Original Article
Head and neck neurovascular trauma: Clinical and angiographic correlation
Interventional Neuroradiology 2015, Vol. 21(1) 108–113 ! The Author(s) 2015 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav DOI: 10.1177/1591019915576666 ine.sagepub.com
Peter Kato Ssenyonga, David Le Feuvre and Allan Taylor
Abstract A retrospective review of all angiograms done for craniocervical trauma, over an eight-year period at Groote Schuur Hospital identified 61 patients out of 823 angiographically studied who had extradural vascular injury and required endovascular treatment. Multiple lesions were identified in nine (14,8%) patients and associated injuries were found in 23 patients (37%). The mechanism of injury was blunt in nine (14.8%) patients and penetrating in 52 (85.2%). There was a statistically significant correlation between the presenting clinical feature and the underlying angiographic lesion. Patients with active bleeding were more likely to have a vessel laceration, an expanding hematoma was associated with false aneurysm and a pulsatile mass with arteriovenous fistula. Endovascular treatment with emphasis on vessel occlusion rather than preservation was successful in all cases except one which required surgical vessel ligation.
Keywords Head and neck, neurovascular, trauma, false aneurysm, arteriovenous fistula
Introduction Blunt and penetrating craniocervical injury is associated with vascular injury in up to 3% and 20% of cases respectively.1–4 Vessel injury can lead to acute hemodynamic and airway compromise from bleeding, as well as neurological deficit from embolism or flow limitation.5 There is a spectrum of clinical presentation and varying degrees and nature of any underlying vascular injury.6,7 We sought to retrospectively review all the cases of craniocervical vascular injury seen over an eight-year period in order to better define the clinical presentation, the underlying vascular injury and success of endovascular treatment in this group of patients. This series is unique in focusing only on extradural vascular injuries of the head and neck and is the largest experience to date. Because the patient numbers were sufficient it was possible to examine the relation between clinical presentation and the underlying vascular finding. Knowing what to look for helps speed up the diagnosis and angiographic analysis in what can be a critical time if the patient is actively bleeding. Our endovascular management strategy focused on trapping injured vessel segments rather than maintaining vessel patency.
of trauma is also unique in that most admissions are the result of interpersonal violence rather than motor vehicle accident or fall. Penetrating injuries due to knife stab are also common, translating to a large number of patients presenting with vascular injury. All angiograms for craniocervical trauma done between January 2006 and December 2013 were retrospectively reviewed to determine the incidence of vascular injury requiring endovascular intervention. Records for the patients who had endovascular treatment were examined to record the presenting symptoms, nature of the vascular injury, treatment and outcome. Presenting symptoms were recorded as either active bleeding, an expanding hematoma or pulsatile mass. Active bleeding was either uncontrolled bleeding from a wound, the oral cavity or epistaxis. An expanding hematoma was a firm enlarging mass related to the site of injury. A pulsatile mass was not firm and in most cases was associated with a bruit or palpable thrill. The preliminary investigation in some patients was a CT angiogram or an ultrasound scan. However, all subjects eventually had a digital subtraction angiogram (DSA) that identified a traumatic vascular injury in
FCS Neurosurgery, University of Cape Town, Cape Town, South Africa
Method Groote Schuur Hospital is a Level 1 trauma referral center that sees a high volume of cases. The pattern
Corresponding author: Allan Taylor, Division of Neurosurgery, University of Cape Town, H53 OMB, Groote Schuur Hospital, Observatory, Cape Town 7925 South Africa. Email: [email protected]
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Results
Figure 1. Left common carotid artery angiogram of a 20-year-old male presenting with epistaxis after he was hit by a cricket ball in the face. Bleeding continued after bilateral PVA embolization of the internal maxillary and facial arteries. This image shows the subtle appearance of contrast leaking from a laceration of the left anterior ethmoidal branch of the ophthalmic artery. Bleeding was controlled by endoscopic surgical clipping of the vessel.
the craniocervical region. The angiograms were reviewed to describe the location of vascular injury, the nature of lesion, modality of treatment and angiographic outcome. Intradural vascular injuries were excluded and only extradural lesions were studied in detail. The dura rather than the skull was used to define intra and extracranial compartments as this is the anatomical boundary between the intracranial and extracranial circulation. The angiographic appearance was described as either vessel laceration, false aneurysms (FAs), fistula or vessel occlusion. A laceration was defined as contrast leakage from a vessel into a hollow viscus such as the pharynx or out of the wound (Figure 1). The appearance of a false aneurysm was contrast filing outside the vessel in a contained space but without any vessel wall (Figure 2) and a fistula as early venous filling through an arteriovenous channel (Figure 3). Our treatment protocol required selective angiography of the regional vessels in the injured territory as well as assessment of collateral flow where required. The aim of treatment when patients were actively bleeding or shocked was rapid closure of the injury by trapping. Proximal vessel occlusion was permitted when treating false aneurysms as long as the vessel was small and the occlusion could be performed close to the injury. Patients presenting with active bleeding and wound tamponade with dressings or an inflated foley catheter inserted into the wound had the tamponade removed immediately after embolization. This was often followed by control angiography to ensure that the injury was treated.
Digital subtraction angiograms were performed for trauma to the craniocervical region in 823 patients at Groote Schuur Hospital in the period from 1 January 2006 to 31 December 2013. One hundred and four patients were identified with extradural and/or intradural vascular injury and required endovascular treatment. Of the 61 patients with extradural vascular injury there were 70 identifiable vascular injuries on DSA. Of the treated patients, 60 (98.4%) were male and one (1.6%) was female. The mean patient age was 27 years and minimum age was 14 years with a maximum age of 62 years. The mechanism of injury was blunt in nine patients with six injuries from assault and three after motor vehicle accidents. All but one of these blunt injuries were associated with active bleeding or an expanding hematoma as a result of facial fractures. Of the 52 patients with penetrating injury, 47 were caused by a stab wound and five by gunshot. Twenty-three (37%) of the patients had an associated injury related to the primary trauma ranging from minor facial fractures to complete spinal cord injury due to penetration of the spinal canal by a knife. Thirty-nine patients presented acutely, usually within hours of injury and seven presented between 24 and 48 hours after sustaining the injury. Fifteen patients had a delayed presentation between three and 76 days following injury. The vertebral artery was the single vessel most likely to be injured with 15 injuries recorded. There were only three internal carotid artery injuries with the remaining injuries (52) distributed among the branches of the external carotid, ascending and deep cervical systems. Three patients had asymptomatic occlusion of the cervical vertebral (2) or carotid (1) artery although they were symptomatic from another injury. One of these patients with an acute vertebral closure at C2 vertebral level had proximal coil closure of the vessel. The other two patients had no intervention for the occluded vessel as retrograde thrombosis had occurred up to the origin of the injured vessel. Twenty-one patients presented with active bleeding, 24 with an expanding hematoma and 14 with a pulsatile mass. Although fistula and false aneurysm could be associated with any of these clinical findings an expanding hematoma was more likely to be associated with a false aneurysm, active bleeding with a laceration and a pulsatile mass with a fistula (Fisher exact test). Two of the patients presented with a different clinical picture, one had a retained knife blade causing a vessel laceration and the other had an acute subdural hematoma with bilateral middle meningeal dural fistulas after blunt trauma (Table 1). Sixty patients had successful endovascular treatment of their vascular lesion using a combination of polyvinyl alcohol, .035 fibred coils, detachable coils,
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Figure 2. A 22-year-old male presented with an expanding hematoma of the right neck after being stabbed. a) CT angiogram at C6 level showing contrast extravasation in the neck soft tissues. b) Left-sided vertebral artery angiogram showing good filling of the basilar circulation. c) Right vertebral angiography shows a large false aneurysm at C6 level. After treatment the false aneurysm has been trapped using a distal 0.035 fibred coil and a proximal detachable balloon. d) Poor choice of the initial coil size and position resulted in displacement of the coil into the false aneurysm lumen without consequence.
Figure 3. A 39-year-old male presented 2 months after blunt assault to the side of the head with a pulsatile mass over the right parotid area. a,b) An angiogram of the right internal maxillary artery (IMA) shows an aneurysmal pouch off the superficial temporal artery (STA) and fistula draining into the internal jugular vein. c) Coils were initially placed into the proximal STA followed by dilute n-BCA injection through a branch of the posterior auricular artery which still filled the aneurysmal pouch. d) Complete occlusion of the pouch and fistula was achieved with symptom resolution.
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Table 1. Clinical presentations and underlying angiographic findings.
Active bleeding Expanding hematoma Pulsatile mass Total
Fistula
False aneurysm
Laceration
Total
p value*
5 4 8 17
11 19 6 36
5 1 0 6
21 24 14 59**
0.018 0.029 0.015
*p values were calculated independently for each presenting symptom and angiographic finding using the Fisher exact test. Bold numbers in each row indicate the angiographic finding correlating with the clinical presentation. **Two patients with differing presentations, one with a retained knife blade and the other with subdural hematoma were excluded from this analysis.
Table 2. Arteries injured and angiographic findings. Vert L FA AVF Occl Total
2 2 9 9 15
Ca.
Fa.
IMa
STa
Lin.
ECa
SP
3
10
4 5
1 7 1
4 2
1 2 3
3
9
6
6
3
1 4
10
9
MMa
Tvs Ce
Ant Ce
Deep Ce
2
1 1
1
2
1
Ant Eth 1
2 2
2
1
L, laceration; FA, false aneurysm; AVF, arteriovenous fistula; Occl, occluded vessel; Vert, vertebral artery; CA, carotid artery; Fa, facial artery; IMA, internal maxilliary artery; STA, superficial temporal artery; Lin, lingual artery; ECa, external carotid artery; SP, sphenopalatine artery; MMa, middle meningeal artery; Tvs Ce, transverse cervical artery; Ant Ce, anterior cervical artery; Deep Ce, deep cervical artery; Ant Eth, anterior ethmoidal artery.
detachable balloons and n-butyl cyanoacrylate (n-BCA). One patient required surgery for active bleeding from a lacerated anterior ethmoidal artery after blunt trauma. The ethmoidal vessel was successfully clipped with control of the patient’s bleeding. Of the 70 recorded vessel injuries (Table 2) in only seven patients was the injured parent artery preserved during treatment. Seventeen patients with a false aneurysm or laceration had proximal vessel closure. Fortytwo had trapping of the lesion either by distal and proximal coil or balloon placement or n-BCA embolization. Three patients had a silent vessel thrombosis (all had other symptomatic injuries) and one small AVF of the left external carotid artery to jugular vein was missed at the time of injury and only detected on image review for the study. One patient had a treatment-related morbidity when a covered stent was placed to cross a large false aneurysm of the cervical internal carotid artery. Although antiplatelet medication was commenced after successful stenting the patient developed an ipsilateral caudate infarct most likely due to embolism. Two technical complications occurred without any clinical consequence. In one patient a fibred 0.035 free coil was displaced into a large C6 vertebral artery false aneurysm during coil placement. The aneurysm was subsequently trapped using another distal coil and a proximal balloon. In another patient with a deep cervical to internal jugular fistula some nBCA progressed into the jugular vein without occlusion of the vein occurring.
Discussion Incidence The incidence of vascular injury in the extracranial head and neck vessels varies depending on the mechanism of injury. With blunt trauma injury occurs mostly to the carotid and vertebral arteries and the reported incidence of injury is between 1% and 3%.8,9 With penetrating trauma the incidence of injury is higher and a previous study at our institution reported a 19% incidence of vascular trauma.4. In this study the overall incidence of vascular injury in patients who had DSA was 8% despite 85% having a penetrating injury. This study probably underestimates the incidence of injury because we did not include patients who had immediate surgical exploration or had surgery after CTA alone. Craniocervical vascular injury in military casualties was reported to be 26.2 % in a study by Bell et al. but this study also included intracranial vessel injuries.2 When intracranial injuries are excluded the incidence of vessel injury was 17.6%, which is similar to reported civilian series.
Pathology There are four reported mechanisms of vessel injury in blunt trauma: hyperextension and rotation, direct vascular blow and intraoral trauma, which result in vessel dissection or direct laceration from bony fracture.3 Vessel dissection is more likely to occur with larger vessels such as the carotid and vertebral arteries and can
112 result in embolic or flow-related distal ischemia.5 The dissection is the result of either intimal stretching and disruption or injury to the internal elastic lamina.10 In our series the mechanism of blunt injury was vessel disruption associated with facial fractures except in one patient who developed a vertebral artery to vertebral venous plexus fistula. This is unusual and is probably because the mechanism of blunt injury in this series was mostly low velocity assault rather than the high velocity motor vehicle accident likely to result in dissection of large vessels. Biffl et al. reported that motor vehicle accidents account for up to 70% of blunt vessel dissecting type injury.11 This study is unique in having such a high incidence of penetrating injury. In a recent study by Kansagra et al. reviewing 100 traumatic arterial injuries, 81% were related to blunt trauma.12 Penetrating trauma leads to disruption of the vessel wall. All the vascular layers, intima, media and adventitia, could be penetrated leading to profuse bleeding. Formation of a clot with associated muscle spasm may taper the active bleeding leading to a false aneurysm. There is a possibility of a tangential penetrating injury that may not penetrate the internal elastic lamina or intima. Bleeding from the vasa vasorum will lead to a dissecting process with resultant luminal stenosis, clot embolism and even complete occlusion. A fistula forms when there is simultaneous disruption of an artery and nearby vein. Blood will flow from the high-pressure artery along the penetrating tract into the low-pressure vein. With time this arteriovenous (AV) channel will endothelialize forming a defined lumen but in the early stage it is only a path through soft tissues. This is an important consideration when treating these lesions. Mature fistulas allow embolic occlusion of the AV channel with preservation of the arterial lumen. In acute lesions the disrupted soft tissues of the injury tract may be further injured by attempts at embolization resulting in fistula persistence or worse bleeding.
Angioarchitecture It is difficult to make comparisons between published series on traumatic craniocervical vascular injuries as intracranial and extracranial injuries were often analyzed together and various terms were used to describe lesions such as traumatic aneurysm and dissection without qualifying how these were angiographically identified.2,12 We sought to focus on extracranial injuries and restrict the description of lesions to what was seen on angiography. In the acute phase vessel spasm or compression by hematoma can be mistaken for dissection.
Interventional Neuroradiology 21(1) most likely to be from a vessel laceration. Laceration with bleeding directly into the injury tract or body cavity can be difficult to visualize on DSA so it is important in active bleeding to obtain good quality images and examine them carefully. In the case of an expanding hematoma a false aneurysm is the most likely finding as more blood escapes the vessel and the surrounding clot enlarges by compressing surrounding soft tissue. When a pulsatile mass is found, particularly if there is a bruit, an AVF can be expected although this finding can also occur with false aneurysms that have a large circulating cavity with a thin wall of surrounding hematoma.
Treatment In their series of wartime traumatic vascular injuries Bell et al. reported only two superficial temporal artery aneurysms with all other injuries being carotid, vertebral or intracranial vessels.2 No comment was made regarding collateral circulation and emphasis was placed on preservation or reconstruction of the injured vessel lumen. Eight patients who required endovascular treatment for cerebrovascular injury in a civilian series reported by Diaz-Daza et al. also had efforts made to preserve the injured vessel lumen.13 Both series used procedural heparin and stents in order to achieve this. Our strategy was rather to trap injured vessels and stop the risk of further bleeding or airway compression as rapidly as possible. This strategy was also effective in preventing symptom recurrence whereas in Bell et al.’s study nine out of 24 patients treated endovascularly required retreatment.2 There were 15 patients with vertebral artery injury in our study and the vessel lumen was preserved in only one patient who had injury to the dominant vessel at C6 with a small false aneurysm that was coiled only. Control angiography the following day showed the aneurysm remained closed and the vertebral artery was open. Of the three carotid artery injuries in the study, one patient with good collateral circulation had trapping of a false aneurysm with a balloon. The two other patients had preservation of the carotid because of inadequate collateral flow, one using a covered stent and the other with coil placement alone into a false aneurysm. The placement of the covered stent resulted in the only complication seen which was an ipsilateral small stroke despite use of antiplatelet medication. Vessel occlusion in the external carotid system was well-tolerated in all of our patients without any ischemia in a distal territory as collateral circulation is well developed in this system. Routine heparin use during procedures was also avoided because of the risk of increasing bleeding.
Clinical correlation No previous study has tried to correlate the clinical presenting features with the underlying angiographic lesion. Although no presentation was specific for the underlying angiographic lesion active bleeding was
Conclusion In this series of 61 patients with extracranial craniocervical vascular injuries clinical presentation with either active bleeding, expanding hematoma or pulsatile mass
Ssenyonga et al. was related to the respective angiographic findings of vessel laceration, false aneurysm and arteriovenous fistula. Endovascular treatment with emphasis on vessel occlusion rather than preservation was successful in all cases except one which required surgical vessel ligation. Funding This research received no specific grant from any funding agency in the public, commercial or not-for-profit sectors.
Conflict of interest The authors declare no conflict of interest.
References 1. Amirjamshidi A, Abbassioun K and Rahmat H. Traumatic aneurysms and arteriovenous fistulas of the extracranial vessels in war injuries. Surg Neurol. 2000; 53: 136–145. doi: 10.1016/S0090-3019(99)00181-0. 2. Bell RS, Alexander H, Roberts R, et al. Wartime traumatic aneurysms: acute presentation, diagnosis, and multimodal treatment of 64 craniocervical arterial injuries. Neurosurgery. 2010; 66: 66–79. doi: 10.1227/ 01.NEU.0000361285.50218.A8. 3. Fusco MR and Harrigan MR. Cerebrovascular dissections: a review. Part II: Blunt cerebrovascular injury. Neurosurgery. 2011; 68: 517–530. doi: 10.1227/ NEU.0b013e3181fe2fda. 4. Van Waes OJ, Cheriex KC, Navsaria PA, et al. Management of penetrating neck injuries. Br. J Surg. 2012; 99(Suppl): 149–154. doi: 10.1002/bjs.7733. 5. Scheid R, Zimmer C, Schroeter ML, et al. The clinical spectrum of blunt cerebrovascular injury. Neurologist. 2006; 12(5): 255–262. doi: 10.1097/01.nrl.0000243977.17242.ab.
113 6. Krings T, Geibprasert S and Lasjaunias PL. Cerebrovascular trauma. Eur Radiol. 2008; 18: 1531–1545. doi: 10.1007/s00330-008-0915-z. 7. Radvany MG, Gailloud PG and Gregg L. Endovascular management of neurosvascular arterial injuries in the face and neck. Neurosurg Clin N Am. 2012; 23(1): 123–131. doi: 10.1016/j.nec.2011.09.009. 8. Hughes KM, Collier B, Greene KA, et al. Traumatic carotid artery dissection: a significant incidental finding. Am Surg. 2000; 66(11): 1023–1027. 9. Stein DM, Boswell S, Sliker CW, et al. Blunt cerebrovascular injuries: does treatment always matter? J Trauma. 2009 66(1): 132–143; discussion 143-144. doi: 10.1097/ TA.0b013e318142d146. 10. Biffl WL, Ray Jr, CE, Moore EE, et al. Treatmentrelated outcomes from blunt cerebrovascular injuries: importance of routine follow-up arteriography. Ann Surg. 2002; 235(5): 699–706; discussion 706–707. doi: 10.1097/00000658-200205000-00012. 11. Biffl WL, Moore EE, Ryu RK, et al. The unrecognized epidemic of blunt carotid arterial injuries: early diagnosis improves neurologic outcome. Ann Surg. 1998; 228(4): 462–470. doi: 10.1097/00000658-199810000-00003. 12. Kansagra AP, Cooke DL, English JD, et al. Current trends in endovascular management of traumatic cerebrovascular injury. J NeuroIntervent Surg. 2014; 6: 47–50. doi: 10.1136/neurintsurg-2012-010605. 13. Diaz-Daza O, Arraiza FJ, Barkley JM, et al. Endovascular therapy of traumatic vascular lesions of the head and neck. Cardiovasc Intervent Radiol. 2003; 26: 213–221. doi: 10.1007/s00270-002-2619-0.
Head and neck neurovascular trauma: Clinical and angiographic correlation
Interventional Neuroradiology 2015, Vol. 21(1) 108–113 ! The Author(s) 2015 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav DOI: 10.1177/1591019915576666 ine.sagepub.com
Peter Kato Ssenyonga, David Le Feuvre and Allan Taylor
Abstract A retrospective review of all angiograms done for craniocervical trauma, over an eight-year period at Groote Schuur Hospital identified 61 patients out of 823 angiographically studied who had extradural vascular injury and required endovascular treatment. Multiple lesions were identified in nine (14,8%) patients and associated injuries were found in 23 patients (37%). The mechanism of injury was blunt in nine (14.8%) patients and penetrating in 52 (85.2%). There was a statistically significant correlation between the presenting clinical feature and the underlying angiographic lesion. Patients with active bleeding were more likely to have a vessel laceration, an expanding hematoma was associated with false aneurysm and a pulsatile mass with arteriovenous fistula. Endovascular treatment with emphasis on vessel occlusion rather than preservation was successful in all cases except one which required surgical vessel ligation.
Keywords Head and neck, neurovascular, trauma, false aneurysm, arteriovenous fistula
Introduction Blunt and penetrating craniocervical injury is associated with vascular injury in up to 3% and 20% of cases respectively.1–4 Vessel injury can lead to acute hemodynamic and airway compromise from bleeding, as well as neurological deficit from embolism or flow limitation.5 There is a spectrum of clinical presentation and varying degrees and nature of any underlying vascular injury.6,7 We sought to retrospectively review all the cases of craniocervical vascular injury seen over an eight-year period in order to better define the clinical presentation, the underlying vascular injury and success of endovascular treatment in this group of patients. This series is unique in focusing only on extradural vascular injuries of the head and neck and is the largest experience to date. Because the patient numbers were sufficient it was possible to examine the relation between clinical presentation and the underlying vascular finding. Knowing what to look for helps speed up the diagnosis and angiographic analysis in what can be a critical time if the patient is actively bleeding. Our endovascular management strategy focused on trapping injured vessel segments rather than maintaining vessel patency.
of trauma is also unique in that most admissions are the result of interpersonal violence rather than motor vehicle accident or fall. Penetrating injuries due to knife stab are also common, translating to a large number of patients presenting with vascular injury. All angiograms for craniocervical trauma done between January 2006 and December 2013 were retrospectively reviewed to determine the incidence of vascular injury requiring endovascular intervention. Records for the patients who had endovascular treatment were examined to record the presenting symptoms, nature of the vascular injury, treatment and outcome. Presenting symptoms were recorded as either active bleeding, an expanding hematoma or pulsatile mass. Active bleeding was either uncontrolled bleeding from a wound, the oral cavity or epistaxis. An expanding hematoma was a firm enlarging mass related to the site of injury. A pulsatile mass was not firm and in most cases was associated with a bruit or palpable thrill. The preliminary investigation in some patients was a CT angiogram or an ultrasound scan. However, all subjects eventually had a digital subtraction angiogram (DSA) that identified a traumatic vascular injury in
FCS Neurosurgery, University of Cape Town, Cape Town, South Africa
Method Groote Schuur Hospital is a Level 1 trauma referral center that sees a high volume of cases. The pattern
Corresponding author: Allan Taylor, Division of Neurosurgery, University of Cape Town, H53 OMB, Groote Schuur Hospital, Observatory, Cape Town 7925 South Africa. Email: [email protected]
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Results
Figure 1. Left common carotid artery angiogram of a 20-year-old male presenting with epistaxis after he was hit by a cricket ball in the face. Bleeding continued after bilateral PVA embolization of the internal maxillary and facial arteries. This image shows the subtle appearance of contrast leaking from a laceration of the left anterior ethmoidal branch of the ophthalmic artery. Bleeding was controlled by endoscopic surgical clipping of the vessel.
the craniocervical region. The angiograms were reviewed to describe the location of vascular injury, the nature of lesion, modality of treatment and angiographic outcome. Intradural vascular injuries were excluded and only extradural lesions were studied in detail. The dura rather than the skull was used to define intra and extracranial compartments as this is the anatomical boundary between the intracranial and extracranial circulation. The angiographic appearance was described as either vessel laceration, false aneurysms (FAs), fistula or vessel occlusion. A laceration was defined as contrast leakage from a vessel into a hollow viscus such as the pharynx or out of the wound (Figure 1). The appearance of a false aneurysm was contrast filing outside the vessel in a contained space but without any vessel wall (Figure 2) and a fistula as early venous filling through an arteriovenous channel (Figure 3). Our treatment protocol required selective angiography of the regional vessels in the injured territory as well as assessment of collateral flow where required. The aim of treatment when patients were actively bleeding or shocked was rapid closure of the injury by trapping. Proximal vessel occlusion was permitted when treating false aneurysms as long as the vessel was small and the occlusion could be performed close to the injury. Patients presenting with active bleeding and wound tamponade with dressings or an inflated foley catheter inserted into the wound had the tamponade removed immediately after embolization. This was often followed by control angiography to ensure that the injury was treated.
Digital subtraction angiograms were performed for trauma to the craniocervical region in 823 patients at Groote Schuur Hospital in the period from 1 January 2006 to 31 December 2013. One hundred and four patients were identified with extradural and/or intradural vascular injury and required endovascular treatment. Of the 61 patients with extradural vascular injury there were 70 identifiable vascular injuries on DSA. Of the treated patients, 60 (98.4%) were male and one (1.6%) was female. The mean patient age was 27 years and minimum age was 14 years with a maximum age of 62 years. The mechanism of injury was blunt in nine patients with six injuries from assault and three after motor vehicle accidents. All but one of these blunt injuries were associated with active bleeding or an expanding hematoma as a result of facial fractures. Of the 52 patients with penetrating injury, 47 were caused by a stab wound and five by gunshot. Twenty-three (37%) of the patients had an associated injury related to the primary trauma ranging from minor facial fractures to complete spinal cord injury due to penetration of the spinal canal by a knife. Thirty-nine patients presented acutely, usually within hours of injury and seven presented between 24 and 48 hours after sustaining the injury. Fifteen patients had a delayed presentation between three and 76 days following injury. The vertebral artery was the single vessel most likely to be injured with 15 injuries recorded. There were only three internal carotid artery injuries with the remaining injuries (52) distributed among the branches of the external carotid, ascending and deep cervical systems. Three patients had asymptomatic occlusion of the cervical vertebral (2) or carotid (1) artery although they were symptomatic from another injury. One of these patients with an acute vertebral closure at C2 vertebral level had proximal coil closure of the vessel. The other two patients had no intervention for the occluded vessel as retrograde thrombosis had occurred up to the origin of the injured vessel. Twenty-one patients presented with active bleeding, 24 with an expanding hematoma and 14 with a pulsatile mass. Although fistula and false aneurysm could be associated with any of these clinical findings an expanding hematoma was more likely to be associated with a false aneurysm, active bleeding with a laceration and a pulsatile mass with a fistula (Fisher exact test). Two of the patients presented with a different clinical picture, one had a retained knife blade causing a vessel laceration and the other had an acute subdural hematoma with bilateral middle meningeal dural fistulas after blunt trauma (Table 1). Sixty patients had successful endovascular treatment of their vascular lesion using a combination of polyvinyl alcohol, .035 fibred coils, detachable coils,
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Figure 2. A 22-year-old male presented with an expanding hematoma of the right neck after being stabbed. a) CT angiogram at C6 level showing contrast extravasation in the neck soft tissues. b) Left-sided vertebral artery angiogram showing good filling of the basilar circulation. c) Right vertebral angiography shows a large false aneurysm at C6 level. After treatment the false aneurysm has been trapped using a distal 0.035 fibred coil and a proximal detachable balloon. d) Poor choice of the initial coil size and position resulted in displacement of the coil into the false aneurysm lumen without consequence.
Figure 3. A 39-year-old male presented 2 months after blunt assault to the side of the head with a pulsatile mass over the right parotid area. a,b) An angiogram of the right internal maxillary artery (IMA) shows an aneurysmal pouch off the superficial temporal artery (STA) and fistula draining into the internal jugular vein. c) Coils were initially placed into the proximal STA followed by dilute n-BCA injection through a branch of the posterior auricular artery which still filled the aneurysmal pouch. d) Complete occlusion of the pouch and fistula was achieved with symptom resolution.
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Table 1. Clinical presentations and underlying angiographic findings.
Active bleeding Expanding hematoma Pulsatile mass Total
Fistula
False aneurysm
Laceration
Total
p value*
5 4 8 17
11 19 6 36
5 1 0 6
21 24 14 59**
0.018 0.029 0.015
*p values were calculated independently for each presenting symptom and angiographic finding using the Fisher exact test. Bold numbers in each row indicate the angiographic finding correlating with the clinical presentation. **Two patients with differing presentations, one with a retained knife blade and the other with subdural hematoma were excluded from this analysis.
Table 2. Arteries injured and angiographic findings. Vert L FA AVF Occl Total
2 2 9 9 15
Ca.
Fa.
IMa
STa
Lin.
ECa
SP
3
10
4 5
1 7 1
4 2
1 2 3
3
9
6
6
3
1 4
10
9
MMa
Tvs Ce
Ant Ce
Deep Ce
2
1 1
1
2
1
Ant Eth 1
2 2
2
1
L, laceration; FA, false aneurysm; AVF, arteriovenous fistula; Occl, occluded vessel; Vert, vertebral artery; CA, carotid artery; Fa, facial artery; IMA, internal maxilliary artery; STA, superficial temporal artery; Lin, lingual artery; ECa, external carotid artery; SP, sphenopalatine artery; MMa, middle meningeal artery; Tvs Ce, transverse cervical artery; Ant Ce, anterior cervical artery; Deep Ce, deep cervical artery; Ant Eth, anterior ethmoidal artery.
detachable balloons and n-butyl cyanoacrylate (n-BCA). One patient required surgery for active bleeding from a lacerated anterior ethmoidal artery after blunt trauma. The ethmoidal vessel was successfully clipped with control of the patient’s bleeding. Of the 70 recorded vessel injuries (Table 2) in only seven patients was the injured parent artery preserved during treatment. Seventeen patients with a false aneurysm or laceration had proximal vessel closure. Fortytwo had trapping of the lesion either by distal and proximal coil or balloon placement or n-BCA embolization. Three patients had a silent vessel thrombosis (all had other symptomatic injuries) and one small AVF of the left external carotid artery to jugular vein was missed at the time of injury and only detected on image review for the study. One patient had a treatment-related morbidity when a covered stent was placed to cross a large false aneurysm of the cervical internal carotid artery. Although antiplatelet medication was commenced after successful stenting the patient developed an ipsilateral caudate infarct most likely due to embolism. Two technical complications occurred without any clinical consequence. In one patient a fibred 0.035 free coil was displaced into a large C6 vertebral artery false aneurysm during coil placement. The aneurysm was subsequently trapped using another distal coil and a proximal balloon. In another patient with a deep cervical to internal jugular fistula some nBCA progressed into the jugular vein without occlusion of the vein occurring.
Discussion Incidence The incidence of vascular injury in the extracranial head and neck vessels varies depending on the mechanism of injury. With blunt trauma injury occurs mostly to the carotid and vertebral arteries and the reported incidence of injury is between 1% and 3%.8,9 With penetrating trauma the incidence of injury is higher and a previous study at our institution reported a 19% incidence of vascular trauma.4. In this study the overall incidence of vascular injury in patients who had DSA was 8% despite 85% having a penetrating injury. This study probably underestimates the incidence of injury because we did not include patients who had immediate surgical exploration or had surgery after CTA alone. Craniocervical vascular injury in military casualties was reported to be 26.2 % in a study by Bell et al. but this study also included intracranial vessel injuries.2 When intracranial injuries are excluded the incidence of vessel injury was 17.6%, which is similar to reported civilian series.
Pathology There are four reported mechanisms of vessel injury in blunt trauma: hyperextension and rotation, direct vascular blow and intraoral trauma, which result in vessel dissection or direct laceration from bony fracture.3 Vessel dissection is more likely to occur with larger vessels such as the carotid and vertebral arteries and can
112 result in embolic or flow-related distal ischemia.5 The dissection is the result of either intimal stretching and disruption or injury to the internal elastic lamina.10 In our series the mechanism of blunt injury was vessel disruption associated with facial fractures except in one patient who developed a vertebral artery to vertebral venous plexus fistula. This is unusual and is probably because the mechanism of blunt injury in this series was mostly low velocity assault rather than the high velocity motor vehicle accident likely to result in dissection of large vessels. Biffl et al. reported that motor vehicle accidents account for up to 70% of blunt vessel dissecting type injury.11 This study is unique in having such a high incidence of penetrating injury. In a recent study by Kansagra et al. reviewing 100 traumatic arterial injuries, 81% were related to blunt trauma.12 Penetrating trauma leads to disruption of the vessel wall. All the vascular layers, intima, media and adventitia, could be penetrated leading to profuse bleeding. Formation of a clot with associated muscle spasm may taper the active bleeding leading to a false aneurysm. There is a possibility of a tangential penetrating injury that may not penetrate the internal elastic lamina or intima. Bleeding from the vasa vasorum will lead to a dissecting process with resultant luminal stenosis, clot embolism and even complete occlusion. A fistula forms when there is simultaneous disruption of an artery and nearby vein. Blood will flow from the high-pressure artery along the penetrating tract into the low-pressure vein. With time this arteriovenous (AV) channel will endothelialize forming a defined lumen but in the early stage it is only a path through soft tissues. This is an important consideration when treating these lesions. Mature fistulas allow embolic occlusion of the AV channel with preservation of the arterial lumen. In acute lesions the disrupted soft tissues of the injury tract may be further injured by attempts at embolization resulting in fistula persistence or worse bleeding.
Angioarchitecture It is difficult to make comparisons between published series on traumatic craniocervical vascular injuries as intracranial and extracranial injuries were often analyzed together and various terms were used to describe lesions such as traumatic aneurysm and dissection without qualifying how these were angiographically identified.2,12 We sought to focus on extracranial injuries and restrict the description of lesions to what was seen on angiography. In the acute phase vessel spasm or compression by hematoma can be mistaken for dissection.
Interventional Neuroradiology 21(1) most likely to be from a vessel laceration. Laceration with bleeding directly into the injury tract or body cavity can be difficult to visualize on DSA so it is important in active bleeding to obtain good quality images and examine them carefully. In the case of an expanding hematoma a false aneurysm is the most likely finding as more blood escapes the vessel and the surrounding clot enlarges by compressing surrounding soft tissue. When a pulsatile mass is found, particularly if there is a bruit, an AVF can be expected although this finding can also occur with false aneurysms that have a large circulating cavity with a thin wall of surrounding hematoma.
Treatment In their series of wartime traumatic vascular injuries Bell et al. reported only two superficial temporal artery aneurysms with all other injuries being carotid, vertebral or intracranial vessels.2 No comment was made regarding collateral circulation and emphasis was placed on preservation or reconstruction of the injured vessel lumen. Eight patients who required endovascular treatment for cerebrovascular injury in a civilian series reported by Diaz-Daza et al. also had efforts made to preserve the injured vessel lumen.13 Both series used procedural heparin and stents in order to achieve this. Our strategy was rather to trap injured vessels and stop the risk of further bleeding or airway compression as rapidly as possible. This strategy was also effective in preventing symptom recurrence whereas in Bell et al.’s study nine out of 24 patients treated endovascularly required retreatment.2 There were 15 patients with vertebral artery injury in our study and the vessel lumen was preserved in only one patient who had injury to the dominant vessel at C6 with a small false aneurysm that was coiled only. Control angiography the following day showed the aneurysm remained closed and the vertebral artery was open. Of the three carotid artery injuries in the study, one patient with good collateral circulation had trapping of a false aneurysm with a balloon. The two other patients had preservation of the carotid because of inadequate collateral flow, one using a covered stent and the other with coil placement alone into a false aneurysm. The placement of the covered stent resulted in the only complication seen which was an ipsilateral small stroke despite use of antiplatelet medication. Vessel occlusion in the external carotid system was well-tolerated in all of our patients without any ischemia in a distal territory as collateral circulation is well developed in this system. Routine heparin use during procedures was also avoided because of the risk of increasing bleeding.
Clinical correlation No previous study has tried to correlate the clinical presenting features with the underlying angiographic lesion. Although no presentation was specific for the underlying angiographic lesion active bleeding was
Conclusion In this series of 61 patients with extracranial craniocervical vascular injuries clinical presentation with either active bleeding, expanding hematoma or pulsatile mass
Ssenyonga et al. was related to the respective angiographic findings of vessel laceration, false aneurysm and arteriovenous fistula. Endovascular treatment with emphasis on vessel occlusion rather than preservation was successful in all cases except one which required surgical vessel ligation. Funding This research received no specific grant from any funding agency in the public, commercial or not-for-profit sectors.
Conflict of interest The authors declare no conflict of interest.
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