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Cervical vessel injury after blunt trauma
Cervical vessel injury after blunt trauma Samir M. Fakhry, M D , Paul F. Jaques, M D , and H e r b e r t J. Proctor, M D ,
Chapel Hill, N.C. Blunt trauma accounts for 3% to 10% of cervical vessel injuries. Death and severe neurologic impairment have been reported in more than 80% of blunt carotid injuries. In our recent experience, 10 patients sustained 18 blunt cervical arterial injuries: two internal carotid artery (ICA) dissections, three ICA transections with pseudoaneurysm, five ICA thromboses, two vertebral artery dissections, one vertebral artery transection with pseudoaneurysm, one vertebral artery thrombosis, one minimal vertebral artery injury, and three caroticocavernous fistulas. A delay of more than 12 hours in making the diagnosis occurred in seven of the 10 patients. The mental status was initially normal in seven patients. The subsequent development of focal neurologic findings incongruent with CT scanning of the head prompted four-vessel angiography. Treatment was individualized and included supportive management, intravenous heparin, ligation, extracranialintracranial bypass, and radiologic embolization. We have developed an angiographic classification that may aid management. Early angiography in patients with neurologic findings incongruent with head CT scan or in whom a normal sensorium and hemiparesis are present may permit improved outcomes. We advocate direct operative repair for accessible lesions of recent onset. For surgically inaccessible lesions, those with delayed presentation or in some cases with a fixed neurologic deficit, intravenous heparin can be started and follow-up angiography, head CT scanning, and the patient's clinical status determine further therapy. (J VAse SURG 1 9 8 8 ; 8 : 5 0 1 - 8 . )
Blunt trauma accounts for only 3% to 10% of cervical vessel injuries. Penetrating injury has received most o f the attention in the surgical literature. In 1803 Fleming 1 successfully ligated the carotid artery of a suicidal sailor. Ligation as primary therapy persisted until the 1950s, despite the pioneering Work of Carrel and Guthrie in vascular repair at the turn of the century. Advances in the techniques of fine-suture repair and blood banking during the Korean Conflict paved the way for the development of present-day management of penetrating cervical injury. Advances in diagnostic and therapeutic radiology have further enhanced treatment, tn part because of their relative infrequency, the management of blunt injuries has lagged behind. A total of 145 patients with blunt cervical injuries have been previously reported in the English language literature. 2-13 Although accessible lesions of recent onset without fixed neurologic deficits are generally manFrom the Departments of Surgery (Drs. Fakhryand Proctor) and Radiology (Dr. Jaques), the University of North Carolina, School of Medicine. Presented at the TwelfthAnnual Meeting of the Southern Association for Vascular Surgery, St. Thomas, Virgin Islands,Jan. 27-30, 1988. Reprint requests: Samir M. Fakhry, MD, University of North Carolina,SchoolofMedicine,Dept. of Surgery,BurnettWomack Bldg., Campus Box 7050, Chapel Hill, NC 275997O5O. .... ~
aged surgically, there is no clear consensus regarding the management of other blunt cervical injuries. A review of the literature and an analysis of our experience suggest that the appropriate management of such lesions can be based on the clinical setting and the angiographic findings with favorable outcomes in selected patients. PATIENTS In t h e 12-year period between 1975 and 1987, 10 patients with 18 nonpenetrating injuries to the cervical vessels were treated at our institution. All but one were treated in the past 3 years. Admission data are summarized in Table I. The mean age of patients was 36 years and motor vehicle accidents accounted for 50% o f injuries. The time from presentation to diagnosis was greater than 12 hours in seven patients. The angiographic findings, treatment, and outcome are summarized in Table II. Follow-up periods ranged from 8 to 24 months with no deaths. The salient features of the individual cases are presented below. Patients 1, 2, and 3 had isolated ophthalmologic abnormalities. Angiography revealed caroticocavernous fistula (CCF) in each (Fig. 1) and all were successfully treated with detachable balloon embolectomy. Follow-up angiograms demonstrated persistent obliteration of the fistulas. 501
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T a b l e I. H i s t o r y and admission findings
Patient 1 2
Age (yr)
Sex
Typeof injury
28 23
F M
MVA Assault
Time to diagnosis
3
88
F
Fall
4
21
M
Athletic injury
6 wk 7 wk 1 mo 4 mo
5
43
F
MVA
1 hr
6 7 8 9 10
17 43 23 3i 45
F M M M F
Assault Fall MVA MVA MVA
6 wk 2 days I mo i hr 1 wk
Neurologicfindings Ptosis; conjunctival hyperemia; bruit; left CN III palsy Ptosis; conjunctival hyperemia; bruit; diplopia Ptosis; decreased acuity Normal mental status; intermittent headache; vertigo; left lower quadrant homonymous hemianopsia Initially normal mental status; then dilated right pupil and right hemiparesis; right CN III palsy Normal mental status; right hemiparesis Global aphasia; right hemiparesis Expressive aphasia; right hemiparesis Combative; moving all extremities; left vocal cord paralysis Normal mental status; left hemiparesis; left CN III palsy
MVA, Motor vehicle accident; CN, cranial nerve.
T a b l e I I . A n g i o g r a p h i c findings, treatment and o u t c o m e
Patient
Angiographic findings
Treatment
1
Lt. CCF
Embolization
2
Rt. CCF
Embolization
3
Lt. CCF
Embolization
4 5
Rt. VA transection and PA Lt. VA dissection
Heparin; embolization Supportive; rehabilitation
6
Rt. ICA occlusion Lt. ICA occlusion
Supportive; rehabilitation
7
Rt. ICA occlusion Lt. ICA occlusion
Heparin; lt. EC-IC bypass; rehabilitation
8
Rt. ICA occlusion Lt. ICA transection and PA
Heparin; ft. EC-IC, ligated rt. ICA; It. EC-IC, occluded It. ICA
9
Lt. and rt. ICA transection and P& It. VA occlusion, ft. VA dissection Lt. and rt. ICA dissection, minimal injury VA
Heparin; vocal cord injection
I0
Heparin
Outcome
Follow-up
Improved proptosis and hyperemia; no bruit Improved proptosis and hyperemia; no bruit Improved proptosis and hyperemia; acuity slightly improved Normal neurologic examination Normal MS and speech; ambulatory; improved left third CN palsy Normal MS; ambulatory with help; dysarthria; moderate residual hemiparesis Normal MS; ambulatory with help; residual expressive aphasia; strength 3/5 RUE Normal MS; ambulatory; mild expressive aphasia; strength 5/5 RLE and 4/5 LLE RUE; 5/5 and 3 -+ 5/5 LUE Normal MS and strength; voice much improved
15 mo
Normal MS; ambulatory; persistent left hand weakness
1 yr 2 yr 2 yr 1 yr 12 yr 8 mo 1 yr
1 yr 20 mo
CCF, Caroticocavernous fistula; V& vertebral artery; PA, pseudoaneurysm; ICA, internal carotid artery; MS, mental status; EC-IC, extracranial-intracranial; RUE, right upper extremity; RLE, right lower extremity; LLE, left lower extremity; LUE, left upper extremity.
Patient 4 exhibited intermittent s y m p t o m s referable to pathologic conditions in the posterior circulation. C T scanning o f the head s h o w e d right cerebellar and occipital infarcts. A n g i o g r a p h y revealed a right vertebral artery transection with pscud o a n c u r y s m (Fig. 2). Because o f the probable emboli c nature o f the symptoms, the patient was treated with intravenous heparin followed by radiologic embolization o f the right vertebral artery and pseudoancurysm. H e completed a 6 - m o n t h course o f warfarin and was completely intact neurologically at the time o f this writing.
Patient 5 sustained a closed head injury with no mass lesion or intracranial bleeding o n C T scanning o f the head. H e r acute deterioration in the emergency department p r o m p t e d arteriography, which revealed left vertebral artery dissection (Fig. 3). After treatm e n t for the closed head injury, she u n d e r w e n t intensive physical therapy. She is presently completely functional with residual diplopia as a result o f aberrant regeneration o f the third cranial nerve. T h e patient has resumed light office work. Patient 6 had been beaten and strangled several days before admission. H e r mental status w a s
Volume 8 Number 4 October 1988
Cervical vessel injury after blunt trauma
503
Fig. 1. Patient 3. Left internal carotid arteriogram shows simultaneous opacification of the ICA and internal jugular vein through a large caroticocavernous fistula.
intact but the hemiparesis prompted an angiogram which showed bilateral internal carotid artery (ICA) occlusion. After supportive management and physical therapy, she entered an intermediate care facility. Patient 7 was initially observed for presumed concussion with a normal CT scan of the head. Hemiparesis and aphasia then developed and he was transferred to our institution. Angiography revealed bilateral ICA occlusion and intravenous heparin was , started. Aphasia and hemiparesis persisted, repeat anglography showed continued bilateral ICA occlusion. Left extracranial-intracranial (EC-IC) bypass was then performed; however, angiography at 6 months revealed occlusion of the bypass. Because of his continued improvement, further surgery was not performed. The patient was unemployed at last follow-up. Patient 8 had subarachnoid blood and a low density area in the left hemisphere on CT scan o f the head obtained at admission. At our institution, angiography revealed left ICA transection with pseudoaneurysm (Fig. 4,A) and right ICA occlusion with collateral filling from the left (Fig. 4, B). Intravenous heparin was started. His speech improved and he became ambulatory within 3 weeks. Repeat angiography at 3 months revealed continued right ICA occlusion. A right EC-IC bypass was performed with ~!gation of the right ICA in the neck. Follow-up
Fig. 2. Patient 4. Right vertebral arteriogram shows small traumatic pseudoaneurysm (arrow).
angiography 3 months later showed a patent right EC-IC graft and a persistent large left ICA pseudoaneurysm. Left EC-IC bypass was accomplished with occlusion of the left ICA by means of a Crutchfield clamp. Angiography 1 month later showed that both EC-IC bypass grafts were patent. Subsequent follow-up at 1 year from admission showed good neurologic recovery but mild expressive aphasia and upper extremity weakness have precluded his return to work. Patient 9 had a normal CT scan obtained at admission. Because of a possible basilar skull fracture, angiography was performed and revealed injury to all four vessels in the neck, including bilateral ICA transection with pseudoaneurysm (Fig. 5) (p. 506). He also had a paralyzed left vocal cord. He was treated with intravenous heparin and improved slowly over several weeks with gradual clearing of his mental status and resolution of multiple other problems related to the injury. The left vocal cord injury was treated with Gelfoam injections. Initial difficulties with swallowing attributed to apparent paralysis of the left side of the pharynx have slowly resolved.
504 Fakhry,Jaques, and Proctor
Fig. 3. Patient 5. Left vertebral arteriogram shows extensive nonobstructive intimal dissection. Follow-up angiography has shown persistence but no enlargement of the bilateral ICA pseudoaneurysms. We plan to continue follow-up for the bilateral pseudoaneurysms. His status returned to normal. Patient 10 was transferred to our institution 1 week after a motor vehicle accident. CT scan of the head showed an atypical right parietal contusion. Angiography revealed bilateral ICA transection with pseudoaneurysm and luminal narrowing (Fig. 6). She also had minimal injury to one vertebral artery (Fig. 7). She was treated with intravenous heparin and completed a course of warfarin. Her mental stares was clear throughout and her strength improved with intensive rehabilitation. Follow-up angiography revealed persistent pseudoaneurysms. One year after her injury, she was ambulatory with assistance and, despite residual upper extremity weakness, was employed. DISCUSSION
Although penetrating injury to the cervical vessels is usually readily suspected, blunt injuries may be
Journal of VASCULAR SURGERY
elusive. Their relative infrequency (3% to I0% of cervical arterial injuries) 11~4 and their common association with other injuries, especially closed head trauma, render their diagnosis more difficult. Characteristically there is a significant delay in making the diagnosis (8 of i0 patients in our series), caused in part by the delayed onset of detectable neurologic deficits. In the collected series reported by Yamada et al)s in 1967, nearly half of the 52 patients were asymptomatic at 10 hours. External signs of cervical trauma were present in only 50% of patients and the admitting diagnosis was correct in only ! of the 52 patients. Thirty-nine percent of patients in this series died and 84% of the survivors had significant neurologic deficit. These findings were reinforced in I980 in a collective review by Krajewski and Hertzer. 2 They added 44 patients with blunt carotid artery trauma to the 52 previously reported by Yamada et al. and found that in blunt carotid trauma, 93% of the injuries were at the carotid bifurcation or higher. Our findings are in agreement with this observation. This is in contrast to penetrating injuries, which involve the common carotid artery, in 50% to 90% of cases. 14'16"~7Krajewsld and Hertzer confirmed the finding by Yamada et al. is that almost all patients with blunt carotid artery injury have monoparesis or hemiparesis. They also substantiated observations made by Jernigan and Gardner ~8 that, although patients with intracranial bleeding become obtunded by the time focal neurologic findings develop, those with blunt carotid injury generally remain alert and oriented. In our series, four of the seven patients with ICA and vertebral artery injuries and all those with CCF had delayed diagnoses with subsequent neurologic or ocular deficits. These sequelae might have been avoided had the injuries been recognized sooner. Once fixed deficits have deveP oped, emergent operative intervention is unlikely to alter the outcome. The mechanism of injury in patients with blunt trauma is not entirely clear. Hyperextension and rotation, direct blows to the neck, intraoral trauma, and basilar or other skull fractures have been suggested as possible mechanisms2 822 In the patient with multiple trauma, it is often difficult to ascertain the exact mechanism of injury. It seems likely that stretching and twisting of the vessels or impalement against the transverse processes of the vertebral bodies or a fractured bony fragment may result in these injuries. No definite evidence exists to support these hypotheses. Whether a local deficiencyin elastic fibers or other structural abnormality2a may account
Volume 8 Number 4 October 1988
Cervical vesselinjury a~er blunt trauma 505
Fig. 4, A. Patient 8. Left carotid arteriogram reveals large pseudoaneurysm arising from the high cervical portion of the ICA. B, Right carotid arteriogram shows the typical tapered occlusion associated with a severe dissection. for the frequent localization of blunt injuries to the ICA has not been established. On the basis of the findings in our study, we developed a system of angiographic classification to assist in the management of these injuries. The most m i n o r injury resulting from nonpenetrating trauma is arterial spasm, which generally resolves promptly without residual effects. Minimal injury or "mural wrinkling" (Fig. 7) is a more severe injury with distortion of one or more layers of the blood vessel wall but without actual disruption of the layers. The extent of this injury determines whether it will heal or progress to a more severe injury. Intimal dissection without narrowing, which we classify radiologically as "linear lucencies within the vessel" (Fig. 3), represents the mildest form of intimal disruption. A more advanced form of this injury is intimal dissection with narrowing causing impairment of flow (Fig. 6) and possible acute total occlusion. Intimal dissection without occlusion may improve spontaneously or with heparin therapy. None of our pa-
tients with such a lesion progressed to delayed total occlusion. In reviewing our arteriograms, we have noted that in all cases of total occlusion there was an oblique, tapering appearance consistent with an intimal flap occluding the lumen. We conclude that occlusion by thrombus alone in a high flow vessel such as the carotid artery is exceedingly uncommon without architectural disruption of the vessel wall, most commonly by intimal dissection (Fig. 4, B). The outcome with acute total occlusion is variable and dependent on the time course over which it occurs, the age of the patient, and the presence of adequate collateral circulation. Because only 20% of the population have a complete circle of Willis and only 50% have adequate collateral circulation, 24 results of traumatic occlusion of the ICA are variable. Transection is a transmural disruption of the vessel wall and may be lethal if not contained immediately. Contained transection (Figs. 4 , A and 5) may progress to the formation of a pseudoaneurysm or, if adjacent vessels are also injured, to an arteriovenous
506
Fakhry,Jaques, and Proctor
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Fig. 5. Patient 9. Composite bilateral carotid arteriograms show bilateral ICA transections with pseudoaneurysms.
fistula, such as the CCFs reported in this series (Fig. 1). We recommend complete four-vessel anglographic evaluation, as we have encountered multiple vessel injuries in approximately 40% of cases. The diagnosis of cervical vessel injury from nonpenetrating trauma should be suspected and angiography strongly considered with any of the following: neurologic findings, incongruent with head CT scan; monoparesis or hemiparesis with a normal mental status; signs or a history of significant external cervical trauma in a patient with an altered neurologic examination; basilar skull fracture in a patient with altered mental status; focal neurologic deficit (including ocular abnormality) inconsistent with head CT scan findings. Many authors 1°'1a'14"16'17 have reported that prompt repair of accessible lesions of recent onset is appropriate whether in blunt or penetrating trauma. Even in the presence of such ominous signs as shock or coma, surgical repair offers as good or better a chance for survival as nonoperative management. Previous fears that revascularization ofischemic areas would result in hemorrhagic infarction as suggested
Fig. 6. Patient 10. Right carotid arteriogram shows typical nonoccluding ICA dissection. Note narrowing of compressed lumen. This patient had a similar lesion involving the left ICA. by Wylie et al. 2s and Bradley24 have not been borne out for patients with acute injuries. In our patients with ICA injuries, delays in diagnosis, fixed neurologic deficits, and relative surgical inaccessibiliv precluded operative intervention. Two of our patients were treated supportively. We used intravenous heparin as initial therapy in five patients. Our indications for the use of anticoagulation were to avoid platelet aggregation, clot formation, and embolic events at areas of intimal disruption; to avoid propagation of already formed thrombus; and possibly to aid in the healing of injured intima by decreasing smooth muscle cell proliferation and intimal thickening as suggested in the rat carotid artery model. 26,27EC-IC bypass is a controversial treatment modality and has been recommended in the management of cervical vessel i n j u r y . 9'28 Our limited experience with this technique in patients with blunt cervical vessel injury does not allow us to support its use. The significant neurologic impairment and high mortality rates encountered in previous reports on
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Cervical vessel injury after blunt trauma
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3.
4.
5.
6.
7.
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common trunk of the carotid itself. Reported by RW Coley. Med Chir J 1817;3:2-4. Krajewski LP, Hertzer NR. Blunt carotid artery trauma: report of two cases and review of the literature. Ann Surg 1980;191:341-6. Marvasti MA, Parker FB Jr, Bredenberg CE. Injuries to arterial branches of the aortic arch. Thorac Cardiovasc Surg 1984;32:293-8. Pellegrini RV, Manzetti GW, DiMarco RF, Bekoe S, Arena SA, Marrangoni AG. The direct surgical management of lesions of the high internal carotid artery. J Cardiovasc Surg (Torino) 1984;25:29-35. Hoffman TH, Richardson JD, Flint LM. Intimal disruption of major cerebral vasculature following blunt trauma. Surgery 1980;87:441-4. Kallero KS, Bjorck CG, Bergqvist D. Carotid artery injury caused by blunt cervical trauma. Case report. Acta Chir Scand 1987;153:155-60. Zdenock GB, Kazmers A, Whitehouse WM Jr, et al. Extracranial internal carotid artery dissections. Arch Surg 1982; 117:425-32.
Fig. 7. Patient 10. Vertebral arteriogram shows minimal injury with "mural wrinkling" (arrow). These lesions are thought to heal without sequelae. b l u n t c a r o t i d t r a u m a reflect t h e severity o f this injury especially w h e n it is associated w i t h total occlusion. W e f o u n d t h a t o t h e r cervical vessel injuries are m o r e amenable to operative and nonoperative managem e n t a n d carry a m o r e favorable p r o g n o s i s . I n summary, o u r experience suggests that patients w i t h cervical vessel injury o c c u r r i n g in b l u n t t r a u m a w i t h d e l a y e d p r e s e n t a t i o n , fixed n e u r o l o g i c deficit, a n d surgically i n a c c e s s i b l e lesions can be safely t r e a t e d n o n o p e r a t i v e l y w i t h i n t r a v e n o u s h e p a r i n a n d in s o m e cases invasive r a d i o l o g i c techniques. 29'a° T h e early use o f four-vessel a n g i o g r a p h y m a y c o n t r i b u t e to decreased m o r t a l i t y a n d m o r b i d i t y in these difficult injuries. We would like to thank Dr. Don W. King for assistance in providing clinical material and Dr. Suzanne L. Kirby for valuable help with the manuscript. REFERENCES
1. Fleming D. Case of rupture of the carotid artery, the wounds of several of its branches, successfully treated by tying the
8. Aranson M, Kramer R. Traumatic disruption of the left common carotid artery following blunt trauma. Surg Rounds 1985;(Dec):47-52. 9. Fry RE, Fry WJ. Extracranial carotid artery injuries. Surgery 1980;88:581-6. 10. Ledgerwood AM, Mullins RJ, Lucas CE. Primary repair vs. ligation for carotid artery injuries. Arch Surg 1980;115:48893. 11. Brown MF, Graham JM, Fdiciano DV, Mattox KL, Beal AC Jr, DeBakey ME. Carotid artery injuries. Am J Surg 1982; 144:748-53. 12. Dragon R, Saranchak H, Lakin P, Stranch G. Blunt injuries to the carotid and vertebral arteries. Am J Surg 1981; 141:497-500. 13. Perry MO, Snyder WM, Thai ER. Carotid artery injury caused by blunt trauma. Ann Surg 1980;192:74-7. 14. Unger SW, Tucker W S Jr, Mrdeza MA, Wellons A Jr, Chandler ]G. Carotid arterial trauma. Surgery 1980;87:47787. 15. Yamada S, Kindt GW, Youmans JR. Carotid artery occlusion due to non-penetrating injmY. J Trauma 1967;7:333-42. 16. Liekweg WG Jr, Greenfield LJ. Management of penetrating carotid injury. Ann Surg 1978;188:587-92. 17. Karlin RM, Marks C. Extracranial carotid artery injury. Current surgical management. Am J Surg 1983;146:225-7. 18. }'emigan WR, Gardner WC. Carotid artery injuries due to closed cervical trauma. J Trauma 1971;11:429-35. 19. Ctissey MM, Bemstein EF. Delayed presentation of carotid intimal tear following blunt craniocervical trauma. Surgery 1974;75:543-9. 20. Woodhurst WB, Robertson WD, Thompson GB. Carotid injury due to intraoral trauma: case report and review of the literature. Neurosurgery 1980;6:559-63. 21. Rosenwasser R, Delgado T, Buchheit W. Cerebrovascular complications of closed neck and head trauma: injuries to the carotid artery. Surg Rounds 1983;0"une):56-65. 22. Pimer SE. Carotid thrombosis due to intraoral trauma: an unusual complication of a common childhood accident. N Engl J Med 1966;274:764-7. 23. Fry WJ, Fry RE. Management of carotid artery injury. In: Bergan JJ, Yao JST, eds. Vascular surgical emergencies. Orlando: Grime & Stratton, Inc, 1987:153-62.
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24. Bradley EL III. Management of penetrating carotid injuries: an alternate approach. J Trauma 1973;13:248-55. 25. Wylie EJ, Hein MF, Adams JE. Intracranial hemorrhage following surgical revascularization for treatment of acute strokes. J Neurosurg 1964;21:212-5. 26. Clowes AW, Clowes MM. Kinetics of cellular proliferation after arterial injury. IV. Heparin inhibits rat smooth muscle mitogenesis and migration. Circ Res 1986;58:839-45. 27. Majesky MW, Schwartz SM, Clowes MM, Clowes AW. Heparin regulates smooth muscle S phase entry in the injured rat carotid artery. Circ Res 1987;61:296-300.
28. Gewertz BL, Sampson DS, Ditmore QM, Bone GE. Management of penetrating injuries of the internal carotid artery at the base of the skull utilizing extracraniai-intracranial bypass. J Trauma 1980;20:365-9. 29. Dory MA. Vertebral artery embotization for control of massive hemorrhage. AJNR 1985;6:641. 30. Tress BM, Thompson KR, Simon AT, King J, Brownhill D, Crawford B. Treatment of carotieocavernous fistula with detachable balloons introduced by percutaneous catheterization. Radiology 1984;150:288.
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Chapel Hill, N.C. Blunt trauma accounts for 3% to 10% of cervical vessel injuries. Death and severe neurologic impairment have been reported in more than 80% of blunt carotid injuries. In our recent experience, 10 patients sustained 18 blunt cervical arterial injuries: two internal carotid artery (ICA) dissections, three ICA transections with pseudoaneurysm, five ICA thromboses, two vertebral artery dissections, one vertebral artery transection with pseudoaneurysm, one vertebral artery thrombosis, one minimal vertebral artery injury, and three caroticocavernous fistulas. A delay of more than 12 hours in making the diagnosis occurred in seven of the 10 patients. The mental status was initially normal in seven patients. The subsequent development of focal neurologic findings incongruent with CT scanning of the head prompted four-vessel angiography. Treatment was individualized and included supportive management, intravenous heparin, ligation, extracranialintracranial bypass, and radiologic embolization. We have developed an angiographic classification that may aid management. Early angiography in patients with neurologic findings incongruent with head CT scan or in whom a normal sensorium and hemiparesis are present may permit improved outcomes. We advocate direct operative repair for accessible lesions of recent onset. For surgically inaccessible lesions, those with delayed presentation or in some cases with a fixed neurologic deficit, intravenous heparin can be started and follow-up angiography, head CT scanning, and the patient's clinical status determine further therapy. (J VAse SURG 1 9 8 8 ; 8 : 5 0 1 - 8 . )
Blunt trauma accounts for only 3% to 10% of cervical vessel injuries. Penetrating injury has received most o f the attention in the surgical literature. In 1803 Fleming 1 successfully ligated the carotid artery of a suicidal sailor. Ligation as primary therapy persisted until the 1950s, despite the pioneering Work of Carrel and Guthrie in vascular repair at the turn of the century. Advances in the techniques of fine-suture repair and blood banking during the Korean Conflict paved the way for the development of present-day management of penetrating cervical injury. Advances in diagnostic and therapeutic radiology have further enhanced treatment, tn part because of their relative infrequency, the management of blunt injuries has lagged behind. A total of 145 patients with blunt cervical injuries have been previously reported in the English language literature. 2-13 Although accessible lesions of recent onset without fixed neurologic deficits are generally manFrom the Departments of Surgery (Drs. Fakhryand Proctor) and Radiology (Dr. Jaques), the University of North Carolina, School of Medicine. Presented at the TwelfthAnnual Meeting of the Southern Association for Vascular Surgery, St. Thomas, Virgin Islands,Jan. 27-30, 1988. Reprint requests: Samir M. Fakhry, MD, University of North Carolina,SchoolofMedicine,Dept. of Surgery,BurnettWomack Bldg., Campus Box 7050, Chapel Hill, NC 275997O5O. .... ~
aged surgically, there is no clear consensus regarding the management of other blunt cervical injuries. A review of the literature and an analysis of our experience suggest that the appropriate management of such lesions can be based on the clinical setting and the angiographic findings with favorable outcomes in selected patients. PATIENTS In t h e 12-year period between 1975 and 1987, 10 patients with 18 nonpenetrating injuries to the cervical vessels were treated at our institution. All but one were treated in the past 3 years. Admission data are summarized in Table I. The mean age of patients was 36 years and motor vehicle accidents accounted for 50% o f injuries. The time from presentation to diagnosis was greater than 12 hours in seven patients. The angiographic findings, treatment, and outcome are summarized in Table II. Follow-up periods ranged from 8 to 24 months with no deaths. The salient features of the individual cases are presented below. Patients 1, 2, and 3 had isolated ophthalmologic abnormalities. Angiography revealed caroticocavernous fistula (CCF) in each (Fig. 1) and all were successfully treated with detachable balloon embolectomy. Follow-up angiograms demonstrated persistent obliteration of the fistulas. 501
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T a b l e I. H i s t o r y and admission findings
Patient 1 2
Age (yr)
Sex
Typeof injury
28 23
F M
MVA Assault
Time to diagnosis
3
88
F
Fall
4
21
M
Athletic injury
6 wk 7 wk 1 mo 4 mo
5
43
F
MVA
1 hr
6 7 8 9 10
17 43 23 3i 45
F M M M F
Assault Fall MVA MVA MVA
6 wk 2 days I mo i hr 1 wk
Neurologicfindings Ptosis; conjunctival hyperemia; bruit; left CN III palsy Ptosis; conjunctival hyperemia; bruit; diplopia Ptosis; decreased acuity Normal mental status; intermittent headache; vertigo; left lower quadrant homonymous hemianopsia Initially normal mental status; then dilated right pupil and right hemiparesis; right CN III palsy Normal mental status; right hemiparesis Global aphasia; right hemiparesis Expressive aphasia; right hemiparesis Combative; moving all extremities; left vocal cord paralysis Normal mental status; left hemiparesis; left CN III palsy
MVA, Motor vehicle accident; CN, cranial nerve.
T a b l e I I . A n g i o g r a p h i c findings, treatment and o u t c o m e
Patient
Angiographic findings
Treatment
1
Lt. CCF
Embolization
2
Rt. CCF
Embolization
3
Lt. CCF
Embolization
4 5
Rt. VA transection and PA Lt. VA dissection
Heparin; embolization Supportive; rehabilitation
6
Rt. ICA occlusion Lt. ICA occlusion
Supportive; rehabilitation
7
Rt. ICA occlusion Lt. ICA occlusion
Heparin; lt. EC-IC bypass; rehabilitation
8
Rt. ICA occlusion Lt. ICA transection and PA
Heparin; ft. EC-IC, ligated rt. ICA; It. EC-IC, occluded It. ICA
9
Lt. and rt. ICA transection and P& It. VA occlusion, ft. VA dissection Lt. and rt. ICA dissection, minimal injury VA
Heparin; vocal cord injection
I0
Heparin
Outcome
Follow-up
Improved proptosis and hyperemia; no bruit Improved proptosis and hyperemia; no bruit Improved proptosis and hyperemia; acuity slightly improved Normal neurologic examination Normal MS and speech; ambulatory; improved left third CN palsy Normal MS; ambulatory with help; dysarthria; moderate residual hemiparesis Normal MS; ambulatory with help; residual expressive aphasia; strength 3/5 RUE Normal MS; ambulatory; mild expressive aphasia; strength 5/5 RLE and 4/5 LLE RUE; 5/5 and 3 -+ 5/5 LUE Normal MS and strength; voice much improved
15 mo
Normal MS; ambulatory; persistent left hand weakness
1 yr 2 yr 2 yr 1 yr 12 yr 8 mo 1 yr
1 yr 20 mo
CCF, Caroticocavernous fistula; V& vertebral artery; PA, pseudoaneurysm; ICA, internal carotid artery; MS, mental status; EC-IC, extracranial-intracranial; RUE, right upper extremity; RLE, right lower extremity; LLE, left lower extremity; LUE, left upper extremity.
Patient 4 exhibited intermittent s y m p t o m s referable to pathologic conditions in the posterior circulation. C T scanning o f the head s h o w e d right cerebellar and occipital infarcts. A n g i o g r a p h y revealed a right vertebral artery transection with pscud o a n c u r y s m (Fig. 2). Because o f the probable emboli c nature o f the symptoms, the patient was treated with intravenous heparin followed by radiologic embolization o f the right vertebral artery and pseudoancurysm. H e completed a 6 - m o n t h course o f warfarin and was completely intact neurologically at the time o f this writing.
Patient 5 sustained a closed head injury with no mass lesion or intracranial bleeding o n C T scanning o f the head. H e r acute deterioration in the emergency department p r o m p t e d arteriography, which revealed left vertebral artery dissection (Fig. 3). After treatm e n t for the closed head injury, she u n d e r w e n t intensive physical therapy. She is presently completely functional with residual diplopia as a result o f aberrant regeneration o f the third cranial nerve. T h e patient has resumed light office work. Patient 6 had been beaten and strangled several days before admission. H e r mental status w a s
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Fig. 1. Patient 3. Left internal carotid arteriogram shows simultaneous opacification of the ICA and internal jugular vein through a large caroticocavernous fistula.
intact but the hemiparesis prompted an angiogram which showed bilateral internal carotid artery (ICA) occlusion. After supportive management and physical therapy, she entered an intermediate care facility. Patient 7 was initially observed for presumed concussion with a normal CT scan of the head. Hemiparesis and aphasia then developed and he was transferred to our institution. Angiography revealed bilateral ICA occlusion and intravenous heparin was , started. Aphasia and hemiparesis persisted, repeat anglography showed continued bilateral ICA occlusion. Left extracranial-intracranial (EC-IC) bypass was then performed; however, angiography at 6 months revealed occlusion of the bypass. Because of his continued improvement, further surgery was not performed. The patient was unemployed at last follow-up. Patient 8 had subarachnoid blood and a low density area in the left hemisphere on CT scan o f the head obtained at admission. At our institution, angiography revealed left ICA transection with pseudoaneurysm (Fig. 4,A) and right ICA occlusion with collateral filling from the left (Fig. 4, B). Intravenous heparin was started. His speech improved and he became ambulatory within 3 weeks. Repeat angiography at 3 months revealed continued right ICA occlusion. A right EC-IC bypass was performed with ~!gation of the right ICA in the neck. Follow-up
Fig. 2. Patient 4. Right vertebral arteriogram shows small traumatic pseudoaneurysm (arrow).
angiography 3 months later showed a patent right EC-IC graft and a persistent large left ICA pseudoaneurysm. Left EC-IC bypass was accomplished with occlusion of the left ICA by means of a Crutchfield clamp. Angiography 1 month later showed that both EC-IC bypass grafts were patent. Subsequent follow-up at 1 year from admission showed good neurologic recovery but mild expressive aphasia and upper extremity weakness have precluded his return to work. Patient 9 had a normal CT scan obtained at admission. Because of a possible basilar skull fracture, angiography was performed and revealed injury to all four vessels in the neck, including bilateral ICA transection with pseudoaneurysm (Fig. 5) (p. 506). He also had a paralyzed left vocal cord. He was treated with intravenous heparin and improved slowly over several weeks with gradual clearing of his mental status and resolution of multiple other problems related to the injury. The left vocal cord injury was treated with Gelfoam injections. Initial difficulties with swallowing attributed to apparent paralysis of the left side of the pharynx have slowly resolved.
504 Fakhry,Jaques, and Proctor
Fig. 3. Patient 5. Left vertebral arteriogram shows extensive nonobstructive intimal dissection. Follow-up angiography has shown persistence but no enlargement of the bilateral ICA pseudoaneurysms. We plan to continue follow-up for the bilateral pseudoaneurysms. His status returned to normal. Patient 10 was transferred to our institution 1 week after a motor vehicle accident. CT scan of the head showed an atypical right parietal contusion. Angiography revealed bilateral ICA transection with pseudoaneurysm and luminal narrowing (Fig. 6). She also had minimal injury to one vertebral artery (Fig. 7). She was treated with intravenous heparin and completed a course of warfarin. Her mental stares was clear throughout and her strength improved with intensive rehabilitation. Follow-up angiography revealed persistent pseudoaneurysms. One year after her injury, she was ambulatory with assistance and, despite residual upper extremity weakness, was employed. DISCUSSION
Although penetrating injury to the cervical vessels is usually readily suspected, blunt injuries may be
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elusive. Their relative infrequency (3% to I0% of cervical arterial injuries) 11~4 and their common association with other injuries, especially closed head trauma, render their diagnosis more difficult. Characteristically there is a significant delay in making the diagnosis (8 of i0 patients in our series), caused in part by the delayed onset of detectable neurologic deficits. In the collected series reported by Yamada et al)s in 1967, nearly half of the 52 patients were asymptomatic at 10 hours. External signs of cervical trauma were present in only 50% of patients and the admitting diagnosis was correct in only ! of the 52 patients. Thirty-nine percent of patients in this series died and 84% of the survivors had significant neurologic deficit. These findings were reinforced in I980 in a collective review by Krajewski and Hertzer. 2 They added 44 patients with blunt carotid artery trauma to the 52 previously reported by Yamada et al. and found that in blunt carotid trauma, 93% of the injuries were at the carotid bifurcation or higher. Our findings are in agreement with this observation. This is in contrast to penetrating injuries, which involve the common carotid artery, in 50% to 90% of cases. 14'16"~7Krajewsld and Hertzer confirmed the finding by Yamada et al. is that almost all patients with blunt carotid artery injury have monoparesis or hemiparesis. They also substantiated observations made by Jernigan and Gardner ~8 that, although patients with intracranial bleeding become obtunded by the time focal neurologic findings develop, those with blunt carotid injury generally remain alert and oriented. In our series, four of the seven patients with ICA and vertebral artery injuries and all those with CCF had delayed diagnoses with subsequent neurologic or ocular deficits. These sequelae might have been avoided had the injuries been recognized sooner. Once fixed deficits have deveP oped, emergent operative intervention is unlikely to alter the outcome. The mechanism of injury in patients with blunt trauma is not entirely clear. Hyperextension and rotation, direct blows to the neck, intraoral trauma, and basilar or other skull fractures have been suggested as possible mechanisms2 822 In the patient with multiple trauma, it is often difficult to ascertain the exact mechanism of injury. It seems likely that stretching and twisting of the vessels or impalement against the transverse processes of the vertebral bodies or a fractured bony fragment may result in these injuries. No definite evidence exists to support these hypotheses. Whether a local deficiencyin elastic fibers or other structural abnormality2a may account
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Cervical vesselinjury a~er blunt trauma 505
Fig. 4, A. Patient 8. Left carotid arteriogram reveals large pseudoaneurysm arising from the high cervical portion of the ICA. B, Right carotid arteriogram shows the typical tapered occlusion associated with a severe dissection. for the frequent localization of blunt injuries to the ICA has not been established. On the basis of the findings in our study, we developed a system of angiographic classification to assist in the management of these injuries. The most m i n o r injury resulting from nonpenetrating trauma is arterial spasm, which generally resolves promptly without residual effects. Minimal injury or "mural wrinkling" (Fig. 7) is a more severe injury with distortion of one or more layers of the blood vessel wall but without actual disruption of the layers. The extent of this injury determines whether it will heal or progress to a more severe injury. Intimal dissection without narrowing, which we classify radiologically as "linear lucencies within the vessel" (Fig. 3), represents the mildest form of intimal disruption. A more advanced form of this injury is intimal dissection with narrowing causing impairment of flow (Fig. 6) and possible acute total occlusion. Intimal dissection without occlusion may improve spontaneously or with heparin therapy. None of our pa-
tients with such a lesion progressed to delayed total occlusion. In reviewing our arteriograms, we have noted that in all cases of total occlusion there was an oblique, tapering appearance consistent with an intimal flap occluding the lumen. We conclude that occlusion by thrombus alone in a high flow vessel such as the carotid artery is exceedingly uncommon without architectural disruption of the vessel wall, most commonly by intimal dissection (Fig. 4, B). The outcome with acute total occlusion is variable and dependent on the time course over which it occurs, the age of the patient, and the presence of adequate collateral circulation. Because only 20% of the population have a complete circle of Willis and only 50% have adequate collateral circulation, 24 results of traumatic occlusion of the ICA are variable. Transection is a transmural disruption of the vessel wall and may be lethal if not contained immediately. Contained transection (Figs. 4 , A and 5) may progress to the formation of a pseudoaneurysm or, if adjacent vessels are also injured, to an arteriovenous
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Fig. 5. Patient 9. Composite bilateral carotid arteriograms show bilateral ICA transections with pseudoaneurysms.
fistula, such as the CCFs reported in this series (Fig. 1). We recommend complete four-vessel anglographic evaluation, as we have encountered multiple vessel injuries in approximately 40% of cases. The diagnosis of cervical vessel injury from nonpenetrating trauma should be suspected and angiography strongly considered with any of the following: neurologic findings, incongruent with head CT scan; monoparesis or hemiparesis with a normal mental status; signs or a history of significant external cervical trauma in a patient with an altered neurologic examination; basilar skull fracture in a patient with altered mental status; focal neurologic deficit (including ocular abnormality) inconsistent with head CT scan findings. Many authors 1°'1a'14"16'17 have reported that prompt repair of accessible lesions of recent onset is appropriate whether in blunt or penetrating trauma. Even in the presence of such ominous signs as shock or coma, surgical repair offers as good or better a chance for survival as nonoperative management. Previous fears that revascularization ofischemic areas would result in hemorrhagic infarction as suggested
Fig. 6. Patient 10. Right carotid arteriogram shows typical nonoccluding ICA dissection. Note narrowing of compressed lumen. This patient had a similar lesion involving the left ICA. by Wylie et al. 2s and Bradley24 have not been borne out for patients with acute injuries. In our patients with ICA injuries, delays in diagnosis, fixed neurologic deficits, and relative surgical inaccessibiliv precluded operative intervention. Two of our patients were treated supportively. We used intravenous heparin as initial therapy in five patients. Our indications for the use of anticoagulation were to avoid platelet aggregation, clot formation, and embolic events at areas of intimal disruption; to avoid propagation of already formed thrombus; and possibly to aid in the healing of injured intima by decreasing smooth muscle cell proliferation and intimal thickening as suggested in the rat carotid artery model. 26,27EC-IC bypass is a controversial treatment modality and has been recommended in the management of cervical vessel i n j u r y . 9'28 Our limited experience with this technique in patients with blunt cervical vessel injury does not allow us to support its use. The significant neurologic impairment and high mortality rates encountered in previous reports on
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common trunk of the carotid itself. Reported by RW Coley. Med Chir J 1817;3:2-4. Krajewski LP, Hertzer NR. Blunt carotid artery trauma: report of two cases and review of the literature. Ann Surg 1980;191:341-6. Marvasti MA, Parker FB Jr, Bredenberg CE. Injuries to arterial branches of the aortic arch. Thorac Cardiovasc Surg 1984;32:293-8. Pellegrini RV, Manzetti GW, DiMarco RF, Bekoe S, Arena SA, Marrangoni AG. The direct surgical management of lesions of the high internal carotid artery. J Cardiovasc Surg (Torino) 1984;25:29-35. Hoffman TH, Richardson JD, Flint LM. Intimal disruption of major cerebral vasculature following blunt trauma. Surgery 1980;87:441-4. Kallero KS, Bjorck CG, Bergqvist D. Carotid artery injury caused by blunt cervical trauma. Case report. Acta Chir Scand 1987;153:155-60. Zdenock GB, Kazmers A, Whitehouse WM Jr, et al. Extracranial internal carotid artery dissections. Arch Surg 1982; 117:425-32.
Fig. 7. Patient 10. Vertebral arteriogram shows minimal injury with "mural wrinkling" (arrow). These lesions are thought to heal without sequelae. b l u n t c a r o t i d t r a u m a reflect t h e severity o f this injury especially w h e n it is associated w i t h total occlusion. W e f o u n d t h a t o t h e r cervical vessel injuries are m o r e amenable to operative and nonoperative managem e n t a n d carry a m o r e favorable p r o g n o s i s . I n summary, o u r experience suggests that patients w i t h cervical vessel injury o c c u r r i n g in b l u n t t r a u m a w i t h d e l a y e d p r e s e n t a t i o n , fixed n e u r o l o g i c deficit, a n d surgically i n a c c e s s i b l e lesions can be safely t r e a t e d n o n o p e r a t i v e l y w i t h i n t r a v e n o u s h e p a r i n a n d in s o m e cases invasive r a d i o l o g i c techniques. 29'a° T h e early use o f four-vessel a n g i o g r a p h y m a y c o n t r i b u t e to decreased m o r t a l i t y a n d m o r b i d i t y in these difficult injuries. We would like to thank Dr. Don W. King for assistance in providing clinical material and Dr. Suzanne L. Kirby for valuable help with the manuscript. REFERENCES
1. Fleming D. Case of rupture of the carotid artery, the wounds of several of its branches, successfully treated by tying the
8. Aranson M, Kramer R. Traumatic disruption of the left common carotid artery following blunt trauma. Surg Rounds 1985;(Dec):47-52. 9. Fry RE, Fry WJ. Extracranial carotid artery injuries. Surgery 1980;88:581-6. 10. Ledgerwood AM, Mullins RJ, Lucas CE. Primary repair vs. ligation for carotid artery injuries. Arch Surg 1980;115:48893. 11. Brown MF, Graham JM, Fdiciano DV, Mattox KL, Beal AC Jr, DeBakey ME. Carotid artery injuries. Am J Surg 1982; 144:748-53. 12. Dragon R, Saranchak H, Lakin P, Stranch G. Blunt injuries to the carotid and vertebral arteries. Am J Surg 1981; 141:497-500. 13. Perry MO, Snyder WM, Thai ER. Carotid artery injury caused by blunt trauma. Ann Surg 1980;192:74-7. 14. Unger SW, Tucker W S Jr, Mrdeza MA, Wellons A Jr, Chandler ]G. Carotid arterial trauma. Surgery 1980;87:47787. 15. Yamada S, Kindt GW, Youmans JR. Carotid artery occlusion due to non-penetrating injmY. J Trauma 1967;7:333-42. 16. Liekweg WG Jr, Greenfield LJ. Management of penetrating carotid injury. Ann Surg 1978;188:587-92. 17. Karlin RM, Marks C. Extracranial carotid artery injury. Current surgical management. Am J Surg 1983;146:225-7. 18. }'emigan WR, Gardner WC. Carotid artery injuries due to closed cervical trauma. J Trauma 1971;11:429-35. 19. Ctissey MM, Bemstein EF. Delayed presentation of carotid intimal tear following blunt craniocervical trauma. Surgery 1974;75:543-9. 20. Woodhurst WB, Robertson WD, Thompson GB. Carotid injury due to intraoral trauma: case report and review of the literature. Neurosurgery 1980;6:559-63. 21. Rosenwasser R, Delgado T, Buchheit W. Cerebrovascular complications of closed neck and head trauma: injuries to the carotid artery. Surg Rounds 1983;0"une):56-65. 22. Pimer SE. Carotid thrombosis due to intraoral trauma: an unusual complication of a common childhood accident. N Engl J Med 1966;274:764-7. 23. Fry WJ, Fry RE. Management of carotid artery injury. In: Bergan JJ, Yao JST, eds. Vascular surgical emergencies. Orlando: Grime & Stratton, Inc, 1987:153-62.
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24. Bradley EL III. Management of penetrating carotid injuries: an alternate approach. J Trauma 1973;13:248-55. 25. Wylie EJ, Hein MF, Adams JE. Intracranial hemorrhage following surgical revascularization for treatment of acute strokes. J Neurosurg 1964;21:212-5. 26. Clowes AW, Clowes MM. Kinetics of cellular proliferation after arterial injury. IV. Heparin inhibits rat smooth muscle mitogenesis and migration. Circ Res 1986;58:839-45. 27. Majesky MW, Schwartz SM, Clowes MM, Clowes AW. Heparin regulates smooth muscle S phase entry in the injured rat carotid artery. Circ Res 1987;61:296-300.
28. Gewertz BL, Sampson DS, Ditmore QM, Bone GE. Management of penetrating injuries of the internal carotid artery at the base of the skull utilizing extracraniai-intracranial bypass. J Trauma 1980;20:365-9. 29. Dory MA. Vertebral artery embotization for control of massive hemorrhage. AJNR 1985;6:641. 30. Tress BM, Thompson KR, Simon AT, King J, Brownhill D, Crawford B. Treatment of carotieocavernous fistula with detachable balloons introduced by percutaneous catheterization. Radiology 1984;150:288.
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