Asymptomatic cervical bruits

ROBERT COTt,* MD, FRCP[C] RENALDO N. BATTISTA,t MD, Sc D, FRCP [cI

Table I-Classification of cervical bruits according to anatomic site* Bruits at the base of the neck or supraclavicular Venous: venous murmurs or hums Arterial: bruits transmitted from the heart (resulting from aortic stenosis) or due to atherosclerosis, thoracic outlet syndrome, arteritis or a hyperdynamic state Vertebral bruits (those posterior to the sternocleidomastoid muscle) Diffuse: radiation of supraclavicular murmurs Localized: due to a structural anomaly or atherosclerosis Carotid bruits (those anterior to the sternocleidomastoid muscle) Diffuse: radiation of supraclavicular murmurs Localized (to the middle or upper portion of the carotid, below the angle of the jaw): due to atherosclerosis (of the internal or external carotid artery), kinking or fibromuscular dysplasia *Adapted from reference 2.

dence rates for stroke and myocardiat infarction in the patients with bruits were more than twice those expected for their age and sex, although no correlation could be found between the cerebral area affected and the site of the bruit. Referral population studies Many patients with asymptomatic cervical bruits who are referred to a specialist have other vascular or systemic diseases or symptoms that would increase the likelihood of conditions that might be attributed to the presence of the bruit. Thompson and associates9 compared the long-term outcome of patients with asymptomatic carotid bruits who underwent endarterectomy with that of a control group of patients who did not undergo this operation. Of the 138 control patients 26.8% suffered transient ischemic attacks within 1 to 99 months after detection of the bruit, 17.4% had a mild to serious stroke within 1 week to 124 months, and 2.2% died of a stroke. Of the 132 who underwent endarterectomy, however, 4.5% suffered transient ischemic attacks within 25 to 100 months postoperatively, 2.3% had a stroke within 11 to 67 months postoperatively and another 2.3% died of a stroke. Thompson and associates thus concluded that endarterectomy would reduce the risk of stroke in patients with asymptomatic carotid bruits. However, the poor prognosis in the control patients reflects a selection bias in their study that produced a different distribution of risk factors in the two groups of patients, the difference favouring those who underwent endarterectomy. Other referral-based follow-up studies have reported a higher incidence of stroke than expected, but they were also flawed by biases in patient selection.10"'

Cooperman and coworkers' study'2 60 patients with asymptomatic carotid bruits who had undergone surgery for peripheral vascular disease were followed up for 3 to 7 years. During the follow-up period 20% of the patients suffered transient ischemic attacks and 15% had a stroke; 35% of the patients died, mainly from coronary artery disease. No information was given regarding correlation between the site of the carotid bruit and subsequent transient ischemic attacks and stroke. From a prospective study of asymptomatic carotid disease Barnes and collaborators'3 reported a high incidence of late neurologic deficits in patients who had undergone surgical procedures for peripheral or coronary artery disease; however, they found no relation between the neurologic deficit and the site of the carotid bruit. They did not recommend prophylactic carotid endarterectomy in such patients. In a more recent prospective study Ropper and colleagues'4 examined 735 patients who had undergone elective surgery and found the prevalence of carotid bruits to be 14%. Only 1 of the 104 patients with a bruit, compared with 4 of the 631 patients without a bruit, had had a stroke immediately after the operation. However, the overall incidence of stroke was 0.7% in both groups of patients. Ropper and colleagues therefore concluded that patients with carotid bruits need not be further evaluated for carotid artery disease before elective surgery if they remain asymptomatic. Management

The current literature provides no justification for systematic screening for cervical bruits in asymptomatic patients. Nevertheless, the family practitioner may detect an asymptomatic cervical bruit during either a routine physical examination or an Preoperative population studies examination prompted by an unrelated problem, or it may be found in Approximately 10% to 20% of a patient in whom elective surgery is patients scheduled for major periph- being contemplated. At present eral vascular or coronary artery by- there are no results of definitive pass surgery have asymptomatic ca- randomized prospective studies to rotid bruits.6 In general these pa- indicate the most valuable investigatients are at a higher long-term risk tional and therapeutic strategies in of cerebral infarction than the pa- patients with asymptomatic cervical tients in population-based studies. In bruits. 998

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Bruits detected during routine physical examination Some investigators have reported a poor prognosis in patients who have been referred because of an asymptomatic carotid bruit; many of them presented with vague neurologic symptoms or were suffering from various vascular conditions.9" In general such studies have suffered from significant methodologic flaws; for example, although prospective studies have shown an increased risk of death from stroke or cardiovascular disease in patients with asymptomatic bruits, the site of the bruits and the type of stroke have been poorly correlated.7'8 Recently it was estimated that the annual stroke rate for patients with asymptomatic bruits is approximately 2%,.". the same as that for patients with symptomatic bruits who have undergone endarterectomy.'6 In other words, the risk of stroke in patients with asymptomatic bruits is so low that the best results of surgery are not superior to the results of a more conservative approach. There is therefore no clear general indication for invasive versus noninvasive diagnostic procedures or for prophylactic surgical correction of an underlying arterial lesion in these patients. Anticoagulant therapy has not been shown to be of any significant value in the prevention of stroke in patients with asymptomatic carotid disease.'7 Although treatment with acetylsalicylic acid has been suggested as a prophylactic measure,"6 there is no evidence that antiplatelet agents prevent ischemic stroke in such patients. Because the presence of a carotid bruit is related to an increased risk of vascular disease, risk factors for cerebrovascular disease (e.g., hypertension, diabetes and hyperlipidemia) should be identified and the patient treated appropriately. Recent studies have shown that the treatment of hypertension results in a significant decrease in morbidity and mortality rates related to vascular disease (including stroke).'8"9 Because symptomatic carotid disease is related to an annual risk of stroke of 5% to 7%,20 patients with asymptomatic bruits should be encouraged to promptly report any symptoms to

their physician. In some patients further investigative and therapeutic maneuvers, including cerebral angiography, carotid endarterectomy, and anticoagulant and antiplatelet therapy, should be considered. It is not known whether some patients with asymptomatic bruits are at a higher risk of stroke than others.'0 In sum, on the basis of current knowledge we believe that patients with asymptomatic cervical bruits should be followed up closely for neurologic symptoms, and if such symptoms occur the patient should be promptly referred to a neurologist for further evaluation and treatment. Risk factors for cerebrovascular disease, especially hypertension, should be identified and the condition treated appropriately. Selected patients (e.g., those less than 50 years of age) should be referred to a neurologist for serial noninvasive testing and further evaluation for progressive stenosis; such testing may also identify the patients who are at a high risk of stroke. The prophylactic use of antiplatelet agents in patients with asymptomatic carotid bruits is controversial. Although such treatment has been suggested by some investigators,"6 there are no firm scientific data to support such a recommendation. We do not recommend routine prophylactic carotid endarterectomy, since randomized prospective studies are needed to prove its efficacy in lowering the risk of ischemic stroke.

Bruits detected preoperatively

dertaken in patients with asymptomatic carotid bruits without any speAlthough many studies have ad- cial arterial investigation. The longdressed the relation of asymptomatic term management of these patients bruits and the perioperative risk of postoperatively is the same as that stroke, none have reported a signifi- of other patients with asymptomatic cant increase in the incidence of cervical bruits. perioperative stroke in patients with Patients in whom symptoms or asymptomatic bruits or carotid ar- signs of transient ischemic attacks tery disease.'3"4'2' -25 However, al- appear should be examined by a though the presence of an asymp- neurologist. Several diagnostic inva. tomatic carotid bruit preoperatively sive and noninvasive tools are availdoes not reliably predict an in- able for defining the underlying anacreased risk of a focal neurologic tomic and physiologic abnormalideficit occurring perioperatively, it ties.3'29 may predict the risk of a late stroke or myocardial infarction, or both. Some investigators have suggested Conclusion an aggressive approach to the evaluation and treatment of asymptomatFew would advocate the use of ic cervical bruits detected preopera- investigational and therapeutic tively on the premise that intraoper- strategies that carry more risk than ative hypotension coupled with ca- the untreated disease. The efficacy rotid occlusive disease is the patho- of early detection and investigation genetic mechanism for most strokes of asymptomatic cervical carotid that occur during surgery.26'27 Re- bruits in preventing stroke is not cently this view has been questioned, established. Indeed, it has been sugand other mechanisms, such as car- gested that the risk of stroke may diogenic embolism and altered not exceed the combined risk of coagulability, have been proposed.28 disability and death related to surgiA review of the literature indi- cal treatment. Clearly, the efficacy cates that prophylactic carotid end- of surgical and pharmacologic treatarterectomy, performed before per- ment will have to be proven by well ipheral vascular surgery or coron- controlled randomized prospective ary artery bypass, does not signifi- studies. The goal of management is cantly reduce the risk of periopera- to reduce the risk of stroke safely tive cerebral ischemia in patients and with due regard for the fact that with asymptomatic carotid disease.2' the greatest risk to the patient is not We therefore believe that any indi- cerebrovascular disease but, rather, cated surgical procedure can be un- death from cardiac disease.

I Most "lost" charts are the victims of lax office procedures. First, never allow charts to leave the office. Complete your notes and dictation before you leave. Keep charts visible at all times, too. Don't put them in a desk drawer or your briefcase where they could be forgotten. Insist that refiling of charts be done at least once a day along with lab reports, consultants' letters, etc. Finally, designate a convenient area in which completed charts and reports can be placed ready for filing. CAN MED ASSOC J, VOL. 130, APRIL 15, 1984

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11. DoR.zio RA, EZZET F, NESBITT NJ: Long-term follow-up of asymptomatic carotid bruits. Am J Surg 1980; 140: 212-2 13 12. COOPERM-AN M, MARTIN EW JR, EVAt.{S WE: Significance of asymptomatic carotid bruits. Arch Surg 1978; 113: 13391340 13. BARNES RW, LIEBMAN PR, MARSZALEK PB, KIRK CL, GOLDMAN MH: The natural history of asymptomatic carotid disease in patients undergoing cardiovascular surgery. Surgery 1981; 90: 10751083 14. ROPPER AH, WECHSLER LR, WILSON LS: Carotid bruit and the risk of stroke in elective surgery. N Engi J Med 1982; 307: 1388-1390 15. WHISNANT JP: The role of the neurologist in the decline of stroke. Ann Neurol 1983; 14: 1-7 16. WHISNANT JP, SANDOK BA, SUNDT TM JR: Carotid endarterectomy for unilateral carotid system transient cerebral ischemia. Mayo Clin Proc 1983; 58: 17 1-175 17. LINDBLAD CI: Asymptomatic internal carotid artery atherosclerotic lesions to treat or not to treat? (C) Lancet 1982; 1: 274 18. Hypertension Detection and Follow-up Program Cooperative Group: Five-year findings of the hypertension detection and follow-up program. III. Reduction in stroke incidence among persons with high blood pressure. JAMA 1982; 247: 633638 19. The Australian therapeutic trial in mild hypertension. Report by the management committee. Lancet 1980; 1:1261-1267 IP, SUNDT TM IR: Guidelines for the management of transient ischemic attacks. Mayo Clin Proc 1978; 53: 665674 21. HART RG, EASTON JD: Management of

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tions. J Thorac Cardiovasc Surg 1981; 82: 765-767 23. TURNIPSEED WD, BERKOFF HA, BELZER FO: Postoperative stroke in cardiac and peripheral vascular disease. Ann Surg 1980; 192: 365-368 24. TREIMAN RL, FORAN RF, COHEN JL, LEVIN PM, COSSMAN DV: Carotid bruit: a follow-up report on its significance in patients undergoing an abdominal aortic operation. Arch Surg 1979; 114: 11381140 25. CARNEY WI JR, STEWART WB, DEPINTO DI, MUCHA SJ, ROBERTS B: Carotid bruit as a risk factor in aortoiliac recon-

struction. Surgery 1977; 81: 567-570 26. FELL G, BRESLAU P, KNOX RA, PHILLIPS D, THIELE BL, STANDNESS DE IR: Importance of noninvasive ultrasonic-Doppler testing in the evaluation of patients with asymptomatic carotid bruits. Am. Heart J 1981; 102: 221-226 27. KARTCHNER MM, MCRAE LP: Guidelines for noninvasive evaluation of asymptomatic carotid bruits. Clin Neurosurg 1981; 28: 418-428 28. HART R, HINDMAN B: Mechanisms of perioperative cerebral infarction. Stroke 1982; 13: 766-773 29. TAVERAS JM: Radiological diagnostic procedures. In SIEKERT RG (ed): Cere-

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In the

Social aspects of low birth weight

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In most Western countries low birth weight is the single most important factor in infant mortality and morbidity. The low-birth-weight ratio is influenced by many variables, including socioeconomic status and education. In his comprehensive article Dr. Henry G. Dunn, from the Children's Hospital in Vancouver, discusses the factors that influence the risk of low birth weight, the determinants of the ultimate level of brain function in children of low birth weight, measures for preventing low birth weight, and means of compensating for social disadvantage.

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