Bilateral traumatic internal carotid artery dissections: Case report Jeffrey L. Ballard, M D , T. J. Bunt, M D , Brian Fitzpatrick, M D , and James M. Malone, M D , Tucson and Phoenix, Ariz. Bilateral internal carotid artery dissections after blunt cervicofacial trauma are rare, with 16 cases being previously published. Management is presumed to be an extension of the dominant therapy for unilateral dissection, that being anticoagulant therapy; however, bilateral stenoses engender questions of threat to total cerebral blood flow. We herein present a patient who suffered bilateral type B dissections and who then had progression of the process on anticoagulant therapy, resulting in an unusual carotid reconstruction. (J VASC SURG)1992;15:431-5.)
The management o f bilateral carotid artery dissection is not well established because o f a paucity o f published experience, l-* Expectant anticoagulant therapy awaiting spontaneous recanalization must be tempered by the possibility o f bilateral hemispheric infarction caused either by embolization or reduction in total cerebral flow. In the latter situation, revascularization by standard extracranial-intracranial bypass for extensive dissections may not provide sufficient acute phase improvement of cerebral flow to prevent infarction. A newly introduced neurosurgical approach to the intrapetrous portion o f the proximal carotid siphon, however, allows large caliber reconstruction o f even extensive dissections. We herein report a case in which this modality was used. CASE R E P O R T A 20-year-old woman was admitted after a motor vehicle accident in which her car was rear-ended at high speed; the steering wheel had been broken from the impact. Initially the patient was alert but disoriented, with a Glasgow Coma Score of 14. Physical examination revealed evidence of blunt trauma to the jaw and neck as well as to the anterior chest. Results of CT scanning of the head were normal. Within the first few hours of admission the patient exhibited right central facial weakness, right hemiparesis, expressive aphasia, and rightward deviation of her tongue. Angiography showed bilateral internal carotid artery dissections initiating above the bifurcations and extending to the base of the skull (Figs. 1,A and B). Intracerebral blood flow was not compromised (Figs. 2, A and B). An
From the Department of Surgery,Maricopa Medical Center, and the Barrow NeurologicalInstitute, Phoenix. Reprint requests: Jeffrey L. Ballard, MD, Maricopa Medical Center, Department of Surgery, P. O. Box 5099, Phoenix, AZ 85010. 24/4/31018
embolus was also seen in the distal angular artery branch of the left middle cerebral artery. The patient was initially treated with heparin anticoagulation and observation; her clinical response was one of improved speech and dramatically improved right hemiparesis. However, repeat head CT scanning at 8 days showed cortical strokes involving the left posterior frontal and the left parietal regions. Follow-up angiography showed more advanced stenoses of the cervical portions of both internal carotid arteries (Figs. 1, C and D). The distal left angular artery was noted to have recanalized; there was some cross-filling from left to right noted (Figs. 2, C and D). The patient was maintained on heparin and continued with progressive clinical improvement. On hospital day 22 a third follow-up angiogram was obtained. On the left, the internal carotid artery was more widely patent, although multiple intimal irregularities were still demonstrated; on the right, there was a long, tightly stenotic segment of the entire cervical internal carotid artery (Figs. 1, E and F). At the same time sequence as the previous angiograms, there was now complete cross-filling from the left to the right hemisphere, indicating on angiography worsening of the right-sided stenosis (Figs. 2, E and F). It was then thought that right-sided revascularization was indicated because of the progressive reduction in flow to the right hemisphere, and threat of complete occlusion. An autologous right, cervical-to-petrous, internal carotid artery bypass was performed by the neurosurgery service. The patient has continued to improve clinically and is currently neurologically intact 15 months after her injury. Follow-up angiography now demonstrates a widely patent right graft and return of the intracerebral flow pattern to normal (Fig. 3). DISCUSSION Unilateral dissection o f the internal carotid artery occurs with a reported incidence o f 2% to 3% in closed neck injuries. 9,1° Dissections afflict all age 431
432
Ballard et al.
Fig. 1. Progression of the right (left column) and left (right column) carotid dissections as demonstrated by angiography on admission (A, B), at 1 week (C, D), and at 3 weeks (E, F) after injury. Black arrows point out the areas of dissection.
Journal of VASCULAR SURGERY
Volume 15 Number 2 February 1992
Traumatic internal carotid artery dissections 433
D
:Fig. 2. Progressive findings on right (left column) and left (right column) intracerebral flow ~rough carotid angiography performed on admission (A, B), at 1 week (C, D), and at 3 weeks (E, F) after injury; There is progressively decreased ipsilateral flow and increased cross-filling !~rom 1 to 3 weeks. These angiographs were taken at the same time after injection of dye.
groups but particularly young adults ( 2 5 to 4 5 years), and may account for 5% or more ofischemic strokes in this age group. ~ Bilateral internal carotid artery dissections in closed neck injuries are much rarer. In a review o f the literature, only 16 other cases o f documented blunt traumatic bilateral internal carotid artery dissections were found; one o f these was
associated with bilateral traumatic disruptions o f the vertebral arteries. 4,5,9,12-~4 Blunt traumatic injury to the internal carotid artery usually results in an intimal tear or mural contusion; a traumatic dissection occurs when the intimal tear is followed by intramedial hemorrhage. Direct inspection at surgical exploration shows a
434
Ballard et aL
Fig. 3. Follow-up angiogram at 8 months demonstrates a widely patent right graft, and prompt fillingof the proximal MCA and ACA.
moderate cylindrical dilation and sharply demarcated dark blue discoloration of the dissected segment. On microscopic examination of excised segments, the dissection is in the outer layer of the media with a characteristic double lumen. A pseudoaneurysm may form between the media and adventia, or hemorrhage and thrombosis around the intima may slowly occlude the vessel completely. Embolization may also occur distally, leading to a variety of presenting symptoms.l,~s The primary indication for carotid angiography is any neurologic deficit that cannot be explained by head CT findings. Early carotid and intracranial angiography should be performed when the diagnosis of a carotid artery lesion is clinically suspected. 7'16q8 The angiographic findings may be classified as follows: type A involves a short segment of the cervical internal carotid not extending to the base of the skull, type B extends to the petrous portion, and type C shows complete occlusion. 8,~5 Intracranial angiography can give additional impor-
lournal of VASCULAR SURGERY
tant information regarding collateral cerebral blood flow and evidence of embolic phenomenon. Therapeutic maneuvers have ranged from distal carotid thrombectomy, carotid ligation, formal resection of the stenotic segment with interposition vein graft reconstruction, and extracranialintracranial bypass, to various anticoagulation regimens. 13'1s-22 Surgical treatment can be difficult because of a more extensive injury than is apparent on the angiograms; distal type B cervical lesions are often inaccessible to the usual modes of vascular repair. Spontaneous resolution of the process on anticoagulant medications is the rule; McNeill et al.21 recommend at least 3 weeks of heparin therapy for a full trial of conservative management. 14,22,23 Other authors have advocated a more aggressive surgical approach, particularly in those without a significant neurologic deficit and/or as a prophylaxis against subsequent neurologic events. Consideration can be made for extracranial-intracranial bypass to restore adequate cerebral perfusion, although its efficacy can be questioned. Ifligation of the internal carotid artery is chosen for a severe ongoing neurologic deficit, there may be propagation of thrombus from the top of the occluded internal carotid artery into the patent middle cerebral artery; adjunctive heparin therapy must therefore be continued. 2,s,1°,14,15,2° Recent introduction of a direct approach to the intrapetrous portion of the distal carotid artery by our neurosurgical colleagues, has allowed us to add an additional possibility to the existing armamentarium. Direct saphenous vein interposition grafts may be placed between the bifurcation and the proximal siphon, bypassing the entire cervical portion of the internal carotid with a large caliber antegrade graft. We have used this twice in the past year; for this case, and for reconstruction of a gunshot wound of the carotid artery at the C1-2 interspace. The indication for reconstruction in this case Was felt to be impending thrombosis of the right internal carotid artery because of angiographically demonstrated worsening stenosis and evidence of progressive left-to-right collateral flow. Follow-up studies indicate normalization of intracerebral flow and a patent graft. REFERENCES 1. Yamada S, Kin& GW, Youmans JR. Carotid artery occlusion due to non-penetrating injury. J Trauma 1967;7:333-42. 2. Thai ER, Snyder WH III, Hay RJ, Perry MO. Management of carotid artery injuries. Surgery 1974;76:955-62. 3. Perry MO, Snyder WH, Thai ER. Carotid artery injuries caused by blunt trauma. Ann Surg 1980;192:74-7. 4. Watridge CB, Muhlbauer MS, Loweruy KD. Traumatic
Volume 15 Number 2 February 1992
5.
6. 7.
8.
9.
10. ~1. 12.
13.
14.
carotid artery dissection: diagnosis and treatment. 1 Neurosurg 1989;71:854-7. Mokri B, Piepgras DG, Houser OW. Traumatic dissections of the extracranial internal carotid artery. I Neurosurg I988;68: I89-96. Hart RG, Easton DJ. Dissections. Stroke i985;16:925-7. Hart RG, Easton DI. Dissections of cervical and cerebral arteries. In: Barnett HJM ed. Cerebrovascular disease. Neurol Clin 1983;1:155-82. Fisher CM, Ojemann RG, Roberson GH. Spontaneous dissection of cervicocerebral arteries. Can J Neurol Surg 1978;5:9-19. Fukuda I, Meguro K, Matsusita S, Shigeta O, Oohashi N, Nakata Y. Traumatic disruption of bilateral vertebral arteries and internal carotid arteries. Case Report. J Trauma 1989;29:263-6. Fry RE, Fry WJ. Extracranial carotid artery injuries. Surgery 1980;88:58i-7. Hart RG, Miller VT. Cerebral infarction in young adults: a practical approach. Stroke 1983;14:110-4. Chakera TM. Bilateral extracranial internal carotid artery injury duc to non-penetrating trauma. Br I Radiol 1979;52: 704-8. Scherman BM, Tucker WS. Bilateral traumatic thrombosis of the internal carotid arteries in the neck: a case report and review of the literature. Neurosurgery 1982;10:751-3. Stringer WL, Kelly lr DL. Traumatic dissection of the
Traumatic internal carotid artery dissections 4 3 5
15. I6. 17.
18. 19.
20. 21.
22. 23.
extracranial internal carotid artery. Neurosurgery 1980;6: 123-30. Ehrenfeld WK, Wylie EJ. Spontaneous dissection of the internal carotid artery. Arch Surg 1986; 111:1294-301. Jernigan WR, Gardner WC. Carotid artery injuries due to closed cervical trauma. J Trauma 1971;11:429-435. Waespe W, Niesper J, Imhof H, Nolavanis A. Lower cranial nerve palsies due to internal carotid dissection. Stroke 1988;19:156i-4. Friedman WA, Day AL, et al. Cervical carotid dissecting aneurysms. Neurosurgery 1980;7:207-i3. Crissey MM, Bernstein EF. Delayed presentation of carotid intimal tear following blunt craniocervical trauma. Surgery 1974;75:543-9. Gee W, Kampp HA, et al. Spontaneous dissection of internal carotid arteries. Arch Surg 1980;115:944-9. McNeill D H Jr, Dreisbach J, Marsden RJ. Spontaneous dissection of the internal carotid artery. Arch Neurol 1980; 37:54-5. Biller T, Hingtgen WL, et al. Cervicocephalic arterial dissections, a ten-year experience. Arch Neurol I986;43:1234-8. Towne JB, Neiss DD, Smith JW. Thrombosis of the internal carotid artery following blunt cervical trauma. Arch Surg 1972; 104: 565-8.
Submitted Feb. 5, 1991; accepted May 15, I991.
The management o f bilateral carotid artery dissection is not well established because o f a paucity o f published experience, l-* Expectant anticoagulant therapy awaiting spontaneous recanalization must be tempered by the possibility o f bilateral hemispheric infarction caused either by embolization or reduction in total cerebral flow. In the latter situation, revascularization by standard extracranial-intracranial bypass for extensive dissections may not provide sufficient acute phase improvement of cerebral flow to prevent infarction. A newly introduced neurosurgical approach to the intrapetrous portion o f the proximal carotid siphon, however, allows large caliber reconstruction o f even extensive dissections. We herein report a case in which this modality was used. CASE R E P O R T A 20-year-old woman was admitted after a motor vehicle accident in which her car was rear-ended at high speed; the steering wheel had been broken from the impact. Initially the patient was alert but disoriented, with a Glasgow Coma Score of 14. Physical examination revealed evidence of blunt trauma to the jaw and neck as well as to the anterior chest. Results of CT scanning of the head were normal. Within the first few hours of admission the patient exhibited right central facial weakness, right hemiparesis, expressive aphasia, and rightward deviation of her tongue. Angiography showed bilateral internal carotid artery dissections initiating above the bifurcations and extending to the base of the skull (Figs. 1,A and B). Intracerebral blood flow was not compromised (Figs. 2, A and B). An
From the Department of Surgery,Maricopa Medical Center, and the Barrow NeurologicalInstitute, Phoenix. Reprint requests: Jeffrey L. Ballard, MD, Maricopa Medical Center, Department of Surgery, P. O. Box 5099, Phoenix, AZ 85010. 24/4/31018
embolus was also seen in the distal angular artery branch of the left middle cerebral artery. The patient was initially treated with heparin anticoagulation and observation; her clinical response was one of improved speech and dramatically improved right hemiparesis. However, repeat head CT scanning at 8 days showed cortical strokes involving the left posterior frontal and the left parietal regions. Follow-up angiography showed more advanced stenoses of the cervical portions of both internal carotid arteries (Figs. 1, C and D). The distal left angular artery was noted to have recanalized; there was some cross-filling from left to right noted (Figs. 2, C and D). The patient was maintained on heparin and continued with progressive clinical improvement. On hospital day 22 a third follow-up angiogram was obtained. On the left, the internal carotid artery was more widely patent, although multiple intimal irregularities were still demonstrated; on the right, there was a long, tightly stenotic segment of the entire cervical internal carotid artery (Figs. 1, E and F). At the same time sequence as the previous angiograms, there was now complete cross-filling from the left to the right hemisphere, indicating on angiography worsening of the right-sided stenosis (Figs. 2, E and F). It was then thought that right-sided revascularization was indicated because of the progressive reduction in flow to the right hemisphere, and threat of complete occlusion. An autologous right, cervical-to-petrous, internal carotid artery bypass was performed by the neurosurgery service. The patient has continued to improve clinically and is currently neurologically intact 15 months after her injury. Follow-up angiography now demonstrates a widely patent right graft and return of the intracerebral flow pattern to normal (Fig. 3). DISCUSSION Unilateral dissection o f the internal carotid artery occurs with a reported incidence o f 2% to 3% in closed neck injuries. 9,1° Dissections afflict all age 431
432
Ballard et al.
Fig. 1. Progression of the right (left column) and left (right column) carotid dissections as demonstrated by angiography on admission (A, B), at 1 week (C, D), and at 3 weeks (E, F) after injury. Black arrows point out the areas of dissection.
Journal of VASCULAR SURGERY
Volume 15 Number 2 February 1992
Traumatic internal carotid artery dissections 433
D
:Fig. 2. Progressive findings on right (left column) and left (right column) intracerebral flow ~rough carotid angiography performed on admission (A, B), at 1 week (C, D), and at 3 weeks (E, F) after injury; There is progressively decreased ipsilateral flow and increased cross-filling !~rom 1 to 3 weeks. These angiographs were taken at the same time after injection of dye.
groups but particularly young adults ( 2 5 to 4 5 years), and may account for 5% or more ofischemic strokes in this age group. ~ Bilateral internal carotid artery dissections in closed neck injuries are much rarer. In a review o f the literature, only 16 other cases o f documented blunt traumatic bilateral internal carotid artery dissections were found; one o f these was
associated with bilateral traumatic disruptions o f the vertebral arteries. 4,5,9,12-~4 Blunt traumatic injury to the internal carotid artery usually results in an intimal tear or mural contusion; a traumatic dissection occurs when the intimal tear is followed by intramedial hemorrhage. Direct inspection at surgical exploration shows a
434
Ballard et aL
Fig. 3. Follow-up angiogram at 8 months demonstrates a widely patent right graft, and prompt fillingof the proximal MCA and ACA.
moderate cylindrical dilation and sharply demarcated dark blue discoloration of the dissected segment. On microscopic examination of excised segments, the dissection is in the outer layer of the media with a characteristic double lumen. A pseudoaneurysm may form between the media and adventia, or hemorrhage and thrombosis around the intima may slowly occlude the vessel completely. Embolization may also occur distally, leading to a variety of presenting symptoms.l,~s The primary indication for carotid angiography is any neurologic deficit that cannot be explained by head CT findings. Early carotid and intracranial angiography should be performed when the diagnosis of a carotid artery lesion is clinically suspected. 7'16q8 The angiographic findings may be classified as follows: type A involves a short segment of the cervical internal carotid not extending to the base of the skull, type B extends to the petrous portion, and type C shows complete occlusion. 8,~5 Intracranial angiography can give additional impor-
lournal of VASCULAR SURGERY
tant information regarding collateral cerebral blood flow and evidence of embolic phenomenon. Therapeutic maneuvers have ranged from distal carotid thrombectomy, carotid ligation, formal resection of the stenotic segment with interposition vein graft reconstruction, and extracranialintracranial bypass, to various anticoagulation regimens. 13'1s-22 Surgical treatment can be difficult because of a more extensive injury than is apparent on the angiograms; distal type B cervical lesions are often inaccessible to the usual modes of vascular repair. Spontaneous resolution of the process on anticoagulant medications is the rule; McNeill et al.21 recommend at least 3 weeks of heparin therapy for a full trial of conservative management. 14,22,23 Other authors have advocated a more aggressive surgical approach, particularly in those without a significant neurologic deficit and/or as a prophylaxis against subsequent neurologic events. Consideration can be made for extracranial-intracranial bypass to restore adequate cerebral perfusion, although its efficacy can be questioned. Ifligation of the internal carotid artery is chosen for a severe ongoing neurologic deficit, there may be propagation of thrombus from the top of the occluded internal carotid artery into the patent middle cerebral artery; adjunctive heparin therapy must therefore be continued. 2,s,1°,14,15,2° Recent introduction of a direct approach to the intrapetrous portion of the distal carotid artery by our neurosurgical colleagues, has allowed us to add an additional possibility to the existing armamentarium. Direct saphenous vein interposition grafts may be placed between the bifurcation and the proximal siphon, bypassing the entire cervical portion of the internal carotid with a large caliber antegrade graft. We have used this twice in the past year; for this case, and for reconstruction of a gunshot wound of the carotid artery at the C1-2 interspace. The indication for reconstruction in this case Was felt to be impending thrombosis of the right internal carotid artery because of angiographically demonstrated worsening stenosis and evidence of progressive left-to-right collateral flow. Follow-up studies indicate normalization of intracerebral flow and a patent graft. REFERENCES 1. Yamada S, Kin& GW, Youmans JR. Carotid artery occlusion due to non-penetrating injury. J Trauma 1967;7:333-42. 2. Thai ER, Snyder WH III, Hay RJ, Perry MO. Management of carotid artery injuries. Surgery 1974;76:955-62. 3. Perry MO, Snyder WH, Thai ER. Carotid artery injuries caused by blunt trauma. Ann Surg 1980;192:74-7. 4. Watridge CB, Muhlbauer MS, Loweruy KD. Traumatic
Volume 15 Number 2 February 1992
5.
6. 7.
8.
9.
10. ~1. 12.
13.
14.
carotid artery dissection: diagnosis and treatment. 1 Neurosurg 1989;71:854-7. Mokri B, Piepgras DG, Houser OW. Traumatic dissections of the extracranial internal carotid artery. I Neurosurg I988;68: I89-96. Hart RG, Easton DJ. Dissections. Stroke i985;16:925-7. Hart RG, Easton DI. Dissections of cervical and cerebral arteries. In: Barnett HJM ed. Cerebrovascular disease. Neurol Clin 1983;1:155-82. Fisher CM, Ojemann RG, Roberson GH. Spontaneous dissection of cervicocerebral arteries. Can J Neurol Surg 1978;5:9-19. Fukuda I, Meguro K, Matsusita S, Shigeta O, Oohashi N, Nakata Y. Traumatic disruption of bilateral vertebral arteries and internal carotid arteries. Case Report. J Trauma 1989;29:263-6. Fry RE, Fry WJ. Extracranial carotid artery injuries. Surgery 1980;88:58i-7. Hart RG, Miller VT. Cerebral infarction in young adults: a practical approach. Stroke 1983;14:110-4. Chakera TM. Bilateral extracranial internal carotid artery injury duc to non-penetrating trauma. Br I Radiol 1979;52: 704-8. Scherman BM, Tucker WS. Bilateral traumatic thrombosis of the internal carotid arteries in the neck: a case report and review of the literature. Neurosurgery 1982;10:751-3. Stringer WL, Kelly lr DL. Traumatic dissection of the
Traumatic internal carotid artery dissections 4 3 5
15. I6. 17.
18. 19.
20. 21.
22. 23.
extracranial internal carotid artery. Neurosurgery 1980;6: 123-30. Ehrenfeld WK, Wylie EJ. Spontaneous dissection of the internal carotid artery. Arch Surg 1986; 111:1294-301. Jernigan WR, Gardner WC. Carotid artery injuries due to closed cervical trauma. J Trauma 1971;11:429-435. Waespe W, Niesper J, Imhof H, Nolavanis A. Lower cranial nerve palsies due to internal carotid dissection. Stroke 1988;19:156i-4. Friedman WA, Day AL, et al. Cervical carotid dissecting aneurysms. Neurosurgery 1980;7:207-i3. Crissey MM, Bernstein EF. Delayed presentation of carotid intimal tear following blunt craniocervical trauma. Surgery 1974;75:543-9. Gee W, Kampp HA, et al. Spontaneous dissection of internal carotid arteries. Arch Surg 1980;115:944-9. McNeill D H Jr, Dreisbach J, Marsden RJ. Spontaneous dissection of the internal carotid artery. Arch Neurol 1980; 37:54-5. Biller T, Hingtgen WL, et al. Cervicocephalic arterial dissections, a ten-year experience. Arch Neurol I986;43:1234-8. Towne JB, Neiss DD, Smith JW. Thrombosis of the internal carotid artery following blunt cervical trauma. Arch Surg 1972; 104: 565-8.
Submitted Feb. 5, 1991; accepted May 15, I991.
