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Surg Neurol 1984;21:110-2
Blunt Trauma to the Carotid Artery with Transient Deficit and Early Repair Paul Kurt Maurer, CPT, MC, U.S.A., Walter Plassche, M.D., and Richard M. Green, M.D. Departments of Surgery and Radiology, University of Rochester Medical Center, Rochester, New York
Maurer PK, Plassche W, Green RM. Blunt trauma to the carotid artery with transient deficit and early repair. Surg Neurol 1984;21:110-2. Blunt trauma to the carotid artery is an uncommon but easily overlooked source of neurological deficit. The prompt diagnosis and angiographic definition of carotid-artery injuries can allow early operative intervention in these potentially devastating lesions. We describe a case report of blunt trauma with transient deficit in a patient who underwent direct repair via Dacron-patch angioplasty. KEY WORDS: Carotid artery; Trauma; Transient neurological deficit; Angiography; Treatment
Blunt trauma to the carotid artery with neurological deficit of subsequent onset is a well-known but uncomm o n entity, accounting for approximately 3 % of carotidartery injuries [6,18]. Following the trauma, the onset of symptoms is generally delayed by m o r e than 1 hour, and has been noted to occur weeks and even months later [1,6,10,11]. T h e injury is usually an intimal tear in the high cervical internal carotid artery, with subsequent delayed thrombosis [ 11,14,18]. With the advent o f routine CT scanning in cases o f head injury, the diagnosis o f carotid-artery injury is often overlooked as a potential source o f neurologic deficit. In reports of prior series, it has been noted that the proper diagnosis was initially entertained in only 6 % of cases [11,18]. The mortality and morbidity in cases o f closed carotid-artery injury have been found to be high, ranging from 2 0 % to 4 0 % in the literature. T h e r e have been approximately 130 case reports o f injury to the artery, with a variety o f conservative and surgical interventions yielding varied results. The natural history and most efficacious manner of dealing with these injuries remains in
Address reprint requests to: Dr. Paul Kurt Maurer, Division of Neurological Surgery, University of Rochester Medical Center, 60 ! Elmwood Ave., Rochester, N.Y. 14642.
© 1984 by ElsevierScience PublishingCo., Inc.
question. We present a case report of blunt trauma to the carotid artery with a transient neurological deficit treated by early operative intervention.
Case Report A 16-year-old white boy was struck in the neck on the right side during a soccer game. H e was only moderately dazed by the impact, and was about to reenter play when he had a sudden onset of numbness in his left upper arm, and mild weakness. This episode passed within 2 to 3 minutes and he was left with no residuum. H e was brought to the emergency department of our institution, and while giving his history had a recurrent episode of weakness, with dysarthric speech being noted. This may have been due to facial weakness, but it is noteworthy that the patient is left-handed. His deficit again cleared in 2 to 3 minutes. Subsequent detailed examination failed to reveal any deficit. A reddened area was evident at the zone of impact on the mid-sternocleidomastoid zone of the right side of the neck. N o h e m a t o m a was present. The patient's carotid pulses were full bilaterally, and no bruits were appreciated. In light of the symptoms suggestive of right hemispheral ischemia, and the absence of cranial trauma, the patient underwent emergent angiography via the transfemoral approach. The angiogram revealed a dilatation of the right internal carotid artery, 5 cm distal to the bifurcation, followed by an intraluminal filling defect that extended superiorly to the carotid siphon (Figures 1 and 2). Operative intervention was undertaken within 5 hours of the injury. A nearly complete occlusion o f the high cervical internal carotid artery was found, with an intimal disruption and dissecting hematoma. In the distal internal carotid artery there was an extensive thrombus. T h e proximal internal carotid artery was free of thrombus. An extended arteriotomy was performed, and the disrupted intima was transsected and tacked in place with 6-0 nylon suture material. A No. 2 Fogarty catheter was 0090-3019/84/$3.00
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The patient had an unremarkable postoperative recovery, and has returned to full scholastic and athletic activity without any deficit.
Discussion Blunt-traumatic injury to the carotid artery is an uncommon cause of neurological deficit, but can be associated with a high rate of mortality and morbidity [1,2,6,11,14,18]. The injury to the vessel is generally ascribed to one of four mechanisms [6,9,11]:
Figure 2. Frontal projection. Arrows outline intraluminal thrombus.
Figure 1. Lateral projection with injection of contrast medium into the right common carotid artery. Lower arrow shows localized outpouching at the site of the artery defect. Upper arrow depicts zone of long intraluminal thrombus.
placed carefully into the carotid siphon, and a large thrombus was readily evacuated. Excellent backflow was evident immediately after removal o f the thrombus. Following the repair of the intimal defect, a Dacron-patch angioplasty was used to repair the arteriotomy in the internal carotid artery. A patch angioplasty was used because o f the small nature o f the internal carotid artery and the length o f the arteriotomy. It was felt this method would improve the long-term patency of the vessel.
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1. Hyperextension and contralateral rotation of the head, which tethers the internal carotid artery over the lateral masses o f C 1 - 2 or the transverse process of C - 3 . This may cause an intimal tear, which can lead to a propagating, delayed thrombosis. 2. A direct blow to the neck. 3. A blunt intraoral trauma. 4. A basal fracture injuring the intrapetrous portion of the vessel. The onset o f s y m p t o m s is frequently delayed for several hours, as the thrombosis forms. Emboli originating from the thrombus can pass to m o r e distal parts o f the intracranial circulation and can cause an acute destabilization of an otherwise stable condition. T h e cornerstone of successful m a n a g e m e n t of the blunt carotid-artery injury is to always entertain the diagnosis in a patient with a neurologic deficit secondary to trauma. In the case presented here the diagnosis was not obscured by associated severe cranial trauma, but as this is often the situation, there is little doubt that many significant carotid injuries are left unrecognized. Early a n g i o g r a p h y - - a n d four-vessel angiography if n e e d e d - - s h o u l d be undertaken. Once the diagnosis has been established, treatment must be individualized on a case-by-case basis. T h e literature includes reports o f conservative management, early operative intervention, anticoagulant therapy, and extracranial-to-intracranial bypass grafting [ 1,5,6,11,14]. Krajewski and H e r t z e r noted death or severe impairm e n t in 8 6 % of patients undergoing nonoperative management and in 5 3 % of those who underwent surgical intervention in a collected series [6]. T h e consensus supports early operative intervention in those patients who have a transient deficit of less than 10 to 12 hours duration [4,6,11]. T h e most c o m m o n form o f intervention is resection o f an intimal tear (if any), thrombectomy, and vein-graft angioplasty. In our case a Dacron graft was utilized, and this would seem to be a viable alternative. In those injuries involving segments of the internal carotid artery that are unlikely to be readily accessible via a routine carotid approach, an extracranialto-intracranial bypass graft may allow some degree of revascularization and a greater degree of safety in a subsequent attempt at carotid reconstruction from below. This was considered in our case, but was deferred because it was felt that successful reconstruction could be achieved. Carotid ligation as the sole means of treatment does not seem justified, and has been associated with an increased morbidity [11]. An extracranial-to-intracranial shunt and reconstruction or reconstruction alone are preferable. Patients with embolization are probably best treated with anticoagulants or a trapping procedure o f the embolic source in concert with bypass revascu-
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larization. The patient with a fixed deficit is less likely to benefit from revascularization, although improvement has been reported in such cases. Nevertheless, the patient with a fixed deficit remains at risk for cerebral embolization by thrombus fragments. The case described here supports the trend toward early operative intervention in blunt trauma to the carotid artery. The most efficacious means for this intervention, be it direct repair, or attempted repair with bypass protection, remains to be m o r e fully established with a m o r e extensive series of patients.
References 1. Crissey MM, Bernstein EF. Delayed presentation of carotid intimal tear following blunt craniocervical trauma. Surgery 1979;75:543-9. 2. Divincentri FC, Weber BB. Traumatic carotid artery injuries in civilian practice. Am Surg 1979;40:277-80. 3. Gurdjian ES, Ardet B, Sibayan RW, Thomas LM. Spasm of the extracranial internal carotid artery resulting from blunt trauma demonstrated by angiography. J Neurosurg 1981;34:742-7. 4. Hoffman TH, Richardson DJ, Flint LM. Intimal disruption of major cerebral vasculature following blunt trauma. Surgery 1980;87:441-9. 5. Hughes JT, Brownell B. Traumatic thrombosis of the internal carotid artery in the neck. J Neurol Neurosurg Psychiatry 1968;31:307-14. 6. Krajewski LP, Hertzer NR. Blunt carotid artery trauma. Ann Surg 1980;191:341-6. 7. Kusunoki T, Rowed DW, Tator CH, Lougheed WM. Thromboendarterectomy for total occlusion of the internal carotid artery: A reappraisal of risks, success rate and potential benefits. Stroke 1978;9:34-8. 8. McGough EC, Helfrich LR, Hughes RK. Traumatic intimal prolapse of the common carotid artery. A m J Surg 1972;123:724-5. 9. New PFJ, Mamose KJ. Traumatic dissection of the internal carotid artery at the atlantoaxial level secondary to non-penetrating injury. Radiology 1969;93:41-9. 10. Olafson RA, Christoferson LA. The syndrome of carotid artery occlusion following minor craniocerebral trauma. J Neurosurg 1980;33:636-9. 11. Perry MO, Snyder WH. Carotid artery injuries caused by blunt trauma. Ann Surg 1980;192:74-7. 12. Schneider RC, Gosch HH, Taren JA, Ferry DJ, Jerva MJ. Blood vessel trauma following head and neck injuries. Clin Neurosurg 1972;19:312-34. 13. Silvernail Wl, Crontcher DL, Byrd BR, Pope DH. Carotid artery injury produced by blunt neck trauma. South Med J 1975;68: 310-3. 14. Stronger WL, Kelly DL. Traumatic dissection of the extracranial internal carotid artery. Neurosurgery 1980;6:123-30. 15. Sullivan HG, Vines FS, Becker UP. Sequelae of indirect internal carotid artery injury. Radiol 1973;109:91-8. 16. Thai ER, Snyder WH, Hayes RJ, Perry MO. Management of carotid artery injuries. Surgery 1974;76:955-62. 17. Towne JB, Neis DD, Smith JW. Thrombosis of the internal carotid artery following blunt cervical trauma. Arch Surg 1972;104:565-8. 18. Yamada S, Kondt GW, Youmans JR. Carotid artery occlusion due to nonpenetrating injury. J Trauma 1967;7:333-42. 19. Zilkha A. Traumatic occlusion of the internal carotid artery. Radiology 1970;97:543-7.