. 14. Wylie EJ, Hein MF, Adams JE. Intracranial hemorrhage following surgical revascularization for treatment of acute strokes. J Neurosurg 1964;21:212-215. 15. DeWeese JA, Rob CG, Satran R, et al. Surgical treatment for occlusive disease of the carotid artery. Ann Surg 1968; 168:85-94. 16. Thompson JE, Kartchner MM, Austin DJ, et al. Carotid endarterectomy for cerebrovascular insufficiency (stroke): follow-up of 359 cases. Ann Surg 1966;163:751-763. 17. Meyer FB, Sundt TM, Jr, Piepgras DG, et al. Emergency carotid endarterectomy for patients with acute carotid occlusion and profound neurological deficits. Ann Surg 1986;203:82-89. 18. Blaisdell WF, Clauss RH, Galbraith JG, et al. Joint study of extracranial arterial occlusion. IV. A review of surgical considerations. JAMA 1969;209:1889-1895. 19. North American Symptomatic Carotid Endarterectomy Trial Collaborators. Benefit of carotid endarterectomy in patients with symptomatic moderate or severe stenosis. N Engl J Med 1998;339:1415-1425. 20. Thompson JE, Patman RD, Talkington CM. Asymptomatic carotid bruit: long-term outcome of patients having endarterectomy compared with unoperated controls. Ann Surg 1978;188:308-316. 21. Hobson RW, 2nd, Weiss DG, Fields WS, et al. Efficacy of carotid endarterectomy for asymptomatic carotid stenosis. The Veteran Affairs Cooperative Study Group. N Engl J Med 1993;328:221-227. 22. Mansoor GA, White WB, Grunnet M, et al. Intracerebral hemorrhage after carotid endarterectomy associated with ipsilateral fibrinoid necrosis: a consequence of the hyperperfusion syndrome? J Vasc Surg 1996;23:147-151. 23. Jansen C, Sprengers AM, Moll FL, et al. Prediction of intracerebral hemorrhage after carotid endarterectomy by clinical criteria and intraoperative transcranial Doppler monitoring. Eur J Vasc Surg 1994;8:303-308.
Carotid endarterectomy is a frequently performed vascular procedure. The most common major perioperative neurologic complication is ischemic stroke. Intracerebral hemorrhage has been traditionally viewed as less common. It has been recently proposed that as technical advances are made, the rate of ischemic stroke and other complications has decreased, causing hemorrhagic stroke to attain increasing importance as a perioperative complication. A review of 2452 consecutive endarterectomies performed by a single surgeon from 1983 to 2000 was performed and rates of ischemic and hemorrhagic strokes were analyzed. There were five hemorrhagic strokes for a rate 0.20% (13.5% of postoperative neurologic complications) and 32 with ischemic strokes for a rate of 1.31% (86.5% of postoperative neurologic complications). From these data we conclude that hemorrhagic stroke remains uncommon and ischemic stroke continues to be the most frequent cause of postoperative neurologic complication after carotid endarterectomy.
INTRODUCTION Carotid endarterectomy (CEA) is a commonly performed vascular procedure with a reported 108,275 cases performed in 1996.1 It has been shown to be beneficial therapy for the treatment of carotid stenosis.2,3 The perioperative complications of CEA include ischemic stroke, intracerebral hemorrhagic stroke (IHS), myocardial infarction, hematoma, infection, cranial nerve injury, and death. The most common perioperative major neurologic complication is ischemic stroke, with rates ranging from 1.8 to 14.5% over the last 30 years.4,5 Recently, the perioperative ischemic stroke rate for asymptomatic patients has been reported to be 0.5-1.4%.4,6 Reported rates of IHS have been 0.41-0.75%.6-10 Ouriel et al.6 reported an increased relative rate of IHS versus ischemic Department of Surgery, University of Kansas School of Medicine– Wichita, Wichita, KS. Correspondence to: Alex D. Ammar, MD, University of Kansas School of Medicine–Wichita, 818 N. Emporia, Suite 200, Wichita, KS 67214, USA, E-mail: [email protected] Ann Vasc Surg 2005; 19: 1-4 DOI: 10.1007/s10016-004-0131-5 Ó Annals of Vascular Surgery Inc. Published online: January 11, 2005
stroke and proposed that as advances in perioperative management and operative technique improved overall morbidity and mortality, IHS would attain increasing importance as a perioperative complication. The purpose of this study was to quantify the rates of perioperative ischemic strokes and IHS in a single surgeonÕs experience.
PATIENTS AND METHODS A written log of consecutive CEAs performed by a single surgeon from 1983 to 2000 was reviewed. This log contained patient name, date of operation, operation performed, and complications suffered. The total number of operations was quantified, as were the number of perioperative ischemic and hemorrhagic strokes. Outpatient clinic and hospital charts of patients experiencing these complications were reviewed and data including age, gender, percent ipsilateral and contralateral stenosis, incidence of coronary artery disease, hypertension, diabetes, history of smoking, previous stroke, and severity of perioperative stroke rate were recorded. All patients had either preoperative carotid arteriography or duplex ultrasound. The degree of 1
2 Wilson and Ammar
Annals of Vascular Surgery
Table I. Comparison of age, comorbidities, carotid stenosis rates, and mortality for patients suffering intracerebral hemorrhage or ischemic strokea Parameter
Intracerebral hemorrhage group
Ischemic stroke group
p
Patients (n) Age (years) Comorbidities Coronary artery disease Hypertension Diabetes Smoking history Previous cerebrovasular accident Degree of carotid artery stenosis Contralateral stenosis Ipsilateral stenosis Death
5 59.8 ± 8.9b
32 69.6 ± 8.9
0.0294
1 4 0 3 0
16 20 13 14 11
0.211 0.446 0.077 0.498 0.159
a
(20) (80) (0) (60) (0)
36% 90% 5 (100)
(50) (63) (41) (44) (34)
39% 72% 4 (13)
0.9056 0.0734 0.001
Data are numbers with percents in parentheses, except where indicated. Mean ± SD.
b
stenosis on arteriogram was calculated by subtracting from one, the ratio of the narrowest diameter at the stenosis to the diameter of the internal carotid artery distal to the stenosis, and multiplying by 100, similar to the method used in the North American Symptomatic Carotid Endarterectomy Trial (NASCET) Collaborators.11 The degree of stenosis was calculated using color duplex sonography in conjunction with internal carotidto-common carotid artery velocity ratios. In all patients with history of prior stroke, endarterectomy was delayed for at least 3 weeks from the time of the stroke, this interval depending on patientÕs clinical status (i.e., resolution of symptoms, degree of stenosis). The operations were performed under general anesthesia. Anticoagulation was attained using heparin (1.5 mg/kg) with partial reversal with protamine. Shunting was used for stump pressures of <50 mmHg, history of previous stroke, or contralateral carotid occlusion. Patch angioplasty with Hema-Shield knitted double-velour Dacron (Meadox, Boston Scientific, Wayne, NJ) was used on redo operations or for small carotid arteries, especially females or young patients with premature atherosclerosis. Low-molecular-weight Dextran was routinely infused intraoperatively and postoperatively since 1991, and all patients were placed on aspirin unless they had aspirin allergy or sensitivity. Postoperative intensive care (ICU) was routinely used prior to 1992. Subsequently, patients were followed in the recovery room for 2 hr and a decision was made regarding the need for ICU admission, usually for hypotension or hypertension or cardiac comorbidities. Stroke was diagnosed by clinical examination demonstrating
acute neurologic deficit. Computed tomography (CT) scans of the brain were performed to differentiate between IHS and ischemic stroke. Postoperative follow-up was between 2 and 3 months.
RESULTS A total of 2452 patients received CEA during the study period. Of these, 32 patients (1.31%) suffered ischemic strokes and 5 (0.20%) had IHS. This accounted for 86.5% and 13.5% of perioperative neurologic complications, respectively. Hemorrhage occurred on postoperative day 2 in one case, day 4 in three cases, and day 9 in one case. History and outcomes for patients suffering IHS versus ischemic stroke are compared in Table I. The average age of patients in the ischemic stroke group was 69.6 years vs. 59.8 for the IHS group. Coronary artery disease was present in 16 (50%) of the ischemic group vs. 1 (20%) in the IHS group. Twenty of the ischemic stroke patients (63%) suffered from hypertension whereas this was a comorbidity in four (80%) of the patients in the IHS group. A history of previous stroke was noted in 11 patients (34%) of the ischemic stroke group and none of the patients in the IHS group. Ipsilateral carotid artery stenosis averaged 90% in the IHS patients compared to 72% average stenosis in the ischemic stroke group. Whereas none of the IHS patients had diabetes, 13 (41%) of the ischemic stroke patients were diabetic. There was a 100% death rate in the IHS group compared to 12.5% of the patients in the ischemic stroke group. Intracerebral hemorrhagic stroke occurred between 2 and 9 days postoperatively, with the last occurring in 1996.
Vol. 19, No. 1, 2005
Ischemic stroke and intracerebral hemorrhage after CEA 3
DISCUSSION
years, it was shown that endarterectomy resulted in a 5.1% stroke rate vs. 11% for nonoperative therapy. Intracerebral hemorrhagic stroke is believed to result from a hyperperfusion syndrome,22 a situation in which long-standing hypoperfusion results in chronic dilatation and loss of the normal compensatory autoregulation and vasoconstriction of cerebral vasculature. With restored blood flow, these dilated vessels then experience supranormal flow rates resulting in rupture and hemorrhage. The rate of IHS has been documented ranging from 0.4 to 2%.6,8,10,23 IHS generally occurred between 1 and 24 days postoperatively. In addition to prior recent stroke, factors identified with IHS are hypertension, headache, and increased flow velocities noted on transcranial Doppler.22,23 Ouriel et al.6 added that younger age and severe cerebrovascular occlusive disease appeared to increase the risk of postoperative IHS. They further postulated that improved preoperative and postoperative management of cardiac disease and operative techniques resulting in decreased morbidity would cause the traditionally stable incidence of IHS to become a relatively more common complication. Our data suggest that IHS remains an infrequent complication. Furthermore, the data in this report agrees with those of Ouriel in that patients with IHS were younger (p = 0.0294) and tended to have more severe cerebrovascular disease. Interestingly, none of our IHS patients suffered a preoperative stroke. Although uncommon, IHS is very significant in that it is often fatal, with 100% mortality among those patients with hemorrhagic stroke in this study. Piepgras et al.9 reported 14 cases of postoperative hemorrhage with 8 deaths, 4 significant neurologic deficits, and 2 complete recoveries. This contrasts somewhat with OurielÕs data, which show that of 11 patients suffering postoperative hemorrhage, 4 died, 3 had partial residual neurologic deficit, and 4 had complete recovery. Reith et al.10 reported two cases, one with devastating neurologic deficit and one with hemiparesis. Despite the low frequency, post-endarterectomy IHS remains significant in terms of its morbidity and mortality. The best treatment for hemorrhagic stroke would appear to be prevention. Control of blood pressure and avoidance of anticoagulation and antiplatelet medication are important. Once IHS is documented, neurosurgical consultation is mandatory; however, the outlook is often poor. Clearly, further study is needed regarding the avoidance of this frequently fatal complication.
The first successful CEA procedures were reported in 195312 and 195413 for patients suffering transient ischemic attacks (TIAs) and mild strokes. Through the next decade, a greater number of these procedures were performed with unclear indications and less than satisfactory results. Historically, CEA was performed as a treatment for stroke on an emergent basis within 24-48 hr from the onset of symptoms. When CEA was performed prematurely after acute stroke, operative mortality ranged from 20 to 60%14-16 while the fraction of patients receiving benefit from this operation was less than 40%.17 The majority of these deaths were due to IHS. Subsequently, patients undergoing endarterectomy greater than 2 weeks after the onset of symptoms were noted to have a lower mortality of 17%.18 Currently, the role of CEA is felt to be preventative in asymptomatic patients or those with TIAs or mild strokes rather than for the treatment of acute severe stroke. Randomized studies definitively quantified the beneficial effect of CEA versus nonoperative treatment for the prevention of stroke in symptomatic patients. In 1991 the NASCET collaborators2 showed that endarterectomy was highly beneficial in preventing strokes in patients with history of stroke or TIA and 70-99% stenosis. Medical therapy yielded stroke rates of 26% over 2 years compared to a 9% rate in those undergoing operative therapy. In 1998 the NASCET collaborators19 published results suggesting that there was a benefit to CEA in symptomatic patients with 50-69% stenosis, with medical therapy resulting in 22.2% 5-year stroke rate vs. 15.7% with surgery. The benefits of endarterectomy were also recognized for asymptomatic patients with carotid stenosis. Although not randomized, a prospective study in 1978 detailed the beneficial effects of endarterectomy.20 Patients undergoing endarterectomy were followed up to 15 years and had symptoms at a rate of 1% per year vs. 3.8% per year for a group of comparable controls that did not undergo operation. In 1993 the results of the Veterans Administration Asymptomatic Trial21 were published as the first randomized study to show benefit in asymptomatic patients. The stroke plus TIA rate was 20.6% in the medical arm vs. 8% in the surgical group. The Asymptomatic Carotid Atherosclerosis Study3 in 1995 was a second randomized study that showed the beneficial effect of endarterectomy for asymptomatic patients with stenosis of >60%. With a follow-up period of 2.7
4 Wilson and Ammar
CONCLUSIONS CEA is a proven safe and effective treatment for symptomatic and asymptomatic carotid stenosis. The vast majority of strokes continue to be ischemic. Although IHS often has devastating results, its relative frequency has not increased. REFERENCES 1. Hsia DC, Moscoe LM, Krushat WM. Epidemiology of carotid endarterectomy among Medical beneficiaries: 1985-1996 update. Stroke 1998;29:346-350. 2. North American Symptomatic Carotid Endarterectomy Trial Collaborators. Beneficial effect of carotid endarterectomy in symptomatic patients with high-grade carotid stenosis. N Eng J Med 1991;325:445-453. 3. Executive Committee for the Asymptomatic Carotid Atherosclerosis Study. Endarterectomy for asymptomatic carotid artery stenosis. JAMA 1995;273:1421-1428. 4. Hertzer NR, OÕHara PJ, Mascha EJ, et al. Early outcome assessment for 2228 consecutive carotid endarterectomy procedures: the Cleveland Clinic experience from 1989 to 1995. J Vasc Surg 1997;26:1-10. 5. Easton JD, Sherman DG. Stroke and mortality rate in carotid endarterectomy: 228 consecutive operations. Stroke 1977;8. 565-568. 6. Ouriel K, Shortell CK, Illig KA, et al. Intracerebral hemorrhage after carotid endarterectomy: incidence, contribution to neurologic morbidity, and predictive factors. J Vasc Surg 1999;29:82-89. 7. Bruetman ME, Fields WS, Crawford ES, et al. Cerebral hemorrhage in carotid artery surgery. Arch NeuroI 1963; 147:458-467. 8. Solomon RA, Loftus CM, Quest DO, et al. Incidence and etiology of intracerebral hemorrhage following carotid endarterectomy. J Neurosurg 1986;64:29-34. 9. Piepgras DG, Morgan MK, Sundt TM, Jr, et al. Intracerebral hemorrhage after carotid endarterectomy. J Neurosurg 1988;68:532-536. 10. Reith HB, Edelmann M, Reith C. Spontaneous intracerebral hemorrhage following carotid endarterectomy. Experience of 328 operations from 1983-1988. Int Surg 1992;77:224-225.
Annals of Vascular Surgery
11. Golledge J, Ellis M, Sabharwal T, et al. Selection of patients for carotid endarterectomy. J Vasc Surg 1999;30. 122-130. 12. DeBakey ME. Successful carotid endarterectomy for cerebrovascular insufficiency. Nineteen-year follow-up. JAMA 1975;233:1083-1085. 13. Eastcott HH, Pickering GW, Rob CG. Reconstruction of internal carotid artery in a patient with intermittent attacks of hemiplegia. Lancet 1954;267:994-996. 14. Wylie EJ, Hein MF, Adams JE. Intracranial hemorrhage following surgical revascularization for treatment of acute strokes. J Neurosurg 1964;21:212-215. 15. DeWeese JA, Rob CG, Satran R, et al. Surgical treatment for occlusive disease of the carotid artery. Ann Surg 1968; 168:85-94. 16. Thompson JE, Kartchner MM, Austin DJ, et al. Carotid endarterectomy for cerebrovascular insufficiency (stroke): follow-up of 359 cases. Ann Surg 1966;163:751-763. 17. Meyer FB, Sundt TM, Jr, Piepgras DG, et al. Emergency carotid endarterectomy for patients with acute carotid occlusion and profound neurological deficits. Ann Surg 1986;203:82-89. 18. Blaisdell WF, Clauss RH, Galbraith JG, et al. Joint study of extracranial arterial occlusion. IV. A review of surgical considerations. JAMA 1969;209:1889-1895. 19. North American Symptomatic Carotid Endarterectomy Trial Collaborators. Benefit of carotid endarterectomy in patients with symptomatic moderate or severe stenosis. N Engl J Med 1998;339:1415-1425. 20. Thompson JE, Patman RD, Talkington CM. Asymptomatic carotid bruit: long-term outcome of patients having endarterectomy compared with unoperated controls. Ann Surg 1978;188:308-316. 21. Hobson RW, 2nd, Weiss DG, Fields WS, et al. Efficacy of carotid endarterectomy for asymptomatic carotid stenosis. The Veteran Affairs Cooperative Study Group. N Engl J Med 1993;328:221-227. 22. Mansoor GA, White WB, Grunnet M, et al. Intracerebral hemorrhage after carotid endarterectomy associated with ipsilateral fibrinoid necrosis: a consequence of the hyperperfusion syndrome? J Vasc Surg 1996;23:147-151. 23. Jansen C, Sprengers AM, Moll FL, et al. Prediction of intracerebral hemorrhage after carotid endarterectomy by clinical criteria and intraoperative transcranial Doppler monitoring. Eur J Vasc Surg 1994;8:303-308.