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The Preoperative Patient with an Asymptomatic Cervical Bruit
Symposium on Medical Evaluation of the Preoperative Preoperatice Patient Sympos'iutn
The Preoperative Patient with an Asymptomatic Cervical Bruit Lourdes Laurdes c. C. Corman, Carman, M.D. M.D."~:~
The general internist is often asked to evaluate patients scheduled for elective noncerebrovascular surgery who on physical examination are found to have a cervical bruit, but who deny any symptoms of occlusive cerebrovascular disease. The preferred approach for these patients is unclear, and recommendations vary. Some advocate deferring the elective surgical procedure until definitive evaluation and surgical treatment is done to document carotid disease. Others favor proceeding with the scheduled surgery and ignoring the finding in the truly asymptomatic patient. This chapter reviews the data on morbidity and mortality of cerebrovascular disease in patients undergoing noncerebrovascular surgery, and among those with cervical bruits. Patients with recent onset of intermittent or progressive neurologic deficits cannot be considered stable, and elective noncerebrovascular surgery should be postponed until suitable medical or surgical treatment is instituted, the patient's condition stabilizes, or both. Rationale Preoperative patients with hypertension, cardiac disease, diabetes mellitus, or transient ischemic attacks may have concomitant cerebrovascular disease. Cardiac patients awaiting myocardial revascularization often have asymptomatic occlusive disease ofthe of the carotid arteries. In these patients management is often approached as a difficult choice between two vascular reconstructive procedures. A study in 1972 of patients with severe coronary artery disease awaiting myocardial revascularization showed a 33 per cent mortality in patients who underwent prophylactic carotid endarterectomy first. In a subsequent similar group of 15 patients, simultaneous carotid endarterectomy and myocardial revascularization were performed with no mortality, but morbidity from cerebrovascular disease was 20 per cent, although only 1 of 3 patients had "Assistant Professor of Medicine, University of Florida College of Medicine, Gainesville, >:'Assistant Florida
America- Vol. 63, No. 6, November 1979 Medical Clinics of North America-Vo!.
1335
1336
LOURDES C. CORMAN
permanent deficits. Despite this group's experience, most authors recom'3 mend carotid endarterectomy prior to myocardial revascularization. 13 The rationale for performing "prophylactic" carotid endarterectomy prior to major elective noncerebrovascular surgery is to prevent intraoperative cerebral infarction should hypotension develop during the surgical procedure. The true risk of cerebral infarction from hypotension is unclear. In normal individuals cerebral blood flow is virtually independent of perfusion pressure except at abnormally high or low pressure, but this autoregulation can be impaired immediately after an 10 hypoxia.1O ischemic insult or during hypercapnia or hypoxia. Patients with advanced occlusive disease can also tolerate transient falls in systemic blood pressure, 12 and atherosclerotic lesions must reduce the lumen of the carotid arteries to less than 1 to 2 mm to produce a substantial decrease in flow. Most symptomatic plaques produce' produce a similar decrease in residual lumen. 11 Prolonged severe intraoperative hypotension has been associated with postoperative neurologic deficits after open heart surgery for valvular diseaseY disease. 17 In aorto-iliac surgery, 11.8 per cent of patients with a 50 per cent drop in systolic pressure intraoperatively had postoperative neurologic deficits as compared to less than 1 per cent of those with lowest systolic pressure above or below 90 mm Hg. However, almost 90 per cent of patients with a severe drop in pressure did not have postoperative neurologic deficits. 41t 4 It appears that strokes can result from any of several mechanisms. In a recent prospective study, strokes were due to large artery thrombosis in 34 per cent of patients, while they were due to lacunar infarctions (most often found in hypertensive patients) in 19 per cent, secondary to embolism (from cardiac sources or ulcerated arterial plaques) in 31 per cent, and due to hematoma or subarachnoid hemorrhage (from aneurysm or arteriovenous malformation) in 16 per cent. 14 cent.'4 The number of strokes ascribed to surgically accessible extracranial carotid arteries has been estimated at 40 per cent. Even among patients with symptoms traditionally ascribed to carotid artery disease (transient monocular blindness and hemispheric attack appropriate to the ips'ilatipsilateral carotid), only half or less of the patients are found to have tight stenosis or occlusion of the carotid artery at arteriography. Among patients with cervical bruits referred for screening to detect significant (;:::40 per cent) carotid artery stenosis, less than 10 per cent were found to (:2:40 have stenosis. 15 IS Because ofthe of the recent recognition ofulcerated of ulcerated nonstenotic carotid plaques as a potential source of emboli, endarterectomy has been recommended even in the absence of significant stenosis.
The Cervical (Carotid) Bruit The coexistence of cervical bruits and occlusive disease of the extracranial carotids was first reported by Fisher in 1957. Since then, the popularity of the cervical bruit as an indicator of occlusive carotid disease has fluctuated. More recently studies based on the character and duration of the sound have been devised to evaluate carotid artery occlusion noninvasively.l Cervical bruits can be secondary to a venous hum, arteriovenous fistula, angiomatous malformations, atherosclerosis of the brachiocephalic, subclavian, vertebral, or carotid arteries, or from murmurs transmitted from the upper mediastinum. 88 Bruits can also be
1337
THE ASYMPTOMATIC CERVICAL BRUIT
Table 1. Postoperative Cerebrovascular Morbidity in Patients with and without Carotid Bruits CAROTID BRUIT PRESENT
CAROTID BRUIT ABSENT
0% (0/40)
1.2% (2/156)
Carney 1977
0% (0/35) 1.8% (21109)" (2/109)~(
1.4% (2/139)
Evans 1978
0% (0/92)
0.8% (4/496)
1.2% (2/167)
1.1 % (8/791)
Treiman 1973
Total
if2 ofbruit *Risk if 2 strokes occurring in 74 patients with the presence of bruit not specified are included.
produced from applying too much pressure over the carotid area, or in any conditions that change flow dynamics, such as thyrotoxicosis or anemia. 12 Bruits secondary to carotid occlusive disease occur over the bifurcation of the common carotid artery opposite the upper end of the thyroid cartilage, are harsh in character and systolic in timing (although with severe stenosis may extend through diastole), and disappear with compression of the ipsilateral artery but increase with compression of the contralateral artery if it is patent. 12 Some authors believe that the presence of a bruit is not as important as its location, quality, and intensity. Others favor specific maneuvers to exclude noncarotid bruits. Compression of an involved artery has been claimed to produce strokes. Bruits may disappear when the residual carotid lumen is 2 mm or less. 11 While to some cervical or "carotid" bruits are fallible indicators of internal carotid artery occlusion, others have used it to identify patients at high risk of stroke and death. In one study 35 per cent of60 patients with an asymptomatic bruit suffered a transient ischemic attack or stroke as compared to 16 per cent of patients with cerebrovascular disease but without a bruit. 55 This was patients, 11 but at least one not the experience in another series of only 14 patients,l1 author claims that prognosis in such patients can be improved by carotid endarterectomy. The prevalence of "carotid" bruits among patients undergoing major vascular procedures has been reported as 14 to 20 per cent but may be higher, since patients in whom no record of cervical auscultation was made were excluded from some series. Among patients referred for evaluation of cervical bruits, 70 per cent have been found to originate in 15 Many young patients the thorax by a combination of noninvasive tests. 15 12 but its presence in a sushave carotid bruits in the absence of disease 12 ceptible patient improves the accuracy of diagnosing a transient ischemic attack. Symptomatic patients (particularly if symptoms are ipsilateral) show a prevaIence of bruits of 61 to 85 per cent, and asymptomatic patients, 21 to 65 per cent. Differences in the figures reported most likely reflect varying populations studied and different definitions of significant bruit and stenosis. The reported prevalence of bruits in patients with stenotic lesions ranges between 27 and 88 per cent for similar reasons. In a prospective study on stroke, the prevalence ofbruit varied according to the diagnosis, 24 per cent being the highest prevalence which was found
1338
LOURDES C. CORMAN
14 Between 10 and 28 per cent of in patients with a thrombotic stroke. 14 patients with bruits can have a normal arteriogram. In conclusion, we would agree with Fields that when a bruit is present in a patient with ipsilateral carotid transient ischemic attack finding.88 Its overall usefulness as a clinical indicator it is a significant finding. of carotid artery stenosis is doubtful.
Risk of Postoperative Stroke Postoperative cerebrovascular accident, like postoperative myocardial infarction, carries a grave prognosis with a mortality of 50 per cent. 4 The reported risk of postoperative morbidity and mortality associated with disease varies in different surgical populations and according to the length of postoperative observation. Since most postoperative strokes occur after the first 24 hours following surgery, 4 figures reported in studies that observed their patients for only one day after surgery may be falsely low. Elderly patients have a postoperative morbidity for cerebrovascular disease of 0.4 to 3.3 per cent, the higher figure being the rate of complications in a group over age 80. Mortality also appeared to be in a similar range. What the risk is at this time is not available from the literature. For general surgery patients, mortality varies from 0 to 2.9 per cent. In these patients morbidity was reported as 1 per cent in one study and not included in any of the others. The risk of cerebrovascular disease in patients undergoing major vascular surgery is 0 to 1.6 per cent. In one series 44 morbidity decreased from 2.2 per cent before 1969 to 0.8 per cent since 1970. Mortality of 0 to 0.8 per cent may be falsely low since length of postoperative observation was not specified. Among patients undergoing open heart surgery, the risk of postoperative cerebrovascular disease varies with the type of surgery. The morbidity and mortality for patients undergoing open heart surgery for valvular heart disease is quite high, although a change in technique halved the risk in one study. 33 Patients undergoing open heart surgery are at risk of emboli secondary to fat, air, silicone material, calcium, and fibrin. In one prospective study, retinal emboli elnboli developed in 4 of 100 patients. However, among patients undergoing myocardial revascularization the risk is much less (0 to 4.5 per cent) and transient. Mortality from cerebrovascular disease after surgery is reported as 0.2 to 0.7 per cent except in one study in which a figure of less than 3.6 per cent ofless is calculated for overall mortality, with cerebrovascular accident as one of the causes listed. Even among 60 patients who had undergone previous myocardial revascularization and who later required one or more major vascular procedures, a cerebrovascular event was not a cause of postoperative complications. 13 Postoperative morbidity and mortality from cerebrovascular disease in patients with previous stroke or transient ischemic attack may be higher than in asymptomatic patients. Patients with cervical bruits would seem from the data (Table 1) to have no worse postoperative prognosis than those without. Morbidity from postoperative cerebrovascular disease was 1.2 per cent for the total reported group with bruits and 1.1 per cent for the patients without. Furthermore, in two prospective studies,
THE ASYMPTOMATIC CERVICAL BRUIT
1339
carotid bruits were not found to place a patient at risk for cardiac morbidity and mortality, 5,9 although preoperative cerebrovascular accident did,55 did. We can conclude that the risk of a postoperative cerebrovascular fatal or nonfatal event may be higher in patients with previous symptomatic cerebrovascular disease, but there are no data that suggest that patients with asymptomatic bruit or carotid stenosis are at higher risk. Since postoperative strokes tend to occur in the first few days after surgery rather than during or immediately after surgery,4 surgerY,4 mechanisms other than intraoperative hypotension are likely involved. A recent case report demonstrated a cerebral embolus histologically histologic ally similar to a thrombus formed at the site of saphenous aortic graft as the cause of death in a patient undergoing myocardial revascularization. Unilateral loss of vision occurred on the eighth day after surgery and the patient died on the fourteenth day, despite heparinization. 22
Other Considerations Angiography has been reported to carry a morbidity of 0.9 to 13 per cent and a mortality of 0.1 to 2.4 per cent. A multitude of noninvasive tests have been developed to help rule in the need for arteriography, but no excellent test has been described. 11 Flow-dependent noninvasive tests do not detect ulcerating plaques unless accompanied by significant stenosis. More recently, pilot studies have appeared using 123I-Iabelled 123I-labelled fibrinogen, 99mTc-DTPA, 99mTc_DTP A, and computed tomography. Arteriography is still the most definitive test available. The recommended approach of prophylactic carotid endarterectomy has been reported as having a very low morbidity and mortality, 0 to 2 per cent in some centers; however, a recent study reports a rate of postoperative stroke of 18.2 per cent in two community hospitals. 66 Furthermore, the beneficial effects of surgery in patients with asymptomatic bruit have not been established in a prospective, randomized manner. While some series include a control group, most do not.
SUMMARY At the time of this writing there appears to be little evidence that cervical bruits are good indicators of stenosis or plaque in the underlying carotid artery in asymptomatic patients, or that the finding of a carotid bruit places the patient at greater risk of postoperative stroke. The mortaland endarterectomy are too high to risk ity and morbidity of angiography an.d their use in a group of asymptomatic patients.
REFERENCES Note: A complete bibliography is available from the author on request. Limitations of space here, prohibited its inclusion here. H,: A perspective on noninvasive diagnosis of carotid disease. Neurology, 1. Ackerman, R. H.: 29 :615, 1979. 29:615, 2. 2, Bounds, J. V., Sandok, B. A., and Barnhorst, V. A.: Fatal cerebral embolism following surgery, Stroke, 7:611, 1976. aorto-coronary bypass graft surgery.
1340
LOURDES C. CORMAN
3. Branthwaite, M. A.: Prevention of neurological damage during open heart surgery. Thorax, 30 :258, 1975. 30:258, 4. Carney, W. I., Stewart, W. B., DePinto, D. J., et al.: Carotid bruit as a factor in aortoiliac reconstruction. Surgery, 81 :567, 1977. 5. Cooperman, M., Evans, W. E., et al.: Significance of asymptomatic carotid bruits. Arch. 113 :1339, 1978. Surg., 113:1339,1978. and Sherman, D. G.: Stroke and mortality rate in carotid endarterectomy: 228 6. Easton, J. J., andSherman, consecutive operations. Stroke, 8 :565, 1977. 7. Evans, W. E., and Cooperman, M.: The significance of asymptomatic unilateral carotid bruits in preoperative patients. Surgery, 83 :522, 1978. 8. Fields, W. S.: The asymptomatic carotid bruit-operate or not? Stroke, 9:269, 1978. Nussbaum, ussbaum, S. R., et al.: Multifactorial index of cardiac risk 9. Goldman, L., Caldera, D. L., N 297:845,1977. in noncardiac surgical procedures. New Eng. J. Med., 297:845, 1977. 1965. 10. Harper, A. M.: Physiology of cerebral blood flow. Brit. J. Anaesthes., 37:225, 37:225,1965. Thl' asymptomatic bruit. Amer. J. Surg., 11. Kanaly, P. J., Peyton, M. D., Cannon, J. P., et al.: The 134:821, 1977. 12. Marshall, J.: The Management of Cerebrovascular Disease. Oxford, Blackwell Scientific Pub!., 3rd ed., 1976. 13. McCollum, C. H., Garcia-Rinaldi, R., Graham, J. M., et al.: Myocardial revascularization prior to subsequent major surgery in patients with coronary artery disease. Surgery, 81 :302, 1977. 14. Mohr, J. P., Caplan, L. R., Melski, J. W., et al.: The Harvard Cooperative Stroke Registry: A prospective study. Neurology, 28:754, 1978. ofnoninvasi\e screening 15. Takaki, H. S., McNamara, M. F., Yas, J. S. T., et al.: Influence ofnoninvash"e in the care of patients with carotid stenosis. In Dietrich, E. B., ed.: Noninvasive Cardiovascular Diagnosis. Baltimore, University Park Press, 1978. 16. Treiman, R. L., Foran, R. F., Shore, E. H., et al.: Carotid bruit-significance in patients undergoing an abdominal aortic operation. Arch. Surg., 106:803, 1973. 17. Tufo, H. M., Ostfeld, A. M., Shekelle, R.: Central nervous system dysfunction following open heart surgery. J.A.M.A., 212:1333, 1970. University of Florida College of Medicine Gainesville, Florida 32610
The Preoperative Patient with an Asymptomatic Cervical Bruit Lourdes Laurdes c. C. Corman, Carman, M.D. M.D."~:~
The general internist is often asked to evaluate patients scheduled for elective noncerebrovascular surgery who on physical examination are found to have a cervical bruit, but who deny any symptoms of occlusive cerebrovascular disease. The preferred approach for these patients is unclear, and recommendations vary. Some advocate deferring the elective surgical procedure until definitive evaluation and surgical treatment is done to document carotid disease. Others favor proceeding with the scheduled surgery and ignoring the finding in the truly asymptomatic patient. This chapter reviews the data on morbidity and mortality of cerebrovascular disease in patients undergoing noncerebrovascular surgery, and among those with cervical bruits. Patients with recent onset of intermittent or progressive neurologic deficits cannot be considered stable, and elective noncerebrovascular surgery should be postponed until suitable medical or surgical treatment is instituted, the patient's condition stabilizes, or both. Rationale Preoperative patients with hypertension, cardiac disease, diabetes mellitus, or transient ischemic attacks may have concomitant cerebrovascular disease. Cardiac patients awaiting myocardial revascularization often have asymptomatic occlusive disease ofthe of the carotid arteries. In these patients management is often approached as a difficult choice between two vascular reconstructive procedures. A study in 1972 of patients with severe coronary artery disease awaiting myocardial revascularization showed a 33 per cent mortality in patients who underwent prophylactic carotid endarterectomy first. In a subsequent similar group of 15 patients, simultaneous carotid endarterectomy and myocardial revascularization were performed with no mortality, but morbidity from cerebrovascular disease was 20 per cent, although only 1 of 3 patients had "Assistant Professor of Medicine, University of Florida College of Medicine, Gainesville, >:'Assistant Florida
America- Vol. 63, No. 6, November 1979 Medical Clinics of North America-Vo!.
1335
1336
LOURDES C. CORMAN
permanent deficits. Despite this group's experience, most authors recom'3 mend carotid endarterectomy prior to myocardial revascularization. 13 The rationale for performing "prophylactic" carotid endarterectomy prior to major elective noncerebrovascular surgery is to prevent intraoperative cerebral infarction should hypotension develop during the surgical procedure. The true risk of cerebral infarction from hypotension is unclear. In normal individuals cerebral blood flow is virtually independent of perfusion pressure except at abnormally high or low pressure, but this autoregulation can be impaired immediately after an 10 hypoxia.1O ischemic insult or during hypercapnia or hypoxia. Patients with advanced occlusive disease can also tolerate transient falls in systemic blood pressure, 12 and atherosclerotic lesions must reduce the lumen of the carotid arteries to less than 1 to 2 mm to produce a substantial decrease in flow. Most symptomatic plaques produce' produce a similar decrease in residual lumen. 11 Prolonged severe intraoperative hypotension has been associated with postoperative neurologic deficits after open heart surgery for valvular diseaseY disease. 17 In aorto-iliac surgery, 11.8 per cent of patients with a 50 per cent drop in systolic pressure intraoperatively had postoperative neurologic deficits as compared to less than 1 per cent of those with lowest systolic pressure above or below 90 mm Hg. However, almost 90 per cent of patients with a severe drop in pressure did not have postoperative neurologic deficits. 41t 4 It appears that strokes can result from any of several mechanisms. In a recent prospective study, strokes were due to large artery thrombosis in 34 per cent of patients, while they were due to lacunar infarctions (most often found in hypertensive patients) in 19 per cent, secondary to embolism (from cardiac sources or ulcerated arterial plaques) in 31 per cent, and due to hematoma or subarachnoid hemorrhage (from aneurysm or arteriovenous malformation) in 16 per cent. 14 cent.'4 The number of strokes ascribed to surgically accessible extracranial carotid arteries has been estimated at 40 per cent. Even among patients with symptoms traditionally ascribed to carotid artery disease (transient monocular blindness and hemispheric attack appropriate to the ips'ilatipsilateral carotid), only half or less of the patients are found to have tight stenosis or occlusion of the carotid artery at arteriography. Among patients with cervical bruits referred for screening to detect significant (;:::40 per cent) carotid artery stenosis, less than 10 per cent were found to (:2:40 have stenosis. 15 IS Because ofthe of the recent recognition ofulcerated of ulcerated nonstenotic carotid plaques as a potential source of emboli, endarterectomy has been recommended even in the absence of significant stenosis.
The Cervical (Carotid) Bruit The coexistence of cervical bruits and occlusive disease of the extracranial carotids was first reported by Fisher in 1957. Since then, the popularity of the cervical bruit as an indicator of occlusive carotid disease has fluctuated. More recently studies based on the character and duration of the sound have been devised to evaluate carotid artery occlusion noninvasively.l Cervical bruits can be secondary to a venous hum, arteriovenous fistula, angiomatous malformations, atherosclerosis of the brachiocephalic, subclavian, vertebral, or carotid arteries, or from murmurs transmitted from the upper mediastinum. 88 Bruits can also be
1337
THE ASYMPTOMATIC CERVICAL BRUIT
Table 1. Postoperative Cerebrovascular Morbidity in Patients with and without Carotid Bruits CAROTID BRUIT PRESENT
CAROTID BRUIT ABSENT
0% (0/40)
1.2% (2/156)
Carney 1977
0% (0/35) 1.8% (21109)" (2/109)~(
1.4% (2/139)
Evans 1978
0% (0/92)
0.8% (4/496)
1.2% (2/167)
1.1 % (8/791)
Treiman 1973
Total
if2 ofbruit *Risk if 2 strokes occurring in 74 patients with the presence of bruit not specified are included.
produced from applying too much pressure over the carotid area, or in any conditions that change flow dynamics, such as thyrotoxicosis or anemia. 12 Bruits secondary to carotid occlusive disease occur over the bifurcation of the common carotid artery opposite the upper end of the thyroid cartilage, are harsh in character and systolic in timing (although with severe stenosis may extend through diastole), and disappear with compression of the ipsilateral artery but increase with compression of the contralateral artery if it is patent. 12 Some authors believe that the presence of a bruit is not as important as its location, quality, and intensity. Others favor specific maneuvers to exclude noncarotid bruits. Compression of an involved artery has been claimed to produce strokes. Bruits may disappear when the residual carotid lumen is 2 mm or less. 11 While to some cervical or "carotid" bruits are fallible indicators of internal carotid artery occlusion, others have used it to identify patients at high risk of stroke and death. In one study 35 per cent of60 patients with an asymptomatic bruit suffered a transient ischemic attack or stroke as compared to 16 per cent of patients with cerebrovascular disease but without a bruit. 55 This was patients, 11 but at least one not the experience in another series of only 14 patients,l1 author claims that prognosis in such patients can be improved by carotid endarterectomy. The prevalence of "carotid" bruits among patients undergoing major vascular procedures has been reported as 14 to 20 per cent but may be higher, since patients in whom no record of cervical auscultation was made were excluded from some series. Among patients referred for evaluation of cervical bruits, 70 per cent have been found to originate in 15 Many young patients the thorax by a combination of noninvasive tests. 15 12 but its presence in a sushave carotid bruits in the absence of disease 12 ceptible patient improves the accuracy of diagnosing a transient ischemic attack. Symptomatic patients (particularly if symptoms are ipsilateral) show a prevaIence of bruits of 61 to 85 per cent, and asymptomatic patients, 21 to 65 per cent. Differences in the figures reported most likely reflect varying populations studied and different definitions of significant bruit and stenosis. The reported prevalence of bruits in patients with stenotic lesions ranges between 27 and 88 per cent for similar reasons. In a prospective study on stroke, the prevalence ofbruit varied according to the diagnosis, 24 per cent being the highest prevalence which was found
1338
LOURDES C. CORMAN
14 Between 10 and 28 per cent of in patients with a thrombotic stroke. 14 patients with bruits can have a normal arteriogram. In conclusion, we would agree with Fields that when a bruit is present in a patient with ipsilateral carotid transient ischemic attack finding.88 Its overall usefulness as a clinical indicator it is a significant finding. of carotid artery stenosis is doubtful.
Risk of Postoperative Stroke Postoperative cerebrovascular accident, like postoperative myocardial infarction, carries a grave prognosis with a mortality of 50 per cent. 4 The reported risk of postoperative morbidity and mortality associated with disease varies in different surgical populations and according to the length of postoperative observation. Since most postoperative strokes occur after the first 24 hours following surgery, 4 figures reported in studies that observed their patients for only one day after surgery may be falsely low. Elderly patients have a postoperative morbidity for cerebrovascular disease of 0.4 to 3.3 per cent, the higher figure being the rate of complications in a group over age 80. Mortality also appeared to be in a similar range. What the risk is at this time is not available from the literature. For general surgery patients, mortality varies from 0 to 2.9 per cent. In these patients morbidity was reported as 1 per cent in one study and not included in any of the others. The risk of cerebrovascular disease in patients undergoing major vascular surgery is 0 to 1.6 per cent. In one series 44 morbidity decreased from 2.2 per cent before 1969 to 0.8 per cent since 1970. Mortality of 0 to 0.8 per cent may be falsely low since length of postoperative observation was not specified. Among patients undergoing open heart surgery, the risk of postoperative cerebrovascular disease varies with the type of surgery. The morbidity and mortality for patients undergoing open heart surgery for valvular heart disease is quite high, although a change in technique halved the risk in one study. 33 Patients undergoing open heart surgery are at risk of emboli secondary to fat, air, silicone material, calcium, and fibrin. In one prospective study, retinal emboli elnboli developed in 4 of 100 patients. However, among patients undergoing myocardial revascularization the risk is much less (0 to 4.5 per cent) and transient. Mortality from cerebrovascular disease after surgery is reported as 0.2 to 0.7 per cent except in one study in which a figure of less than 3.6 per cent ofless is calculated for overall mortality, with cerebrovascular accident as one of the causes listed. Even among 60 patients who had undergone previous myocardial revascularization and who later required one or more major vascular procedures, a cerebrovascular event was not a cause of postoperative complications. 13 Postoperative morbidity and mortality from cerebrovascular disease in patients with previous stroke or transient ischemic attack may be higher than in asymptomatic patients. Patients with cervical bruits would seem from the data (Table 1) to have no worse postoperative prognosis than those without. Morbidity from postoperative cerebrovascular disease was 1.2 per cent for the total reported group with bruits and 1.1 per cent for the patients without. Furthermore, in two prospective studies,
THE ASYMPTOMATIC CERVICAL BRUIT
1339
carotid bruits were not found to place a patient at risk for cardiac morbidity and mortality, 5,9 although preoperative cerebrovascular accident did,55 did. We can conclude that the risk of a postoperative cerebrovascular fatal or nonfatal event may be higher in patients with previous symptomatic cerebrovascular disease, but there are no data that suggest that patients with asymptomatic bruit or carotid stenosis are at higher risk. Since postoperative strokes tend to occur in the first few days after surgery rather than during or immediately after surgery,4 surgerY,4 mechanisms other than intraoperative hypotension are likely involved. A recent case report demonstrated a cerebral embolus histologically histologic ally similar to a thrombus formed at the site of saphenous aortic graft as the cause of death in a patient undergoing myocardial revascularization. Unilateral loss of vision occurred on the eighth day after surgery and the patient died on the fourteenth day, despite heparinization. 22
Other Considerations Angiography has been reported to carry a morbidity of 0.9 to 13 per cent and a mortality of 0.1 to 2.4 per cent. A multitude of noninvasive tests have been developed to help rule in the need for arteriography, but no excellent test has been described. 11 Flow-dependent noninvasive tests do not detect ulcerating plaques unless accompanied by significant stenosis. More recently, pilot studies have appeared using 123I-Iabelled 123I-labelled fibrinogen, 99mTc-DTPA, 99mTc_DTP A, and computed tomography. Arteriography is still the most definitive test available. The recommended approach of prophylactic carotid endarterectomy has been reported as having a very low morbidity and mortality, 0 to 2 per cent in some centers; however, a recent study reports a rate of postoperative stroke of 18.2 per cent in two community hospitals. 66 Furthermore, the beneficial effects of surgery in patients with asymptomatic bruit have not been established in a prospective, randomized manner. While some series include a control group, most do not.
SUMMARY At the time of this writing there appears to be little evidence that cervical bruits are good indicators of stenosis or plaque in the underlying carotid artery in asymptomatic patients, or that the finding of a carotid bruit places the patient at greater risk of postoperative stroke. The mortaland endarterectomy are too high to risk ity and morbidity of angiography an.d their use in a group of asymptomatic patients.
REFERENCES Note: A complete bibliography is available from the author on request. Limitations of space here, prohibited its inclusion here. H,: A perspective on noninvasive diagnosis of carotid disease. Neurology, 1. Ackerman, R. H.: 29 :615, 1979. 29:615, 2. 2, Bounds, J. V., Sandok, B. A., and Barnhorst, V. A.: Fatal cerebral embolism following surgery, Stroke, 7:611, 1976. aorto-coronary bypass graft surgery.
1340
LOURDES C. CORMAN
3. Branthwaite, M. A.: Prevention of neurological damage during open heart surgery. Thorax, 30 :258, 1975. 30:258, 4. Carney, W. I., Stewart, W. B., DePinto, D. J., et al.: Carotid bruit as a factor in aortoiliac reconstruction. Surgery, 81 :567, 1977. 5. Cooperman, M., Evans, W. E., et al.: Significance of asymptomatic carotid bruits. Arch. 113 :1339, 1978. Surg., 113:1339,1978. and Sherman, D. G.: Stroke and mortality rate in carotid endarterectomy: 228 6. Easton, J. J., andSherman, consecutive operations. Stroke, 8 :565, 1977. 7. Evans, W. E., and Cooperman, M.: The significance of asymptomatic unilateral carotid bruits in preoperative patients. Surgery, 83 :522, 1978. 8. Fields, W. S.: The asymptomatic carotid bruit-operate or not? Stroke, 9:269, 1978. Nussbaum, ussbaum, S. R., et al.: Multifactorial index of cardiac risk 9. Goldman, L., Caldera, D. L., N 297:845,1977. in noncardiac surgical procedures. New Eng. J. Med., 297:845, 1977. 1965. 10. Harper, A. M.: Physiology of cerebral blood flow. Brit. J. Anaesthes., 37:225, 37:225,1965. Thl' asymptomatic bruit. Amer. J. Surg., 11. Kanaly, P. J., Peyton, M. D., Cannon, J. P., et al.: The 134:821, 1977. 12. Marshall, J.: The Management of Cerebrovascular Disease. Oxford, Blackwell Scientific Pub!., 3rd ed., 1976. 13. McCollum, C. H., Garcia-Rinaldi, R., Graham, J. M., et al.: Myocardial revascularization prior to subsequent major surgery in patients with coronary artery disease. Surgery, 81 :302, 1977. 14. Mohr, J. P., Caplan, L. R., Melski, J. W., et al.: The Harvard Cooperative Stroke Registry: A prospective study. Neurology, 28:754, 1978. ofnoninvasi\e screening 15. Takaki, H. S., McNamara, M. F., Yas, J. S. T., et al.: Influence ofnoninvash"e in the care of patients with carotid stenosis. In Dietrich, E. B., ed.: Noninvasive Cardiovascular Diagnosis. Baltimore, University Park Press, 1978. 16. Treiman, R. L., Foran, R. F., Shore, E. H., et al.: Carotid bruit-significance in patients undergoing an abdominal aortic operation. Arch. Surg., 106:803, 1973. 17. Tufo, H. M., Ostfeld, A. M., Shekelle, R.: Central nervous system dysfunction following open heart surgery. J.A.M.A., 212:1333, 1970. University of Florida College of Medicine Gainesville, Florida 32610