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Blunt trauma to the carotid arteries
Blunt trauma to the carotid arteries R o n a l d F. Martin, M D , Jens Eldrup-Jorgensen, M D , David E. Clark, M D , and Carl E. Bredenberg, M D , Portland, M~tine, and Syracuse, N.Y. Blunt carotid artery trauma is an uncommon but potentially dangerous clinical entity. We report eight: patients from a 10-year interval who sustained blunt injuries to the carotid arteries. Six of eight patients suffered a hyperextension injury or had a cervical spine fracture or both. Artedography revealed four arterial dissections and four thrombotic occlusions. 'two asymptomatic common carotid artery occlusions and one dissection with transient ischemic attacks had successful arterial reconstructions. Five patients were treated nonoperatively: three internal carotid artery dissections with minor or no neurologic deficit; one asymptomatic thrombosis; and one internal carotid artery thrombosis with a major fixed neurologic deficit that did not improve. No patient died, and seven of eight made a complete neurologic recovery or remained asymptomatic. The diagnosis of blunt carotid artery injuries should be suspected in patients with neck hyperextens.ion injuries or with cervical spine fractures as well as in patients with neurologic deficits not explained by intraeranial trauma. Duplex scanning may be a useful noninvasive study. Surgery is indicated for selected patients with accessible lesions who have minor or no neurologic deficits. Asymptomatic patients with small intimal flaps or dissections may be successfully treated nonoperatively. (J VASC SURG 1991;14:789-95.)
Blunt trauma to carotid arteries occurs infrequently and accot~nts for only 3% to 10% of all reported carotid injuries. 15 Mortality rates for injury are reported from 120% to 40% in larger series, 3,6s and permanent neurologic deficits range from 40% t o 80%. 5fi'9 The injury is often not recognized at the time the patient is a,~nitted, ~,6,~°and hence treatment may be delayed. PATIENTS AND METHODS Medical records from the Maine Medical Center (Portland, Maine) and SUNY Health Science Center (Syracuse, N.Y.) from 1981 to 1991 listing a diagnosis of carotid injury were reviewed. Patients with carotid injuries as a result of penetrating trauma or iatrogenic procedures were excluded. A summary of the eight remaix~ng cases is given in Table I. Six of the eight patients were men (75%). The mean age was 22 years, with a range of 12 to 43 years. The mechanism of injury varied among the eight patients. Six patients had hyperextension injuries to the neck: one was an unstable cervical spine ligamenFrom the Department of Surgery, Maine Medical Center, Portland, and the Depamnent of Surgery,State Universityof New York Health ScienceCenter, Syracuse. Presented at the Fifth Annual Meeting of the Eastern Vascular Society, Pittsburgh, Pa., May 4, 1991. Reprint requests: RonaldF. Martin,MD, Departmentof Surgery, Maine MedicalCenter, 22 BramhallSt., Portland, ME 04]i02. 24/6]32076
tous injury (five a result of motor vehicle accidents and one because of a fall); one had a case of blunt intraoral trauma that occurred while the patient was sledding, and one patient had a crush injury to the chest and neck. Three of the eight patients were admitted with neurologic deficits. Two had lateralizing motor signs (left hemiplegia and left hemiparesis), and one was comatose. The patient in coma (S.T.), however, had a complicated injury in that he also had a closed head injury and a significantly elevated blood alcohol level. His level of consciousness improved significantly with a decrease in blood alcohol content. One patient later had transient ischemic attacks with right arm and leg weakness. In only one of the eight patients was carotid artery injury suspected at the time of initial evaluation. In six patients the injury was incidentally detected during radiographic imaging for other injuries. In four patients (50%) the diagnosis of carotid injury was made during arteriography for suspicion of transected thoracic aorta: one of these four had a dissection of the left common carotid artery near its origin; one had bilateral internal carotid artery dissections; one had a thrombosed left common carotid artery near its origin; and one had a thrombosed right internal carotid artery. Two patients with thromboses were incidentally detected while undergoing CT scanning of the head and neck. In these two patients CT scanning of the neck revealed an in789
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Martin et al.
Table I. Summary of cases Patient
Age/sex
EB
12/M
MB
25/M
MN
Neurologic deficit
Mechanism of injury
Left hemiplegia None
Intraoral trauma
15/M
Left hemiparesis
Hyperextension MVA
ST
20/M
KG
22/F
Comatose (alcohol, CIM) None
DU
20/M
GS
20/M
Transient cerebral ischemia None
Hyperextension MVA Hyperextension MVA Hyperextension MVA Crush chest/neck
BH
43/F
None
Hyperextension/fall
Hyperextension MVA
Diagnostic study CT scan/arteriography CT scan/arteriography CT scan/Doppler/arteriography Arteriography (? TTA) CT scan/arteriography Atteriography (? TTA) Arteriography (? TTA) Arteriography (? TEA)
Type of injury
Treatment
Outcome
Thrombosis RICA Thrombosis/intimat flap RCCA Dissection RICA
Support ~
Support
No deficit
Thrombosis RICA Dissection LICA Dissection LCCA Thrombosis/avulsion LCCA Dissection bilateral ICA
Support
No deficit
IV heparin/warfarin LSCA-LCCA bypass Interposition graft Support
No deficit
Interposition graft
Left hemiplegia No deficit
No deficit No deficit No deficit
CT, Computed tomography; RICA, right internal carotid artery; LICA, left internal carotid artery; ICA, internal carotid artery; LSCA, left subclavian artery; CHI, closed head injury; MVA, motor vehicle accident; RCCA, right common carotid artery; LCCA, left common carotid artery; TTA, transected thoracic aorta; Support, observation and rehabilitative care.
creased density in the carotid artery. Arteriography confirmed thrombosis of the right common carotid artery in one patient and a thrombosed right internal carotid artery in the other. One patient had left hemiparesis and underwent a CT scan of the head for suspected cerebral injury. Because no intracranial injury was detected in the presence of the left hemiparesis, a Doppler examination of the neck was performed, which revealed a decreased flow velocity pattern in the right internal carotid artery. Arteriography confirmed dissection of the right internal carotid artery. The final patient (E.B.) was promptly studied with four-vessel cerebral arteriography for early suspicion of a thrombosed right internal carotid artery after CT scanning revealed a pale infarct in the right middle cerebral artery distribution in the setting of left hemiplegia. Three patients were treated operatively and five were managed nonoperatively. Of the three patients undergoing operation, two had asymptomatic occlusions of the common carotid artery (one avulsion/thrombosis and one intimal flap/thrombosis), which were repaired with synthetic interposition grafts. The third patient was initially asymptomatic with a documented dissection of the left common carotid artery near its origin. After having transient ischemic attacks he underwent extraanatomic bypass from the left subclavian artery to the left
common carotid artery with ligation of the proximal left common carotid artery. Five patients were managed nonoperatively. Three of these patients had dissections with minor or no neurologic deficits; one was given heparin for systemic anticoagulation, and two received no specific treatment. The remaining two cases, which were managed nonoperatively, had thromboses of the internal carotid artery of unclear origin. One had a dense left hemiplegia and on CT scanning evidence of a right parietal stroke, and one was asymptomatic. Both were managed supportively with observation and rehabilitative care only. Seven of eight patients made a complete neurologic recovery or remained asymptomatic. One individual with dense left hemiplegia after blunt intraoral trauma made no clinical improvement with expectant management. DISCUSSION
Blunt carotid artery trauma is a rare clinical entity that comprises 3 % to 10% of all carotid injuries.~'2,~'~ An estimated incidence of 0.08% in the blunt trauma population is reported in one large series. H Several possible mechanisms of injury have been postulated. Hyperextension of the neck with contralateral rotation of the head, direct blows to the neck, blunt intraoral trauma, basilar skull fractures
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injuring the intrapetrous portion of the vessel, therapeutic and diagnostic carotid massage, 3,6,12,13 and attempted strangulation ~4 have all been suggested as etiologic mechanisms for injury to the carotid artery. Findings commonly associated with blunt carotid artery trauma include the following: (1) lateral neck hematoma formation; (2) ipsilateral Horner's syndrome; (3) transient ischemic attacks; (4) lucid interval with development of a focal neurologic deficit; and (5) progressive limb paresis in an alert and oriented patient. 15 Less commonly associated findings include aphasia, seizures, drowsiness, retrograde amnesia, and isolated motor or sensory deftcits. 9 Associated injuries are common and frequently include closed heact injuries, cervical spine injuries, and long bone fractures, n'~6 The diagnosis of blunt carotid artery trauma can frequently be difficult at the time of initial presentation. In a collective: review of 96 patients with blunt carotid arterial injuries, diagnosis was delayed in 94% of patients because symptoms resembled those of closed head trauma or a latent interval existed between the time of injury and the onset of symptoms. At least 50% of patients had no visible evidence of cervical trauma. 6 Blunt carotid arterial injury was frequently first suspected during evaluation for other injuries. Fifty percent of patients in our series were diagnosed ~dth carotid artery injm~¢ while undergoing aortography for suspected transected thoracic aorta. This is similar to the experience of Rosenberg et al.~6 who reported that 28 of 30 patients with blunt injury to the aortic arch vessels were diagnosed at arteriographic examination for aortic ruptnre. 16 The diagnosis is rarely suspected in asymptomatic patients with blunt upper thoracic or cervical tramna. Two of the patients in our series had the injury discovered incidentally while undergoing CT scanning of the head and neck (Fig. 1), and arteriography played a confirmatory role. If the diagnosis is considered, a reluctance exists to subject patients to arteriography to identify such an uncommon problem. Increased use of the carotid duplex scan can aid in making the diagnosis. Davis et al.n report a series of 14 blunt carotid artery dissections, and five patients were studied with duplex scanning. Two internal carotid occlusions were correctly identified as well as bilateral intimal flaps in one patient. In one patient turbulent flow was shown; it was later confirmed by arteriography to be an irregular vessel.
Blunt trauma to the carotid arteries
791
Fig. 1. CT scan of the neck revealing a hypodense area in the right common carotid artery indicating thrombosis (arrow).
One patient was thought to have an occluded internal carotid artery by duplex scanning which was later shown to be an irregular but patent vessel by arteriography. Other reports have supported the use of ultrasonography for the diagnosis or screening of this i n j u r y . 17-19 Therapeutic alternatives include observation, 2,s,n anticoagulation, 2,n,2° ligation of the carotid artery with or without extracranial-intracranial bypass, 2,s and arterial reconstructionY ,6,um,22 Reported success of these treatment modalities is highly variable. Mortality rates as high as 40% and morbidity rates as high as 80% have been reported for this injury. 3'5,6,7,9 Anatomic location of the arterial injury, type of arterial defect, neurologic and cardiovascular status, and associated injuries are all important considerations in the treatment of these patients. Thrce of eight patients in our series sustained common carotid artery injuries, and all patients who were treated surgically had common carotid artery injuries and were initially asymptomatic. Patients with injuries of the distal internal carotid artery pose special problems. Thrombosis of the internal carotid artery is more likely to cause stroke than occlusion of the common carotid artery with preservation of collateral
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flow to a patent internal carotid artery. In addition, surgical access to the internal carotid artery near the base of the skull can be difficult. Although there are surgical techniques to improve access to this region,22 a group of lesions remains where this is probably too hazardous to justify operation. This includes intimal flaps or dissections that may extend to the base of the skull. Furthermore, associated cervical spine injuries may preclude the use of some techniques used for improved exposure. The primary goal of therapy is to prevent the development of neurologic deficits. Patients with major fixed neurotogic deficits do not respond well to any treatment. Patients with lesions of the distal internal carotid artery are not good operative candidates, and anticoagulation should be considered. Patients with demonstrated lesions of the carotid artery that are surgically accessible should undergo vascular repair if there is evidence of transient cerebral ischemia or completed mild neurologic deficit. 6,22,2s Small dissections or intimal flaps are treated conservatively. A clinical review of intimal arterial injuries showed no difference in outcome between patients treated operatively or with anticoagulation for small intimal injuries.24 An experimental canine model suggests that intimal injuries that are not hemodynamically significant may not require surgical repair. 2s Patients with evidence of thrombosis into the intracranial portion of the artery or extensive intracerebral embolization should not be treated surgically and should undergo systemic anticoagulation to prevent distal propagation of thrombus unless contraindicated by associated injuries or coagulopathy. 3's'21 Other contraindications to surgical reconstruction include coma or significant cardiovascular instability, s,21 In summary, blunt carotid arterial trauma is a rare entity that is frequently diagnosed in a delayed fashion. We emphasize the importance of an early raised index of suspicion. We support attempting to identify this injury in patients undergoing arteriography for suspected aortic rupture as well as extending the field of study caudally to include the cervical carotid artery in patients undergoing cerebral CT scanning with neurologic deficits that are not explained by intracranial findings. Duplex scanning for selected patients based on mechanism of injury, associated physical findings, or associated injuries may be useful for earlier detection of these injuries. Surgery is indicated for patients with accessible
lesions and evidence of transient cerebral ischemia or minor neurologic deficits or for asymptomatic patients with thrombosis of the common carotid artery. Whether attempts should be made to revasctthrize occluded internal carotid arteries when there is minor neurologic deficit remains controversial. Small intireal dissections or intimal flaps may be managed conservatively, and anticoagulation should be considered unless contraindications exist because of other injuries. Surgery is contraindicated in patients with profound neurologic deficits or significant cardiovascular instability. REFERENCES 1. Dragon R, Saranchak H, Lakin P, Strauch G. Blunt injuries to the carotid and vertebral arteries. Am J Surg 1981;141:497500. 2. Fakhry SM, Jacques PR, Proctor HI. Cervical vessel injury after blunt trauma. J VAsc SURG 1988;8:501-7. 3. Perry MO, Snyder WH, Thai ER. Carotid artery injuries produced by blunt trauma. Ann Surg 1980;192:74-7. 4. Rubio PA, Reul GJ Jr, Beall AC, et al. Acute carotid artery injury: 25 years' experience. J Trauma 1974;14:967-73. 5. Yamada S, Kin& GW, Youmans JR. Carotid artery occlusion due to non-penetrating injury. 1 Trauma 1967;7:733-42. 6. Krajewski LP, Hertzer NR. Blunt carotid artery trauma. Alan Surg 1980;191:341-6. 7. Manrer PK, Plassche W, Green RM. Blunt trauma to the carotid artery with transient deficit and early repair. Surg Neurology 1984;21:110-2. 8. Towne JP, Neiss ND, Smith JW. Thrombosis of the internal carotid artery following cervical trauma. Arch Surg 1972;104: 565-8. 9. Mears GD, Leonard RB. Blunt carotid artery trauma: a case report. J Emerg Med 1988;6:281-4. 10. Welling RE, Saul TG, Tew JM~ Tomisch TA, Kremchek TE, Bellamy MI. Management of blunt injury to the internal carotid artery. J Trauma 1987;27:1221-6. 11. Davis JW, Holbrook TL, Hoyt DB, Mackersie RC, Field TO, Shackford SR. Blunt carotid artery dissection: incidence, associated injuries, screening, and treatment. J Trauma 1990;30:1514-7. 12. Crissey MM, Bernstein EF. Delayed presentation of carotid intimal tear following blunt craniocervical trauma. Surgery 1974;75:543-9. 13. New PFI, Mamose KJ. Traumatic dissection of the internal carotid artery at the aflantoaxial level secondary to nonpenetrating injury. Radiology 1969;93:41-9. 14. Milligan N, Anderson M. Conjugal disharmony: a hitherto unrecognized cause of strokes. BMJ 1980;281:421-2. 15. Jernigan WR, Gardner WC, Carotid injuries due to closed cervical trauma. J Trauma 1971;11:429-35. 16. Rosenberg JM, Bredenberg CE, Marvasti MA, Bucknam C, Conti C, Parker FB Jr. Blunt injuries to the aortic arch vessels. Ann Thoracic Surg 1989;48:508-13. 17. Bashour TT, Crew JP~ Dean M. Ultrasonic imaging of common carotid artery dissections. J Clin Ultrasound 1985; 13:210-1.
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18. Bluth EI, Shyn PB, Sullivan MA, et al. Doppler color flow imaging of carotid artery dissection. J Ultrasound Med 1989,8:149-53. 19. Zurbrugg HR, Leupi F, Shupbach P, et al. Duplex scanner study of carotid artery dissection following surgical treatment of aortic dissection, Type A. Stroke 1988;19:970-6. 20. Watridge CB, Muhlbauer MS, Lowery RD. Trauaxaatic carotid artery dissection: diagnosis and treatment. J Neurosurg 1989;71:854-7. 21. Goldstone J, Moo:reWS. Emergency carotid artery surgery in neurologically unstable patients. Arch Surg 1976; 111:128491. 22. Pelligrini RV, Manzetti GW, DiMarco RF, Bekoe S, Arena S,
Blunt trauma to the carotid arteries 793
Marrangoni AG. The direct surgical management of lesions of the high internal carotid artery. J Cardiovasc Surg 1984;25: 29-35. 23. Thal ER, Snyder WH, Hays RJ, Perry MO. Management of carotid artery injuries. Surgery 1974;79:955-62. 24. Kestenberg WL. Rcview of intimal arterial injuries. Surgery versus conservative management. Am Surg 1990;56:504-6. 25. Sawchuk AP, Eldrup-Jorgcnsen J, Tober C, et al. The natural history of intimal flaps in a canine model. Arch Surg 1990; 125:1614-6. Submitted May 13, 1991; accepted June 28, 1991.
DISCUSSION
Dr. Frank Padberg (East Orange, N.J.). The anthors have addressed a difficult and uncommon clinical problem. With improved recognition and earlier treatment, mortality and morbidity rates should decrease. The authors have attributed their improved results largely to the location anatomically in the common carotid artery. Blunt carotid injury has usually gone undetected until neurologic symptoms intervene; note that 50% of the patients in the authors' series were asymptomatic. The authors report: only one patient who developed symptoms belatedly in contrast to the 50% noted in these previous reports. The absence of death and the single, permanent deficit are a dramatic improvement when compared with prior literature summaries from multiple institutions. I suspect that this is largely because ofearlicr recognition, and I request that the authors delineate the time course of diagnosis after injury. Perhaps the authors would speculate on the probability of cause and effect between prompt initiation of therapy and reduction of mortality and morbidity rates from this injury. We agree with the use of increased surveillance for this injury. If thc CT scan is negative and the patient has focal findings, suspicion of blunt carotid injury should he heightened. Although the duplex Doppler examination would seem ideal for this purpose, it has several major drawbacks. First, imaging is often difficult when the patient's neck is surrounded by stabilization hardware; second, blunt injury often involves the distal internal carotid artery, which is poorly visualized by these scanners; finally, the accuracy of the duplex examination is highly dependent on the technician, a problem for patients who usually arrive outside of the usu~ working hours. Alternative choices include angiography or perhaps MRI or CT scanning as the authors suggest; expensive, invasive examinations that may be difficult to justify on the basis of the yield for these rare clinical problems. Management of the intirnal flap remains controversial
and may involve observation, anticoagulation, or repair, all of which can be supported by the literature. The authors contend that many intimal flaps may be innocuous, a concept also supported by experimental work from our laboratory and other clinical reports presented at national trauma and vascular forums. Selection of the appropriate flap, in nonoperative management in the cerebrovascular circulation, however, requires further definition. I have several questions. First, mortality rates seem to be declining, and most patients in this series were asymptomatic. Is this related to earlier intervention, preventing both stroke and death? Second, this presentation, like other recent reports, has described several bilateral injuries. Should this alter the treatment plan? Third, vertebral artery injury is even rarer, but should occur from the same mechanisms. Was this seen? Fourth, although sensitive to bifurcation disease, duplex examination is restricted by immobilization and distal anatomic injury in the internal carotid artery. What alternative diagnostic modalities do you advocate in this setting and how should these be applied? H o w can more invasive and usually more expensive examinations be justified with such a low incidence of positive findings? Finally, if we agree that some intimal injuries are benign, how do we decide which? If the criteria are hemodynamic, please define this for us. Dr. Ronald Martin. I thank Dr. Padberg for his comments and questions. I shall take them in order, if I may. With regard to the declining mortality rates that we report in our series and that have been reported in some of the more recent small series as well, I am not sure whether we can take too much credit for that in our series in that this is a retrospective review and no two of these patients were treated by the same operative team. With regard to the patients in our series being asymptomatic, I think that that largely reflects the fact that they are being evaluated as part of multitranma protocols,
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and their injuries were picked up serendipitously at that time. In particular with respect to the CT scans, were it not for the fact that in one patient CT intravenous contrast was given for a head CT scan, which is not our routine protocol, the injury would not have been picked up at all, and with respect to the other one, she had had a CT scan of her head followed by a CT scan of her abdomen where she was given contrast and then had a CT scan of her neck for a C3-C4 subluxation, which revealed her injuries. So both of those were extremely lucky. And similarly with respect to whether or not early intervention prevents both stroke and death, in our series we intervened in only three patients, all of whom did well, and we did not intervene significantly in four of the remaining five patients with any therapy, and all but one of those did extremely well. As far as bilateral injuries go, I think that is a difficult question. Whether or not one should attempt to revascularize one side, monitor the patient and revascularize the other, I could only speculate on, and we did not have the oppommity in our series to do that. The one patient we did have with a bilateral injury had bilateral internal carotid artery dissections, and she was treated with supportive measures only and made a complete neurologic recovery. We had no experience with vertebral artery injuries in our series whatsoever. As to duplex scanning, although the largest series reported by Hertzer shows that 87% of these injuries appear between the bifurcation and the base of the skull, we did not find that to be the case with ours. Even our internal carotid artery injuries were fairly low with the exception of one patient who underwent anticoagulation who had a small intimal flap at the level of C-2. As far as alternate diagnostic modalities go, arteriography obviously is the gold standard for this injury. Most of our patients come in with multitrauma injuries being their main problem, and using the M R I at that time could be quite difficult, considering that a great many of them are paralyzed and on ventilation before starting. As far as which intimal injuries we would treat and not treat, one retrospective study looks at approximately 50 patients with intimal injuries, and out of those eight had what they considered small injuries; four of these were treated surgically and four were treated with anticoagulation, and all made a complete recovery and showed healing on subsequent arteriograms. Other than doing noninvasive studies and measuring velocity rates, I do not know how else we would assess the hemodynamic consequences. Dr. R i c h a r d Curl (Buffalo, N.Y.). I am curious about the rationale for repairing a thrombosed carotid artery in the asymptomatic patient, particularly if there has been a significant delay between the time of injury and the time of diagnosis. Do you feel that the presence of this thrombosed artery puts these patients at risk for subsequent events? Dr. Martin. Both patients that we had with thrombosed common carotid artery lesions had patent internal carotid vessels. Both of these patients were picked up at the
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time of admission, so they were diagnosed within several hours of their injury. We were fortunate in that regard. Dr. Joseph Buda (New York, N.Y.). Were these patients symptomatic? Dr. Martin. Neither of these patients were symptomatic. Dr. Curl. What if there had been a significant delay between the time of injury and diagnosis, would you still recommend repair of an asymptomatic carotid thrombosis? Dr. Martin. I am not sure that I would. We feel that the main role for surgical intervention in this procedure is obviously not to fix anybody, but it is prophylactic in nature. And when they have a patent internal carotid, if one can successfully extricate the clot and revasoalarize them, as shown by Dr. Perry's series, all of these patients did much better. In his series, those that they could not revascularize had about a 55% mortality rate, and that was delayed. So I think based on that one could infer it, but based on our data we could not substantiate that. Dr. John Bivona (Newburgh, N.Y.). In my experience of one case it was picked up because the patient had complained of buzzing in his ear, got an angiogram and found an intimal flap, and this was a week after his accident, and the neurologist said leave him alone; he had seen many of them. I listened to him, put him on aspirin, and within a year the buzz went away, and on duplex scanning he had a clean vessel again. My question for you is, have you followed any of these up that you have not operated on to see what they looked like down the road? Dr. Buda. What was the lesion that you saw on the arteriogram? Dr. Bivona. It was approximately 1 cm up from the bifurcation of the internal carotid. Dr. Buda. It was an intimal flap? Dr. Bivona. Hematoma, a subintimal hematoma. Dr. Martin. We have followed up several of these patients. Some of them because o f their nature of being transient in the state of Maine we have not been able to follow; they have been vacationers who have been injured on the highways. But some o f the ones that we have from almost 10 years ago have been followed, and people with small injuries have shown significant healing, although some still have some residual defect on their arteriogram. Dr. Richard P u r d y (Lawrence, Pa.). I would like to just make one comment. After a tragedy that we had where a man was minimally injured, came in with virtually no neurologic signs or symptoms, had been concussed, very little question about weakness in the right hand, we diagnosed his carotid problem in the morning from a CT scan with clot in his middle cerebral artery. H e eventually died. In reviewing the literature, what we could divine from it, and it seemed true in our situation, is that the key to the discasc as you sce it clinicallyin trauma centers is if you have a neurologic deficit and a negative CT scan you must do an
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Blunt trauma to the carotid arteries 795
angiogram to pick this condition up. Yours were very fortuitous, you had closed vessels and no neurologic signs or symptoms, and chances are they would have done well if left. Dr. William Gee (Allentown, Pa.). Blunt carotid injuries are infrequently diagnosed and often difficult to
evaluate in the multitrauma patient, especially when significant head injury is present or suspected. Our observations suggest ocular pneumoplethysmography (OPG-Gee) as a rapid (30 to 45 seconds) simple test for the detection of carotid lesions of hemodynamic consequence.
E. J. W Y L I E T R A V E L I N G F E L L O W S H I P OF T H E E D U C A T I O N A L FOUNDATION OF T H E S O C I E T Y FOR VASCULAR SURGERY The Educational Foundation of the Society for Vascular Surgery (with financial assistance from W. L. Gore & Associates, Inc.) has established an E. J. Wylie Traveling Fellowship. The purpose of the fellowship is to enable young surgeons to visit centers of excellence in vascular surgery in the United States and abroad. The benefits of educational travel for the maintenance and enhancement of excellence in the practice of vascular surgery are obvious. To be considered for selection a candidate must: 1. Be younger than 40 years of age at the time the traveling fellowship is awarded 2. Have completed a postgraduate vascular training program or have considerable experience in vascular surgery supplemental to general surgical training 3. Be committed to an academic career in vascular surgery and have obtained an academic appointment in a medical school or freestanding clinic devoted to excellence in medical education 4. Have a demonstrated record of success in pursuing clinical or basic science research sufficient to assure academic excellence in his or her pursuit of a career in vascular surgery Selection will be made without regard to the candidate's geographic location. A candidate submitting documentation for consideration for selection must furnish an up-to-date curriculum vitae and a list of publications, research projects, current research support, and a list of the centers that he or she wishes to visit. Three letters of recommendation are required, including one from the Division Head and another from the Chairman of the Department of Surgery of the institution in which the candidate holds a faculty appointment. A 500-word essay describing the objectives of the candidate's travel plans and linking these to his or her career goals must be appended. The Travel Fellowship Award is $10,000, granted to one person for use during a time limit and for expenses of travel, research, and clerical help. Application for the Fellowship award shall be made in a letter containing the information and documents as detailed. The deadline for receiving applications is March 1, 1992. Letter of nomination or intent should be directed to: Ronald J. Stoney, MD, FACS Chairman, E. J. Wylie Traveling Fellowship Committee Division of Vascular Surgery University of California Medical Center 505 Parnassus Ave., M-488 San Francisco, CA 94143
Blunt trauma to carotid arteries occurs infrequently and accot~nts for only 3% to 10% of all reported carotid injuries. 15 Mortality rates for injury are reported from 120% to 40% in larger series, 3,6s and permanent neurologic deficits range from 40% t o 80%. 5fi'9 The injury is often not recognized at the time the patient is a,~nitted, ~,6,~°and hence treatment may be delayed. PATIENTS AND METHODS Medical records from the Maine Medical Center (Portland, Maine) and SUNY Health Science Center (Syracuse, N.Y.) from 1981 to 1991 listing a diagnosis of carotid injury were reviewed. Patients with carotid injuries as a result of penetrating trauma or iatrogenic procedures were excluded. A summary of the eight remaix~ng cases is given in Table I. Six of the eight patients were men (75%). The mean age was 22 years, with a range of 12 to 43 years. The mechanism of injury varied among the eight patients. Six patients had hyperextension injuries to the neck: one was an unstable cervical spine ligamenFrom the Department of Surgery, Maine Medical Center, Portland, and the Depamnent of Surgery,State Universityof New York Health ScienceCenter, Syracuse. Presented at the Fifth Annual Meeting of the Eastern Vascular Society, Pittsburgh, Pa., May 4, 1991. Reprint requests: RonaldF. Martin,MD, Departmentof Surgery, Maine MedicalCenter, 22 BramhallSt., Portland, ME 04]i02. 24/6]32076
tous injury (five a result of motor vehicle accidents and one because of a fall); one had a case of blunt intraoral trauma that occurred while the patient was sledding, and one patient had a crush injury to the chest and neck. Three of the eight patients were admitted with neurologic deficits. Two had lateralizing motor signs (left hemiplegia and left hemiparesis), and one was comatose. The patient in coma (S.T.), however, had a complicated injury in that he also had a closed head injury and a significantly elevated blood alcohol level. His level of consciousness improved significantly with a decrease in blood alcohol content. One patient later had transient ischemic attacks with right arm and leg weakness. In only one of the eight patients was carotid artery injury suspected at the time of initial evaluation. In six patients the injury was incidentally detected during radiographic imaging for other injuries. In four patients (50%) the diagnosis of carotid injury was made during arteriography for suspicion of transected thoracic aorta: one of these four had a dissection of the left common carotid artery near its origin; one had bilateral internal carotid artery dissections; one had a thrombosed left common carotid artery near its origin; and one had a thrombosed right internal carotid artery. Two patients with thromboses were incidentally detected while undergoing CT scanning of the head and neck. In these two patients CT scanning of the neck revealed an in789
790
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Table I. Summary of cases Patient
Age/sex
EB
12/M
MB
25/M
MN
Neurologic deficit
Mechanism of injury
Left hemiplegia None
Intraoral trauma
15/M
Left hemiparesis
Hyperextension MVA
ST
20/M
KG
22/F
Comatose (alcohol, CIM) None
DU
20/M
GS
20/M
Transient cerebral ischemia None
Hyperextension MVA Hyperextension MVA Hyperextension MVA Crush chest/neck
BH
43/F
None
Hyperextension/fall
Hyperextension MVA
Diagnostic study CT scan/arteriography CT scan/arteriography CT scan/Doppler/arteriography Arteriography (? TTA) CT scan/arteriography Atteriography (? TTA) Arteriography (? TTA) Arteriography (? TEA)
Type of injury
Treatment
Outcome
Thrombosis RICA Thrombosis/intimat flap RCCA Dissection RICA
Support ~
Support
No deficit
Thrombosis RICA Dissection LICA Dissection LCCA Thrombosis/avulsion LCCA Dissection bilateral ICA
Support
No deficit
IV heparin/warfarin LSCA-LCCA bypass Interposition graft Support
No deficit
Interposition graft
Left hemiplegia No deficit
No deficit No deficit No deficit
CT, Computed tomography; RICA, right internal carotid artery; LICA, left internal carotid artery; ICA, internal carotid artery; LSCA, left subclavian artery; CHI, closed head injury; MVA, motor vehicle accident; RCCA, right common carotid artery; LCCA, left common carotid artery; TTA, transected thoracic aorta; Support, observation and rehabilitative care.
creased density in the carotid artery. Arteriography confirmed thrombosis of the right common carotid artery in one patient and a thrombosed right internal carotid artery in the other. One patient had left hemiparesis and underwent a CT scan of the head for suspected cerebral injury. Because no intracranial injury was detected in the presence of the left hemiparesis, a Doppler examination of the neck was performed, which revealed a decreased flow velocity pattern in the right internal carotid artery. Arteriography confirmed dissection of the right internal carotid artery. The final patient (E.B.) was promptly studied with four-vessel cerebral arteriography for early suspicion of a thrombosed right internal carotid artery after CT scanning revealed a pale infarct in the right middle cerebral artery distribution in the setting of left hemiplegia. Three patients were treated operatively and five were managed nonoperatively. Of the three patients undergoing operation, two had asymptomatic occlusions of the common carotid artery (one avulsion/thrombosis and one intimal flap/thrombosis), which were repaired with synthetic interposition grafts. The third patient was initially asymptomatic with a documented dissection of the left common carotid artery near its origin. After having transient ischemic attacks he underwent extraanatomic bypass from the left subclavian artery to the left
common carotid artery with ligation of the proximal left common carotid artery. Five patients were managed nonoperatively. Three of these patients had dissections with minor or no neurologic deficits; one was given heparin for systemic anticoagulation, and two received no specific treatment. The remaining two cases, which were managed nonoperatively, had thromboses of the internal carotid artery of unclear origin. One had a dense left hemiplegia and on CT scanning evidence of a right parietal stroke, and one was asymptomatic. Both were managed supportively with observation and rehabilitative care only. Seven of eight patients made a complete neurologic recovery or remained asymptomatic. One individual with dense left hemiplegia after blunt intraoral trauma made no clinical improvement with expectant management. DISCUSSION
Blunt carotid artery trauma is a rare clinical entity that comprises 3 % to 10% of all carotid injuries.~'2,~'~ An estimated incidence of 0.08% in the blunt trauma population is reported in one large series. H Several possible mechanisms of injury have been postulated. Hyperextension of the neck with contralateral rotation of the head, direct blows to the neck, blunt intraoral trauma, basilar skull fractures
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injuring the intrapetrous portion of the vessel, therapeutic and diagnostic carotid massage, 3,6,12,13 and attempted strangulation ~4 have all been suggested as etiologic mechanisms for injury to the carotid artery. Findings commonly associated with blunt carotid artery trauma include the following: (1) lateral neck hematoma formation; (2) ipsilateral Horner's syndrome; (3) transient ischemic attacks; (4) lucid interval with development of a focal neurologic deficit; and (5) progressive limb paresis in an alert and oriented patient. 15 Less commonly associated findings include aphasia, seizures, drowsiness, retrograde amnesia, and isolated motor or sensory deftcits. 9 Associated injuries are common and frequently include closed heact injuries, cervical spine injuries, and long bone fractures, n'~6 The diagnosis of blunt carotid artery trauma can frequently be difficult at the time of initial presentation. In a collective: review of 96 patients with blunt carotid arterial injuries, diagnosis was delayed in 94% of patients because symptoms resembled those of closed head trauma or a latent interval existed between the time of injury and the onset of symptoms. At least 50% of patients had no visible evidence of cervical trauma. 6 Blunt carotid arterial injury was frequently first suspected during evaluation for other injuries. Fifty percent of patients in our series were diagnosed ~dth carotid artery injm~¢ while undergoing aortography for suspected transected thoracic aorta. This is similar to the experience of Rosenberg et al.~6 who reported that 28 of 30 patients with blunt injury to the aortic arch vessels were diagnosed at arteriographic examination for aortic ruptnre. 16 The diagnosis is rarely suspected in asymptomatic patients with blunt upper thoracic or cervical tramna. Two of the patients in our series had the injury discovered incidentally while undergoing CT scanning of the head and neck (Fig. 1), and arteriography played a confirmatory role. If the diagnosis is considered, a reluctance exists to subject patients to arteriography to identify such an uncommon problem. Increased use of the carotid duplex scan can aid in making the diagnosis. Davis et al.n report a series of 14 blunt carotid artery dissections, and five patients were studied with duplex scanning. Two internal carotid occlusions were correctly identified as well as bilateral intimal flaps in one patient. In one patient turbulent flow was shown; it was later confirmed by arteriography to be an irregular vessel.
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Fig. 1. CT scan of the neck revealing a hypodense area in the right common carotid artery indicating thrombosis (arrow).
One patient was thought to have an occluded internal carotid artery by duplex scanning which was later shown to be an irregular but patent vessel by arteriography. Other reports have supported the use of ultrasonography for the diagnosis or screening of this i n j u r y . 17-19 Therapeutic alternatives include observation, 2,s,n anticoagulation, 2,n,2° ligation of the carotid artery with or without extracranial-intracranial bypass, 2,s and arterial reconstructionY ,6,um,22 Reported success of these treatment modalities is highly variable. Mortality rates as high as 40% and morbidity rates as high as 80% have been reported for this injury. 3'5,6,7,9 Anatomic location of the arterial injury, type of arterial defect, neurologic and cardiovascular status, and associated injuries are all important considerations in the treatment of these patients. Thrce of eight patients in our series sustained common carotid artery injuries, and all patients who were treated surgically had common carotid artery injuries and were initially asymptomatic. Patients with injuries of the distal internal carotid artery pose special problems. Thrombosis of the internal carotid artery is more likely to cause stroke than occlusion of the common carotid artery with preservation of collateral
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Martin et al.
flow to a patent internal carotid artery. In addition, surgical access to the internal carotid artery near the base of the skull can be difficult. Although there are surgical techniques to improve access to this region,22 a group of lesions remains where this is probably too hazardous to justify operation. This includes intimal flaps or dissections that may extend to the base of the skull. Furthermore, associated cervical spine injuries may preclude the use of some techniques used for improved exposure. The primary goal of therapy is to prevent the development of neurologic deficits. Patients with major fixed neurotogic deficits do not respond well to any treatment. Patients with lesions of the distal internal carotid artery are not good operative candidates, and anticoagulation should be considered. Patients with demonstrated lesions of the carotid artery that are surgically accessible should undergo vascular repair if there is evidence of transient cerebral ischemia or completed mild neurologic deficit. 6,22,2s Small dissections or intimal flaps are treated conservatively. A clinical review of intimal arterial injuries showed no difference in outcome between patients treated operatively or with anticoagulation for small intimal injuries.24 An experimental canine model suggests that intimal injuries that are not hemodynamically significant may not require surgical repair. 2s Patients with evidence of thrombosis into the intracranial portion of the artery or extensive intracerebral embolization should not be treated surgically and should undergo systemic anticoagulation to prevent distal propagation of thrombus unless contraindicated by associated injuries or coagulopathy. 3's'21 Other contraindications to surgical reconstruction include coma or significant cardiovascular instability, s,21 In summary, blunt carotid arterial trauma is a rare entity that is frequently diagnosed in a delayed fashion. We emphasize the importance of an early raised index of suspicion. We support attempting to identify this injury in patients undergoing arteriography for suspected aortic rupture as well as extending the field of study caudally to include the cervical carotid artery in patients undergoing cerebral CT scanning with neurologic deficits that are not explained by intracranial findings. Duplex scanning for selected patients based on mechanism of injury, associated physical findings, or associated injuries may be useful for earlier detection of these injuries. Surgery is indicated for patients with accessible
lesions and evidence of transient cerebral ischemia or minor neurologic deficits or for asymptomatic patients with thrombosis of the common carotid artery. Whether attempts should be made to revasctthrize occluded internal carotid arteries when there is minor neurologic deficit remains controversial. Small intireal dissections or intimal flaps may be managed conservatively, and anticoagulation should be considered unless contraindications exist because of other injuries. Surgery is contraindicated in patients with profound neurologic deficits or significant cardiovascular instability. REFERENCES 1. Dragon R, Saranchak H, Lakin P, Strauch G. Blunt injuries to the carotid and vertebral arteries. Am J Surg 1981;141:497500. 2. Fakhry SM, Jacques PR, Proctor HI. Cervical vessel injury after blunt trauma. J VAsc SURG 1988;8:501-7. 3. Perry MO, Snyder WH, Thai ER. Carotid artery injuries produced by blunt trauma. Ann Surg 1980;192:74-7. 4. Rubio PA, Reul GJ Jr, Beall AC, et al. Acute carotid artery injury: 25 years' experience. J Trauma 1974;14:967-73. 5. Yamada S, Kin& GW, Youmans JR. Carotid artery occlusion due to non-penetrating injury. 1 Trauma 1967;7:733-42. 6. Krajewski LP, Hertzer NR. Blunt carotid artery trauma. Alan Surg 1980;191:341-6. 7. Manrer PK, Plassche W, Green RM. Blunt trauma to the carotid artery with transient deficit and early repair. Surg Neurology 1984;21:110-2. 8. Towne JP, Neiss ND, Smith JW. Thrombosis of the internal carotid artery following cervical trauma. Arch Surg 1972;104: 565-8. 9. Mears GD, Leonard RB. Blunt carotid artery trauma: a case report. J Emerg Med 1988;6:281-4. 10. Welling RE, Saul TG, Tew JM~ Tomisch TA, Kremchek TE, Bellamy MI. Management of blunt injury to the internal carotid artery. J Trauma 1987;27:1221-6. 11. Davis JW, Holbrook TL, Hoyt DB, Mackersie RC, Field TO, Shackford SR. Blunt carotid artery dissection: incidence, associated injuries, screening, and treatment. J Trauma 1990;30:1514-7. 12. Crissey MM, Bernstein EF. Delayed presentation of carotid intimal tear following blunt craniocervical trauma. Surgery 1974;75:543-9. 13. New PFI, Mamose KJ. Traumatic dissection of the internal carotid artery at the aflantoaxial level secondary to nonpenetrating injury. Radiology 1969;93:41-9. 14. Milligan N, Anderson M. Conjugal disharmony: a hitherto unrecognized cause of strokes. BMJ 1980;281:421-2. 15. Jernigan WR, Gardner WC, Carotid injuries due to closed cervical trauma. J Trauma 1971;11:429-35. 16. Rosenberg JM, Bredenberg CE, Marvasti MA, Bucknam C, Conti C, Parker FB Jr. Blunt injuries to the aortic arch vessels. Ann Thoracic Surg 1989;48:508-13. 17. Bashour TT, Crew JP~ Dean M. Ultrasonic imaging of common carotid artery dissections. J Clin Ultrasound 1985; 13:210-1.
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18. Bluth EI, Shyn PB, Sullivan MA, et al. Doppler color flow imaging of carotid artery dissection. J Ultrasound Med 1989,8:149-53. 19. Zurbrugg HR, Leupi F, Shupbach P, et al. Duplex scanner study of carotid artery dissection following surgical treatment of aortic dissection, Type A. Stroke 1988;19:970-6. 20. Watridge CB, Muhlbauer MS, Lowery RD. Trauaxaatic carotid artery dissection: diagnosis and treatment. J Neurosurg 1989;71:854-7. 21. Goldstone J, Moo:reWS. Emergency carotid artery surgery in neurologically unstable patients. Arch Surg 1976; 111:128491. 22. Pelligrini RV, Manzetti GW, DiMarco RF, Bekoe S, Arena S,
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Marrangoni AG. The direct surgical management of lesions of the high internal carotid artery. J Cardiovasc Surg 1984;25: 29-35. 23. Thal ER, Snyder WH, Hays RJ, Perry MO. Management of carotid artery injuries. Surgery 1974;79:955-62. 24. Kestenberg WL. Rcview of intimal arterial injuries. Surgery versus conservative management. Am Surg 1990;56:504-6. 25. Sawchuk AP, Eldrup-Jorgcnsen J, Tober C, et al. The natural history of intimal flaps in a canine model. Arch Surg 1990; 125:1614-6. Submitted May 13, 1991; accepted June 28, 1991.
DISCUSSION
Dr. Frank Padberg (East Orange, N.J.). The anthors have addressed a difficult and uncommon clinical problem. With improved recognition and earlier treatment, mortality and morbidity rates should decrease. The authors have attributed their improved results largely to the location anatomically in the common carotid artery. Blunt carotid injury has usually gone undetected until neurologic symptoms intervene; note that 50% of the patients in the authors' series were asymptomatic. The authors report: only one patient who developed symptoms belatedly in contrast to the 50% noted in these previous reports. The absence of death and the single, permanent deficit are a dramatic improvement when compared with prior literature summaries from multiple institutions. I suspect that this is largely because ofearlicr recognition, and I request that the authors delineate the time course of diagnosis after injury. Perhaps the authors would speculate on the probability of cause and effect between prompt initiation of therapy and reduction of mortality and morbidity rates from this injury. We agree with the use of increased surveillance for this injury. If thc CT scan is negative and the patient has focal findings, suspicion of blunt carotid injury should he heightened. Although the duplex Doppler examination would seem ideal for this purpose, it has several major drawbacks. First, imaging is often difficult when the patient's neck is surrounded by stabilization hardware; second, blunt injury often involves the distal internal carotid artery, which is poorly visualized by these scanners; finally, the accuracy of the duplex examination is highly dependent on the technician, a problem for patients who usually arrive outside of the usu~ working hours. Alternative choices include angiography or perhaps MRI or CT scanning as the authors suggest; expensive, invasive examinations that may be difficult to justify on the basis of the yield for these rare clinical problems. Management of the intirnal flap remains controversial
and may involve observation, anticoagulation, or repair, all of which can be supported by the literature. The authors contend that many intimal flaps may be innocuous, a concept also supported by experimental work from our laboratory and other clinical reports presented at national trauma and vascular forums. Selection of the appropriate flap, in nonoperative management in the cerebrovascular circulation, however, requires further definition. I have several questions. First, mortality rates seem to be declining, and most patients in this series were asymptomatic. Is this related to earlier intervention, preventing both stroke and death? Second, this presentation, like other recent reports, has described several bilateral injuries. Should this alter the treatment plan? Third, vertebral artery injury is even rarer, but should occur from the same mechanisms. Was this seen? Fourth, although sensitive to bifurcation disease, duplex examination is restricted by immobilization and distal anatomic injury in the internal carotid artery. What alternative diagnostic modalities do you advocate in this setting and how should these be applied? H o w can more invasive and usually more expensive examinations be justified with such a low incidence of positive findings? Finally, if we agree that some intimal injuries are benign, how do we decide which? If the criteria are hemodynamic, please define this for us. Dr. Ronald Martin. I thank Dr. Padberg for his comments and questions. I shall take them in order, if I may. With regard to the declining mortality rates that we report in our series and that have been reported in some of the more recent small series as well, I am not sure whether we can take too much credit for that in our series in that this is a retrospective review and no two of these patients were treated by the same operative team. With regard to the patients in our series being asymptomatic, I think that that largely reflects the fact that they are being evaluated as part of multitranma protocols,
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and their injuries were picked up serendipitously at that time. In particular with respect to the CT scans, were it not for the fact that in one patient CT intravenous contrast was given for a head CT scan, which is not our routine protocol, the injury would not have been picked up at all, and with respect to the other one, she had had a CT scan of her head followed by a CT scan of her abdomen where she was given contrast and then had a CT scan of her neck for a C3-C4 subluxation, which revealed her injuries. So both of those were extremely lucky. And similarly with respect to whether or not early intervention prevents both stroke and death, in our series we intervened in only three patients, all of whom did well, and we did not intervene significantly in four of the remaining five patients with any therapy, and all but one of those did extremely well. As far as bilateral injuries go, I think that is a difficult question. Whether or not one should attempt to revascularize one side, monitor the patient and revascularize the other, I could only speculate on, and we did not have the oppommity in our series to do that. The one patient we did have with a bilateral injury had bilateral internal carotid artery dissections, and she was treated with supportive measures only and made a complete neurologic recovery. We had no experience with vertebral artery injuries in our series whatsoever. As to duplex scanning, although the largest series reported by Hertzer shows that 87% of these injuries appear between the bifurcation and the base of the skull, we did not find that to be the case with ours. Even our internal carotid artery injuries were fairly low with the exception of one patient who underwent anticoagulation who had a small intimal flap at the level of C-2. As far as alternate diagnostic modalities go, arteriography obviously is the gold standard for this injury. Most of our patients come in with multitrauma injuries being their main problem, and using the M R I at that time could be quite difficult, considering that a great many of them are paralyzed and on ventilation before starting. As far as which intimal injuries we would treat and not treat, one retrospective study looks at approximately 50 patients with intimal injuries, and out of those eight had what they considered small injuries; four of these were treated surgically and four were treated with anticoagulation, and all made a complete recovery and showed healing on subsequent arteriograms. Other than doing noninvasive studies and measuring velocity rates, I do not know how else we would assess the hemodynamic consequences. Dr. R i c h a r d Curl (Buffalo, N.Y.). I am curious about the rationale for repairing a thrombosed carotid artery in the asymptomatic patient, particularly if there has been a significant delay between the time of injury and the time of diagnosis. Do you feel that the presence of this thrombosed artery puts these patients at risk for subsequent events? Dr. Martin. Both patients that we had with thrombosed common carotid artery lesions had patent internal carotid vessels. Both of these patients were picked up at the
Journal of VASCULAR SURGERY
time of admission, so they were diagnosed within several hours of their injury. We were fortunate in that regard. Dr. Joseph Buda (New York, N.Y.). Were these patients symptomatic? Dr. Martin. Neither of these patients were symptomatic. Dr. Curl. What if there had been a significant delay between the time of injury and diagnosis, would you still recommend repair of an asymptomatic carotid thrombosis? Dr. Martin. I am not sure that I would. We feel that the main role for surgical intervention in this procedure is obviously not to fix anybody, but it is prophylactic in nature. And when they have a patent internal carotid, if one can successfully extricate the clot and revasoalarize them, as shown by Dr. Perry's series, all of these patients did much better. In his series, those that they could not revascularize had about a 55% mortality rate, and that was delayed. So I think based on that one could infer it, but based on our data we could not substantiate that. Dr. John Bivona (Newburgh, N.Y.). In my experience of one case it was picked up because the patient had complained of buzzing in his ear, got an angiogram and found an intimal flap, and this was a week after his accident, and the neurologist said leave him alone; he had seen many of them. I listened to him, put him on aspirin, and within a year the buzz went away, and on duplex scanning he had a clean vessel again. My question for you is, have you followed any of these up that you have not operated on to see what they looked like down the road? Dr. Buda. What was the lesion that you saw on the arteriogram? Dr. Bivona. It was approximately 1 cm up from the bifurcation of the internal carotid. Dr. Buda. It was an intimal flap? Dr. Bivona. Hematoma, a subintimal hematoma. Dr. Martin. We have followed up several of these patients. Some of them because o f their nature of being transient in the state of Maine we have not been able to follow; they have been vacationers who have been injured on the highways. But some o f the ones that we have from almost 10 years ago have been followed, and people with small injuries have shown significant healing, although some still have some residual defect on their arteriogram. Dr. Richard P u r d y (Lawrence, Pa.). I would like to just make one comment. After a tragedy that we had where a man was minimally injured, came in with virtually no neurologic signs or symptoms, had been concussed, very little question about weakness in the right hand, we diagnosed his carotid problem in the morning from a CT scan with clot in his middle cerebral artery. H e eventually died. In reviewing the literature, what we could divine from it, and it seemed true in our situation, is that the key to the discasc as you sce it clinicallyin trauma centers is if you have a neurologic deficit and a negative CT scan you must do an
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Blunt trauma to the carotid arteries 795
angiogram to pick this condition up. Yours were very fortuitous, you had closed vessels and no neurologic signs or symptoms, and chances are they would have done well if left. Dr. William Gee (Allentown, Pa.). Blunt carotid injuries are infrequently diagnosed and often difficult to
evaluate in the multitrauma patient, especially when significant head injury is present or suspected. Our observations suggest ocular pneumoplethysmography (OPG-Gee) as a rapid (30 to 45 seconds) simple test for the detection of carotid lesions of hemodynamic consequence.
E. J. W Y L I E T R A V E L I N G F E L L O W S H I P OF T H E E D U C A T I O N A L FOUNDATION OF T H E S O C I E T Y FOR VASCULAR SURGERY The Educational Foundation of the Society for Vascular Surgery (with financial assistance from W. L. Gore & Associates, Inc.) has established an E. J. Wylie Traveling Fellowship. The purpose of the fellowship is to enable young surgeons to visit centers of excellence in vascular surgery in the United States and abroad. The benefits of educational travel for the maintenance and enhancement of excellence in the practice of vascular surgery are obvious. To be considered for selection a candidate must: 1. Be younger than 40 years of age at the time the traveling fellowship is awarded 2. Have completed a postgraduate vascular training program or have considerable experience in vascular surgery supplemental to general surgical training 3. Be committed to an academic career in vascular surgery and have obtained an academic appointment in a medical school or freestanding clinic devoted to excellence in medical education 4. Have a demonstrated record of success in pursuing clinical or basic science research sufficient to assure academic excellence in his or her pursuit of a career in vascular surgery Selection will be made without regard to the candidate's geographic location. A candidate submitting documentation for consideration for selection must furnish an up-to-date curriculum vitae and a list of publications, research projects, current research support, and a list of the centers that he or she wishes to visit. Three letters of recommendation are required, including one from the Division Head and another from the Chairman of the Department of Surgery of the institution in which the candidate holds a faculty appointment. A 500-word essay describing the objectives of the candidate's travel plans and linking these to his or her career goals must be appended. The Travel Fellowship Award is $10,000, granted to one person for use during a time limit and for expenses of travel, research, and clerical help. Application for the Fellowship award shall be made in a letter containing the information and documents as detailed. The deadline for receiving applications is March 1, 1992. Letter of nomination or intent should be directed to: Ronald J. Stoney, MD, FACS Chairman, E. J. Wylie Traveling Fellowship Committee Division of Vascular Surgery University of California Medical Center 505 Parnassus Ave., M-488 San Francisco, CA 94143