CAROTID SINUS SYNDROME: NEW SURGICAL CONSIDERATIONS R. S. GARDNER, M.D., G. J. MAGOVERN, M.D., S. B. PARK, M.D., W. J. CUSHING, M.D., G. A. LIEBLER, M.D., AND R. HUGHES

Carotid sinus syndrome is a relatively rare disorder with a sparsity of’ reports in the literature and is not to be confused with carotid body tumors (figure 1). In 1886 Cermak reported that palpation of a nodule in the side of his neck produced a slowing of’ his pulse.’ The reasons for this eluded precise medical explanation until 1923, when Hering in a comprehensive study determined that carotid sinus syndrome was caused by stimulation of a dilated area of the proximal internal carotid artery. Pressure on the carotid sinus excites a number of’ sensory nerve fibers which are embedded in the thickened adventitia and are known variously as baroreceptors, pressoreceptors or stretch receptors. These impulses are conduced through many small branches, which occasionally form a large trunk-Hering’s nerve. These impulses progress along the glossopharyngeal nerve to the vagus nerve and finally to the heart. 10 By the early thirties several investigators, but particularly Weiss and Baker,30 described the causes and effect of’ the syndrome much as we know it

today, namely: 1. Pathway of stimulation

of’ carotid sinus syndrome (figure 2) 2. Clinical classification of’ carotid sinus syndrome A. Cardioinhibitor (vagal type) B. Vasodepressor C. Primary cerebral Today the pathophysiology is more apparent. The cardioinhibitor effect which is the mechanism for 50 to 75% of’ cases of the syndrome is caused predominantly by increased vagal activity and to a lesser degree by decreased sympathetic activity and decreased circulating adrenalin. The vasodepressor effect which represents 5 to 10% of’ cases is mediated in much the same way with the additional involvement of’ the medullary reticular formation to the vasodepressor center to the peripheral circulation. The primary cerebral type is rare (less than 5%’). Its pathway is not clear but is thought to be centrally through the glossopharyngeal nerve. Carotid sinus stimulation also causes depression of respiration, diminished skeletal muscle tone and minor viseral changes. Clinically, the syndrome appears as a form of transient dizzy spells or unconsciousness. With close questioning there is usually an associated history of pressure to the carotid sinus which may be caused by turning the head, tight collar or actual direct pressure to the neck. Contributing factors may be digitalis, arteriosclerosis, hypertension, arteriosclerotic heart disease, diabetes and insulin. All make the carotid sinus more sensitive. The dizzy spells

Department of Surgery, Allegheny

General

Hospital, Pittsburgh, Pennsylvania 204

Downloaded from ves.sagepub.com at MICHIGAN STATE UNIV LIBRARIES on June 2, 2015

15212.

205

FIG. 2.

referred to as hyperreactive carotid sinus reflex are asystoles lasting 3-5 seconds with a blood pressure drop of 30-50 mm Hg. Normally, carotid sinus stimulation produces slight bradycardia and a blood pressure drop of 10 mm Hg. The more severe form of the syndrome comprising 5-20% of the total and known as carotid sinus syncope requires a 5 second or more asystole and a greater than 50 mm Hg. blood pressure drop. The syndrome is rarely found below the age of 30 and increases directly with age and degree of arteriosclerosis. It is twice as frequent in males. It can manifest itself as blurring or darkness of vision, general weakness, pressure or fullness in the head, tinnitus, paresthesias of the hand, dyspnea, headache, confusion, nausea and sweating. These varied symptoms can make borderline hyperactive patients difficult to

Downloaded from ves.sagepub.com at MICHIGAN STATE UNIV LIBRARIES on June 2, 2015

206 on the other hand is usually somewhat easier to diagnose. it can present atypically as convulsions or can be instances Even so in certain mimicked by carotid insufficiency .31 Symptoms of both the hyperreactive and the syncope patient should occur with pressure to the carotid sinus and should fail to occur after infiltration of the sinus with procain.3 Several important features should be remembered in examining these

diagnose. Syncope

patients. 1. Initially the neck should be examined with the patient in the supine position. 2. Only one side of the neck should be massaged at a time with a light gradually increasing pressure until symptoms are elicited. 3. Cerebral damage has occurred following examinations. Therefore, in cases of syncope, the elective production of symptoms should be kept at a

minimum. TREATMENT

A first treatment is generally conservative with the use of atropine or like drugs for bradycardia and ephedrine or Benzedrine for hypotension. Instructions are given to avoid physical stimulation of the sensitive area. As the syndrome has become better known, it is apparent that most cases of syncope will not respond to medication and most are refractory to conservative methods of treatment. 1, 22, 23 Surgery for carotid sinus syncope has proved to be a method that can give permanent cure. 2 0, 2 2, 1, 5, 3l Unfortunately, two aspects of surgical treatment were undesirable, a high recurrence rate of’ up to 50% and unpredictable sudden deaths or permanent central nervous system damage. 1. 11, 14, 16. 23, 26 These problems are interrelated in such a manner that success in one is achieved at the expense of the other. A well anesthetized sinus prevents the long asystoles or hypotension that caused death or central nervous damage during surgery, but also made it difficult to determine the adequacy of the resection, with resultant frequent recurrences. 21 Conversely, an unanesthetized sinus can be easily checked to determine if any cardiac depression remains, but the associated complications of cardiac asystole are

high. Concern about postoperative hypertension is unwarranted since it is usually of short nature. However, bilateral denervation may cause troublesome

long-term postural hypotension. In 1971 because of these problems a number of investigators began to advocate the use of permanently implanted pacemakers to control the patient with carotid sinus syndrome refractory to medical management.’, 1, 27, 28. 29 It can be done with relatively little risk under local anesthesia and provides good control of intermittent bradycardias and asystoles. DISCUSSION

Our opinion is that surgical denervation of the carotid sinus is still the procedure of choice if it is done as safely as pacemaker insertion for the

following

reasons:

Downloaded from ves.sagepub.com at MICHIGAN STATE UNIV LIBRARIES on June 2, 2015

207 1. Pacemakers

are

not

permanent since they require replacement

every two

years while malfunction may result in an earlier replacement. 2. Pacemakers are not without morbidity (i.e. infections, cardiac perforations, extrusions, etc.) 7, 15, 18, 19, 25 Several large series have shown major complications over 30%.13, 144 3. Pacemakers do not cure the vasodepressor or cerebral type of carotid sinus syncope. 28 In addition recurrence rates might be lower if’ the surgeon could have a method of determining the completeness of denervation at that time of

surgery.

Because of this, the following is advocated for the treatment of’ confirmed selected cases of carotid sinus syncope refractory to medical management. Preoperative carotid angiograms to confirm absence of’ arteriosclerotic carotid insufficiency.3’ At the same time temporary endocardial pacing leads are inserted to allow a safely conducted anesthesia. This also provides for an easy way to determine the sensitive sites of the carotid sinus without the danger of a fatal asystole. The EKG demonstrates the areas of sensitivity which show demand cardiac pacing when stimulated and permits a complete excision of the necessary tissue. An electrical nerve stimulator facilitates this search. The procedure offers little difficulty or risk, and is comparable to the risks and complications of periodic pacemaker insertions. CASE REPORT

Mr. W. L. is a 63 year old male who complained of’ fainting spells for two years. These fainting spells would occur when he experienced any pressure to his right neck and this, at first, cause him to buy larger collars. His symptoms progressed until any twisting of his head to the left caused fainting. He finally sought medical consultation since he was a traveling salesman and feared an automobile accident during one of his spells. Initial examination by his private physician revealed an extremely sensitive right carotid sinus the lightest palpation of which produced syncope and a 5 second asystole. He was referred to the cardiovascular service for treatment. Routine laboratory studies were within normal limits. In addition, four vessel cerebral angiograms were obtained and were found to be within normal limits. At the same time, a temporary endocardial pacer was placed. He was seen in consultation by the neurology service which concurred with the diagnosis of carotid sinus syncope. OPERATIVE DESCRIPTION

The patient was premedicated with Atropine and Vistal and under general endotracheal anesthesia using Pentothal, Nitrous oxide and Halothane an incision along the anterior border of the right sternoclediomastoid muscle was made to expose the right carotid bufurcation. By the use of a nerve stimulator and by mechanical stimulation the sensitive areas on the carotid (carotid sinus) and surrounding nerves (Hering’s nerve) could be accurately determined. This was easily done by observing the cardiac monitor. The pacemaker

Downloaded from ves.sagepub.com at MICHIGAN STATE UNIV LIBRARIES on June 2, 2015

208

the patient’s normal rate, and the sensitive areas of the carotid sinus were showed when scope dramatically stimulated. The entire carotid sinus and afferent nerve supply were easily and quickly mapped out. (figure 3). Denervation of’ the carotid sinus was easily performed. The operation went smoothly and the patient showed no adverse effect throughout the entire procedure. At no time did the heart rate drop below the desired rate set on the pacemaker. was

set at

a

rate of’ 10 per minute lower than

POSTOPERATIVE COURSE

On the first postoperative day compression of’ the operative site produced a 10 per minute rate depression. The blood pressure showed a 30 mm Hg. rise

preoperative levels. By the third postoperative day, no cardiac rate depression could be elicited and the blood pressure had returned to normal. over

Examination at nine months showed no residual carotid sinus function right and the patient had been completely asymptomatic.

on

the

CONCLUSION

This case was reported to illustrate an approach to carotid sinus surgery that is both safe and capable of’ a complete denervation without the long-term

FIG. 3. Tapes are around common, internal and external carotid arteries. Silk ligature at 1 o’clock is around usual location for nerves from the carotid sinus (Hering’s nerve). Silk ligature at 7 o’clock shows fine nerve fibers that were found with nerve stimulation and mechanical stimulation. These nerves were embeded in the areolar tissue several cm’s lateral to the usual distribution of nerves from the carotid sinus. If’ local anesthesia had been used, stimulation of the area would have had no effect and these nerves would have been missed. The above picture is somewhat misleading since the nerves appear very obvious following their dissection from the covering tissue.

Downloaded from ves.sagepub.com at MICHIGAN STATE UNIV LIBRARIES on June 2, 2015

209

problems associated with pacemakers or the complications connected with earlier surgical procedures. It is felt that this approach will result in better cure

rates. ’

SUMMARY

surgical denervation of the carotid sinus would long-term results for carotid sinus syncope.

1. Direct

best

appear to offer the

2. Carotid sinus denervation should be done under temporary cardiac pacing for safety and for completeness of’ denervation. 3. Arteriography is indicated to eliminate those cases of cerebral vascular insufficiency that might mimic carotid sinus syndrome. Credit must be given to Dr. R. Hughes, Clearfield, Pa., who recognized this diagnosis and referred the patient for therapy.

Robert S. Gardner, M.D.

Department of Surgery Allegheny General Hospital Pittsburgh, Pennsylvania 15212 REFERENCES

Bahl, O. P., Ferguson, J. B., Oliver, G. C. and Parker, B. M.: Treatment of carotid sinus syncope with demand pacemaker. Chest 59: 262-5, 1971. 2. Bonchek, L. I.: New methods in the management of extruded and infected cardiac pacemakers. Ann. Surgery 176: 686-9, 1972. 3. Chusid, J. G.: Correlative neuroanatomy and functional neurology. Lang. Med. Publication, Los Altos, Cal. pp. 392-4, 1970. 4. Craig, W. M. and Smith, H. L.: The surgical treatment of hypersensitive carotid sinus 1.

reflexes: A report of thirteen cases. Yale J. Biol. Med. 11: 415-22, 1938-9. 5. DeTakots: Vascular Surgery; The carotid sinus syndrome pp. 457-64, W. B. Sanders, 1959. 6. Dunst, M.: Cardiac pacemakers. Med. Clinic of North America 57: 1515-24, 1973. 7. Escher, D. J. W.: Types of pacemakers and their complications. Circulation, XLVII: 1119-31, 1973. 8. Fearon, R. E.: Demand pacing in carotid sinus syncope. American Heart Journal 81: 581, 1971. 9. Ham, A. W.: Histology. pp. 590 Fifth Edition, J. B. Lippincott Co. 1965. 10. Hering, H. E.: Die sinusreflexe vom sinus caroticus werden durch einen nerven (sinusvert) vermittelt der ein ast des nervus glossopharyngeus ist. Munchen Med. Eschr. 71: 1265-66, 1924. 11. Heron, J. R., Anderson, E. G. and Noble, I. M.: Cardiac abnormalities associated with carotid sinus syndrome. Lancet, ii, 214-6, 1965. 12. Hoffman, E. and Rochbery, S.: The hypersensitive carotid sinus reflex. Amer. J. Surg. 84: 693-95, 1952. 13. Imparato, A. M. and Kim, G. E.: Electrode complications in patients with permanent cardiac pacemakers. Arch. Surg. 105: 705-10, 1972. 14. Lambertsen, C. S.: Medical Physiology. pp. 183-90 C. V. Mosby Co. Edited by Mountcastle, V. B. 1968. 15. McLaughlin, J. S., Cohen, M. L., Singleton, R., Attar, S., Scherlis, L. and Cowley, A.: Permanent transvenous catheter pacing. J. Thoracic and Cardiovascular Surgery 66: 771-7, 1973. 16. Merritt: Testbook of Neurology. pp. 745-6 Lea and Febiger, 1963. 17. Palmer, R. A.: The treatment of carotid sinus syncope with propontheline. Cad. Med. Assoc. J. 104: 923-5, 1971. 18. Parsonnet, V., Feldman, S., Parsonnet, J. and Rothfeld, E. L.: Arrhythmias induced by exercise in paced patients. Am. Heart Journal 87: 76-82, 1974. 19. Parsonnet, V., Gilbert, L. and Zucker, I. R.: The natural history of pacemaker wires. J. Thoracic and Cardiovascular Surgery 65: 315-22, 1973. 20. Ray, B. S. and Stewart, H. J.: Observations and surgical aspects of the carotid sinus reflex in man. Surgery 11: 915-38, 1942. 21. Reich, N. E.: The versatility of the carotid sinus in diagnosis and treatment. Angiology 8: 328-36, 1957.

Downloaded from ves.sagepub.com at MICHIGAN STATE UNIV LIBRARIES on June 2, 2015

210 22. 23. 24.

25. 26. 27. 28.

R. E., Faller, C. P. and Quickel, K. E.: The treatment of the carotid sinus syndrome. Amer. J. Cardiology 2: 351-6, 1958. Salomon, S.: The carotid sinus syndrome. Amer. J. Cardiology 2: 342-350, 1958. Schowengerdt, C. G. and Masangkay, M. P.: Implantation of cardiac pacemakers. (a review of complications) Ohio State Med. Journal 68: 1015-8, 1972. Seremetis, M. G., DeGuzman, V. C., Lyons, W. S. and Peabody, J. W.: Cardiac pacemakers (clinical experience with 289 patients) Am. Heart Journal 85: 739-48, 1973. Thomas, J. E.: Hyperactive carotid sinus reflex and carotid sinus syncope. Mayo Clinic Proceedings 44: 127-39, 1969. Von Lehe, D. P., Jr.: Carotid sinus syncope treated with demand pacemaker. J. Science Med. Assoc. 67: 7-9, 1971. Von Maur, K., Nelson, E. W., Holsinger, J. W., Jr. and Eliot, R. S.: Hypersensitive carotid sinus syncope treated by implantable demand cardiac pacemaker. Am. J. Cardiology 29:

Rosco,

109-10, 1972. 29. Voss, D. M. and Magnin, G. E.: Demand pacing and carotid sinus syncope. Am. Heart Journal 79: 544-7, 1970. 30. Weiss, S. and Baker, J. P.: The carotid sinus reflex in health and disease: its role in the causation of fainting and convulsions. Medicine 12: 297-354, 1933. 31. Wertheimer, M., Hughes, R. and Castle, H.: Superior vena cava syndrome: complication of permanent transvenous endocardial cardiac pacing. JAMA 224: 1172-3, 1973. 32. White, J. C., Smithwick, R. M. and Sineone, F. A.: The Autonomic Nervous System, Anatomy, Physiology and Surgical Application. pp. 234-9, Third Edition, N.Y. The Macmillan Co., 1952. 33. Willis, W. D. Jr. and Grossman, R. G.: Medical Neurobiology. pp. 301, The C. V. Mosby Co., St. Louis 1973. 34. Wright, I. S.: The year book of cardiovascular medicine and surgery. pp. 324, Year Book Medical Publishers, Chicago 1972.

Downloaded from ves.sagepub.com at MICHIGAN STATE UNIV LIBRARIES on June 2, 2015

Carotid sinus syndrome: new surgical considerations.

1. Direct surgical denervation of the carotid sinus would appear to offer the best long-term results for carotid sinus syncope. 2. Carotid sinus dener...
439KB Sizes 0 Downloads 0 Views